768 Sentences With "murine" | Random Sentence Generator

These findings were replicated in subsequent experiments with four other murine breeds.

But as murine middle age approached, at around the animals' first birthdays, differences began to manifest themselves.

Work in mice has proved that early stimulation of their immune systems protects against a murine version of ALL.

Flea-borne typhus, also called endemic or murine typhus, is transmitted to humans when they are bitten by fleas infected with Rickettsia typhi or R. felis.

To investigate, he and his team infected one group of mice with a murine influenza virus, and the other with Listeria monocytogenes, a bacterium that causes food poisoning.

Not much is currently known about what all those squeaks mean, but Coffey hopes that once enough biologists compile enough calls, a sort of murine "Rosetta Stone" will emerge.

Once scientists took their murine turn, the benefits of continuing down that road were self-reinforcing; the more they learned to do with mice, the more they wanted to do.

Cases of the flea-borne form of the disease—called endemic or murine typhus—are seen in the area every year, according to the Los Angeles County Department of Public Health.

But in order to study how that activity affects human brains at the cellular level, researchers at the University of Oregon managed to put murine brains into a somewhat equivalent state.

Indeed, the next project in his lab is to explore whether clearing senescent cells from the brains of mice that are already suffering from the murine version of Alzheimer's might allow their already damaged brains to recover.

On the other hand, early infection with a different common pathogen, Yersinia pseudotuberculosis, affects murine immune systems in a way that leaves mice more open to subsequent attack, rather than less so—the reverse of the hygiene hypothesis.

A nice example which the two researchers found of the hygiene hypothesis at work is that stopping laboratory mice being infected with murine cytomegalovirus, which is common in their wild kin, damages their immune response to a host of other pathogens, bacterial as well as viral.

He then monitored all four groups for signs of murine multiple sclerosis, such as loss of tail tone, unsteady gait and limb paralysis, When the experiment began, he and his colleagues expected that the disease would progress more slowly in the experimental group than in the control groups, and that its rate of progress in all three control groups would be the same, since any effect of exposure to ultraviolet would be negated by the sunscreen.

CD300lf has been shown to function as the primary receptor for murine norovirus in mice, Human norovirus does not use the same receptor in viral entry. Human and murine CD300lf proteins have about 59% identity in their immunoglobulin domains, with most of that variation occurring in parts of the protein called CDR3 and the CC’loop. Murine norovirus binds to a cleft between these domains. The differences between murine and human CD300lf contribute to murine norovirus host species restriction, as incorporating murine CD300lf into human cells makes them susceptible to infection by the murine virus.

Sca-1 is a murine hematopoietic stem cell antigen. Lin is a series of lineage marker antigens that identify mature murine blood cells.

Antibodies may also referred to as murine, chimeric, humanized or human. Murine antibodies are from mice and carry a risk of immune reaction. Chimeric antibodies attempt to reduce murine antibodies' immunogenicity by replacing part of the antibody with the corresponding human counterpart, known as the constant region. Humanized antibodies are almost completely human; only the complementarity determining regions of the variable regions are derived from murine sources.

Agouti signaling protein (ASP) is the human homologue of murine agouti. It is encoded by the human agouti gene on chromosome 20 and is a protein consisting of 132 amino acids. It is expressed much more broadly than murine agouti and is found in adipose tissue, pancreas, testes, and ovaries, whereas murine agouti is solely expressed in melanocytes. ASP has 85% similarity to the murine form of agouti.

PAK3 was initially cloned from a murine fibroblast cDNA library and from a murine embryo cDNA library. Like other group I PAKs, PAK3 is stimulated by activated Cdc42 and Rac1.

Murine UL16 binding protein-like transcript (MULT-1) is a murine cell surface glycoprotein encoded by MULT-1 gene located on murine chromosome 10. MULT-1 is related to MHC class I and is composed of α1α2 domain, a transmembrane segment, and a large cytoplasmic domain. MULT-1 functions as a stress-induced ligand for NKG2D receptor.

A recent study detected a murine astrovirus in laboratory mice held at more than half of the US and Japanese institutes investigated. Murine astrovirus was found in nine mice strains, including NSG, NOD-SCID, NSG-3GS, C57BL6-Timp-3−/−, uPA- NOG, B6J, ICR, Bash2, and BALB/C, with various degrees of prevalence. The pathogenicity of the murine astrovirus was not known.

The function of ASP differs to murine agouti. ASP effects the quality of hair pigmentation whereas murine agouti controls the distribution of pigments that determine coat color. ASP has neuroendocrine functions consistent with murine agouti, as it agonizes via AgRP neurons in the hypothalamus and antagonizes MSH at MC4Rs which reduce satiety signals. AgRP acts as an appetite stimulator and increases appetite while decreasing metabolism.

However, cytarabine treatment was only effective for herpesvirus infection in a murine model.

Murine coronavirus (M-CoV) is a species of coronavirus which infects mice. It is an enveloped, positive-sense, single-stranded RNA virus which enters its host cell by binding to the CEACAM1 receptor. It has, like other coronaviruses from genus Betacoronavirus, subgenus Embecovirus, an additional hemagglutinin esterase (HE) gene. The Murine coronavirus is a coronavirus that causes an epidemic murine illness with high mortality, especially among colonies of laboratory mice.

The murine Mta3 gene contains nine transcripts, six of which are predicted to code proteins ranging from 251 amino acids to 591 amino acids while one transcript codes for 40 amino acids polypeptide. The murine Mta3 gene contains two predicted non-coding RNAs.

This gene was discovered using a non- virulent protein of murine leukemia virus. This protein will block replication of some murine leukemia virus strains following reverse transcription. The restriction of the virus depends on the interaction of the protein and the invading virus.

A expressional decrease of KDM4C was found during cardiac differentation of murine embryonic stem cells.

For example, lymphocyte T-cell immunomodulator inhibits viral growth in the murine model of influenza.

A truncated murine NLRC4 was the first member of this family whose crystal structure was solved.

Vasorelaxant and hypotensive activity in vitro and in vivo in a murine model by intravenous infusion.

The murine homolog of EMR1, F4/80, is a well- known and widely used marker of murine macrophage populations. The N-terminal fragment (NTF) of EMR1 contains 4-6 Epidermal Growth Factor-like (EGF-like) domains in human and 4-7 EGF-like domains in the mouse.

In addition, NS2 is required for efficient infection in its natural murine host, but is dispensable in experimental infection in human cell lines. Although not fully understood, in murine A9 fibroblasts NS2 interacts with nuclear export factor Crm1 resulting in efficient nuclear egress of progeny virions.

DNMT3A is a 130 kDa protein encoded by 23 exons found on chromosome 2p23 in humans. There exists a 98% homology between human and murine homologues. Due to splicing, there exist two main murine RNA isoforms, Dnmt3a1 and Dnmt3a2. These isoforms exist in different cell types.

To reduce murine antibody immunogenicity (attacks by the immune system against the antibody), murine molecules were engineered to remove immunogenic content and to increase immunologic efficiency. This was initially achieved by the production of chimeric (suffix -ximab) and humanized antibodies (suffix -zumab). Chimeric antibodies are composed of murine variable regions fused onto human constant regions. Taking human gene sequences from the kappa light chain and the IgG1 heavy chain results in antibodies that are approximately 65% human.

Coronaviruses infect laboratory animals. Mouse hepatitis virus (MHV), which is a member of the species Murine coronavirus, causes an epidemic murine illness with high mortality, especially among colonies of laboratory mice. Prior to the discovery of SARS-CoV, MHV was the best-studied coronavirus both in vivo and in vitro as well as at the molecular level. Some strains of MHV cause a progressive demyelinating encephalitis in mice which has been used as a murine model for multiple sclerosis.

Feb 2017 Co-blockade of TIGIT and PD-1 pathways elicits tumor rejection in preclinical murine models.

KDM6B was found to be expressional increased during cardiac and endothelial differentation of murine embryonic stem cells.

After the stimulation of interferon gamma, GPB2 murine is expressed in the innate and adaptive immune cells.

CD34 is expressed in roughly 20% of murine hematopoietic stem cells, and can be stimulated and reversed.

In 1900, he was born in Kikuchi District, Kumamoto Prefecture. He graduated from Kumamoto Medical School in 1924 and entered the Kyushu Sanatorium. In 1934, he became a Ph.D. for his study on murine leprosy. He found a large house where 23% of mice were infected with murine leprosy.

KSL cells are an early form of mouse/murine hematopoietic stem cells. Characteristics are Kit (+), Sca-1 (+) and Lin (-). HSCs [Hematopoietic stem cells] in murine cultures show phenotypic markers as being CD34-, CD150+, and Flt3- for LTR [long-term reconstitution]. Kit (CD117) is the receptor of Stem Cell Factor.

Initially, murine antibodies were obtained by hybridoma technology, for which Jerne, Köhler and Milstein received a Nobel prize. However the dissimilarity between murine and human immune systems led to the clinical failure of these antibodies, except in some specific circumstances. Major problems associated with murine antibodies included reduced stimulation of cytotoxicity and the formation complexes after repeated administration, which resulted in mild allergic reactions and sometimes anaphylactic shock. Hybridoma technology has been replaced by recombinant DNA technology, transgenic mice and phage display.

BMP-7 has been shown in murine animal models to reverse the loss of glomeruli due to sclerosis.

LXR agonists are effective for treatment of murine models of atherosclerosis, diabetes, anti-inflammation, Alzheimer's disease, and cancer.

Gross was a major proponent of the possibility that some cancers can be caused by viruses and began a long search for viral causes of murine leukemia. In the course of these studies, he isolated the Gross murine leukemia virus strain as well as the first polyomavirus, so named for its proclivity to cause cancers in multiple tissue types. Gross murine leukemia virus is a retrovirus whose counterpart in humans is human T cell lymphotropic virus I (HTLV-I), while murine polyomavirus is closely related to the human Merkel cell polyomavirus that causes most forms of Merkel cell carcinoma. Thus, Gross identified two critical animal viruses that serve as models for viruses causing cancer in humans.

Sphingulus is a genus of moths in the family Sphingidae, containing only one species, Sphingulus mus, the murine hawkmoth.

There are two types, human (hMICL) and murine (mMICL). Human MICL is expressed as a monomer primarily on myeloid cells, including granulocytes, monocytes, macrophages and dendritic cells. Murine MICL is expressed as dimer on granulocytes, monocytes but also on B lymfocytes and can be also found on NK cells surface in bone marrow.

Radioimmunotherapy (RIT) involves the use of radioactively-conjugated murine antibodies against cellular antigens. Most research involves their application to lymphomas, as these are highly radio-sensitive malignancies. To limit radiation exposure, murine antibodies were chosen, as their high immunogenicity promotes rapid tumor clearance. Tositumomab is an example used for non-Hodgkin's lymphoma.

Mus musculus B16F10 skin melanoma cells in laboratory. B16 melanoma is a murine tumor cell line used for research as a model for human skin cancers. B16 cells are useful models for the study of metastasis and solid tumor formation, and were one of the first effective murine tools for metastasis research.

SNX8 plays an antiviral role against Listeria monocytogenes through the IFNγ-triggered IKKβ-mediated noncanonical signaling pathway; murine cells expressing SNX8 under this infection showed a higher expression and secretion of IFNβ and IL6 cytokines in blood and lower presence of bacteria in liver and spleens, which resulted in a reduction of Listeria monocytogenes lethality, in comparison to SNX8-negative induced murine cells. In addition, SNX8 plays an antiviral role against DNA viruses such as HSV-1 through the MITA-mediated activation of the IFNβ promoter; murine cells expressing SNX8 under this infection showed a higher expression and secretion of IFNβ and IL6 cytokines in blood and a decreased presence of cerebral viral titers, which resulted in a reduction of HSV-1 lethality, in comparison to SNX8-negative induced murine cells. Finally, SNX8 also plays an antiviral role against RNA viruses such as SeV (Sendai virus) through VISA- mediated activation of the IFNβ promoter; murine cells expressing SNX8 under this infection showed a higher expression and secretion of IFNβ and IL6 cytokines in blood and a reduced presence of viral accumulations, which resulted in a reduction of SeV lethality, in comparison to SNX8-negative induced murine cells.

Leke pursued her PhD, entitled 'Murine plasmodia: chronic, virulent and self-limiting infections', at the Université de Montréal in 1975.

Theiler's Murine Encephalomyelitis Virus (TMEV) is a single-stranded RNA murine cardiovirus from the family Picornaviridae. It has been used as a mouse model for studying virally induced paralysis, as well as encephalomyelitis comparable to Multiple sclerosis. Depending on the mouse and viral strain, viral pathogenesis can range from negligible, to chronic or acute encephalomyelitis.

In one example of producing an anti-idiotypic vaccine, antibodies that bind tumor-associated antigens (TAA) are isolated and injected into mice. To the murine immune system, the TAA antibodies are antigens and cause an immunogenic reaction producing murine antibodies that can bind to the "TAA idiotype" and is said to be "anti-idiotypic". The resulting murine antibodies are harvested and used to vaccinate other mice. The resulting antibodies in the second set of mice have a three-dimensional binding site that mimics the original antibodies that bind tumor-associated antigens.

PHF8 was found to be expressional increased during endothelial differentation and significantly decreased during cardial differentation of murine embryonic stem cells.

This reduces immunogenicity, and thus increases serum half-life. Humanised antibodies are produced by grafting murine hypervariable regions on amino acid domains into human antibodies. This results in a molecule of approximately 95% human origin. Humanised antibodies bind antigen much more weakly than the parent murine monoclonal antibody, with reported decreases in affinity of up to several hundredfold.

Genetic engineering has led to the generation of humanized and chimeric antibodies, by exchanging the murine constant and complementary regions of the immunoglobulin chains with the human counterparts. Although this has reduced the sometimes extreme immunogenicity associated with murine mAbs, the anticipation that all fully human mAbs would have not possess unwanted immunogenic properties remains unfulfilled.

A 3D representation of a Gammaretrovirus core encapsidation signal. This is a view of the NMR structure for the 101-nucleotide core encapsidation signal of the Moloney murine leukemia virus. A 3D representation of a Gammaretrovirus. This structure shows the packaging of the dimeric genome of Moloney murine leukaemia virus, of which the encapsidation signal forms a part.

The murine leukemia viruses (MLVs or MuLVs) are retroviruses named for their ability to cause cancer in murine (mouse) hosts. Some MLVs may infect other vertebrates. MLVs include both exogenous and endogenous viruses. Replicating MLVs have a positive sense, single-stranded RNA (ssRNA) genome that replicates through a DNA intermediate via the process of reverse transcription.

Linnaeus's mouse opossum (Marmosa murina), also known as the common or murine mouse opossum, is a South American marsupial of the family Didelphidae.

Human anti-mouse antibody or human anti-murine antibody (HAMA) is an antibody found in humans which reacts to immunoglobins found in mice.

The Abelson murine leukemia virus (Ab-MLV or A-MuLV) is a retrovirus (Class VI) used to induce transformation of murine lymphoid cells. As a retrovirus, it has a single-stranded, positive sense RNA genome which replicates via a DNA intermediate mediated by a reverse transcriptase. The Abelson murine leukemia virus is named for the American pediatrician Herbert T. Abelson, who together with Louise S Rabstein, first described and isolated it. A-MuLV causes a rapidly progressive lymphosarcoma known as Abelson disease in mice, which is a type of leukemia that does not involve the thymus.

Thus common biological activities of LIF and OSM are mediated through the type I receptor and OSM specific activities are mediated through the type II receptor. The murine homologue of OSM was not discovered until 1996, whereas the murine OSMR homologue was not cloned until 1998. Until recently, it was thought that mOSM only signals through the murine type II receptor, namely through mOSMR/mgp130 complexes, because of a low affinity for the type I receptor counterpart. However, it is now known that, in bone at least, mOSM is able to signal through both mOSMR/mgp130 and mLIFR/mgp130.

NAGly powerfully stimulates oxygen consumption in multiple cell lines, including murine C2C12 myoblasts and human HEK293T cells. This respiratory bioactivity of NAGly is by increased uncoupled (state4u) mitochondrial respiration and depends on the presence of fatty acid desaturation. NAGly respiration bioactivity can be also abrogated in the presence of serum albumin, which functions as an NAGly carrier in murine blood plasma.

Most studies of uNKs use murine cells to model the human equivalent: unless stated otherwise, this section focuses on murine uNKs only. uNKs are large, granular, rounded or oval lymphocytes. On microscopic examination, they may have one or more cytoplasmic projections and/or be binucleate. Characteristically they contain eosinophilic granules that stain darkly with PAS, indicating the presence of glycoproteins.

In murine polyomavirus the minor proteins have been reported to induce apoptosis in the infected cell, and in SV40 they have been identified as viroporins.

In addition, a mutation in Dock5 has been associated with the rupture of murine lens cataracts. In zebrafish Dock5 has been implicated in myoblast fusion.

Genetic recombination can occur when at least two RNA viral genomes are present in the same infected host cell. RNA-RNA recombination between different strains of the murine coronavirus was found to occur at a very high frequency both in tissue cultureMakino S, Keck JG, Stohlman SA, Lai MM. High-frequency RNA recombination of murine coronaviruses. J Virol. 1986 Mar;57(3):729-37.

A study of PDE4 inhibition in a murine model of allergic asthma showed that piclamilast significantly improves the pulmonary function, airway inflammation and goblet cell hyperplasia.

Human HPS90AB1 shares 60% overall homology to its closest relative HSP90AA1. Murine HSP90AB1 was cloned in 1987 based on homology of the corresponding Drosophila melanogaster gene.

CpG-S sequences have also been used as external adjuvants for both DNA and recombinant protein vaccination with variable success rates. Other organisms with hypomethylated CpG motifs have demonstrated the stimulation of polyclonal B-cell expansion. The mechanism behind this may be more complicated than simple methylation – hypomethylated murine DNA has not been found to mount an immune response. Most of the evidence for immunostimulatory CpG sequences comes from murine studies.

While major publications have identified these cells as CPC's and have found a very large number in the murine and human heart, recent publications have found very few Isl1+ cells in the murine fetal heart and attribute their localization to the sinoatrial node, which is known as an area that contributes to heart pacemaking. The role of these cells and their niche are under intense research and debate.

TOL101, is a murine-monoclonal antibody specific for the human αβ T cell receptor. In 2010 it was an Investigational New Drug under development by Tolera Therapeutics, Inc.

Levy, J.A., Xenotropic viruses: murine leukemia viruses associated with NIH Swiss, NZB, and other mouse strains. Science, 1973. 182: p. 1151-1153.Levy, J.A., Xenotropic type C viruses.

TRPV6 mRNA is expressed in the apical domain of murine osteoclasts of cortical bone. Cortical and trabecular osteocytes do not express TRPV6 mRNA whereas osteoblasts show weak expression.

Human MDSCs are less characterized, and they are generally defined as myeloid cells expressing CD33, CD14 and low levels of HLA DR. The absence of the human equivalent to the murine GR1 marker makes it difficult to compare murine and human MDSCs. Although they functionally resemble murine MDSCs, their characterization and classification into different subsets remains to be resolved as there is () no international consensus on how human subsets of MDSC should be defined. However, A combination of CD33 and CD15 has been found to identify two major subsets of the MSDC in the peripheral blood of bladder cancer patients into granulocyte-type CD15(high) CD33(low) cells and monocyte-type CD15(low) CD33(high) cells.

In the first system, a wild-type Moloney Murine Leukemia Virus (M-MLV) reverse transcriptase was fused to the Cas9 H840A nickase C-terminus. Detectable editing efficiencies were observed.

The striped field mouse is a common agricultural pest within its range, particularly in years of population outbreaks, and a natural vector of diseases commonly associated with murine rodents.

Feline calicivirus (FCV)—a member of the Vesivirus—represents an important pathogen of cats. Sapovirus, Norovirus, and Vesivirus have been detected in pigs, making this animal species of particular interest in the study of calicivirus pathogenesis and host range. The first mouse norovirus, murine norovirus 1 (MNV-1), was discovered in 2003. Since then, numerous murine norovirus strains have been identified and they were assigned a new genogroup in the genus Norovirus.

As ectopic expression of murine agouti leads to the development of the yellow obese syndrome, this is expected to be consistent in humans. The yellow obese syndrome increases the development of many chronic diseases, including obesity, type II diabetes mellitus and tumorigenesis. ASP has similar pharmacological activation to murine agouti, as melanocortin receptors are inhibited through competitive antagonism. Inhibition of melanocortin by ASP can also be through non-competitive methods, broadening its range of effects.

For example, major differences in telomere regulation enable murine cells to bypass the requirement for telomerase upregulation, which is a rate-limiting step in human cancer formation. As another example, certain ligand-receptor interactions are incompatible between mice and humans. Additionally, experiments have demonstrated important and significant differences in the ability to transform cells, compared with cells of murine origin. For these reasons, it remains essential to develop models of cancer that employ human cells.

Most animal testing for TB vaccines has been conducted on murine, bovine and non-primate species. Recently, a study deemed zebrafish a potentially suitable model organism for preclinical vaccine development.

Murodermin (INN), also known as recombinant murine epidermal growth factor (rmEGF), is a recombinant form of mouse epidermal growth factor (EGF) and an EGF receptor agonist which was never marketed.

The antibody, originally called G5/44, was created by grafting the complementarity-determining regions and some framework residues from the murine anti-CD22 mAb m5/44, onto human acceptor frameworks.

In neurons, murine ortholog Wwp1 and its homolog Wwp2 control polarity acquisition, formation, and branching of axons, as well as migration of newly born nerve cells into the cortical plate.

Ileibacterium valens is a Gram-positive bacterium from the genus of Ileibacterium which has been isolated from the intestine of a murine from New York City in the United States.

2012.0198 (2012). Co-culturing 3T3-L1 pre- adipocytes in 3D with murine endothelial bEND.3 cells creates a vascular-like network assembly with concomitant lipogenesis in perivascular cells. See figure below.

Akt regulates cellular survival and metabolism by binding and regulating many downstream effectors, e.g. Nuclear Factor-κB, Bcl-2 family proteins, master lysosomal regulator TFEB and murine double minute 2 (MDM2).

Austyn was educated at the University of Oxford where he was awarded a Doctor of Philosophy degre in for research investigating monoclonal antibodies against the murine macrophage supervised by Siamon Gordon.

The reason that they are so useful is because their genomes are very simple and easy to use. Retroviruses have the ability to integrate into host cell genomes very well, which allows for the long term expression of their genome. One specific gammaretrovirus that is commonly used as a retroviral vector is the Moloney murine leukemia virus. A specific gammaretrovirus called xenotropic murine leukemia virus-related virus (XMRV) has been found to infect prostate cancer tissue in laboratories.

VIS1 (viral integration site 1), also known as HIS-1, is a long non-coding RNA. It was originally identified in mice in a screen for genes involved in the development of myeloid leukemia. In murine myeloid leukemias, this gene is a common site of viral insertion by the murine ecotropic retrovirus CasBrM It is conserved amongst vertebrates, including human, mice, cats, pigs, cattle and dogs. Expression of VIS1 is restricted to epithelial cells, leukemias and carcinomas.

Sodium-dependent phosphate transporter 1 is a protein that in humans is encoded by the SLC20A1 gene. Retrovirus receptors allow infection of human and murine cells by various retroviruses. The receptors that have been identified at the molecular level include CD4 (MIM 186940) for human immunodeficiency virus, Rec1 for murine ecotropic virus, and GLVR1 for gibbon ape leukemia virus (see MIM 182090). These 3 proteins show no homology to one another at the DNA or protein level.

Knockout mouse studies have implicated FFAR3 in diabetes, colitis, hypertension and asthma. However, discrepancies between the pathways activated by FFAR3 agonists in human cells and the equivalent murine counterparts have been observed.

An in vitro study showed that extracts of devil's club might inhibit tuberculosis. Another study suggested devil's club may reduce leukemia burden in mice engrafted with murine C1498 acute myeloid leukemia cells.

Anderson, W.F.: Human Gene Therapy. Science, 256: 808-813, 1992.Anderson, W.F., McGarrity, G.J., Moen, R.C.: Report to the NIH Recombinant DNA Advisory Committee on murine replication-competent retrovirus (RCR) assays. Hum.

Ludwik Gross (September 11, 1904 – July 19, 1999) was a Polish-American virologist who discovered two different tumor viruses, murine leukemia virus and mouse polyomavirus, capable of causing cancers in laboratory mice.

The murine GBP2 gene is not just highly activated by the interferon-gamma during macrophages activation but also by the stimulation of Toll-like receptors, Tumor necrosis factor (TNF) and Interleukin 1 beta.

Humphries, R.K.; Berg, P.; DiPietro, J.; Bernstein, S.; Baur, A.; Nienhuis, A.W.; Anderson, W.F.: Transfer of human and murine globin-gene sequences into transgenic mice. Am. J. Hum. Genet.• 37: 295-310, 1985.

Gammaretrovirus is a genus in the retroviridae family. Example species are the murine leukemia virus and the feline leukemia virus. They cause various sarcomas, leukemias and immune deficiencies in mammals, reptiles and birds.

Muromonab-CD3 was developed before the WHO nomenclature of monoclonal antibodies took effect, and consequently its name does not follow this convention. Instead, it is a contraction from "murine monoclonal antibody targeting CD3".

Human monoclonal antibodies (suffix -umab) are produced using transgenic mice or phage display libraries by transferring human immunoglobulin genes into the murine genome and vaccinating the transgenic mouse against the desired antigen, leading to the production of appropriate monoclonal antibodies. Murine antibodies in vitro are thereby transformed into fully human antibodies. The heavy and light chains of human IgG proteins are expressed in structural polymorphic (allotypic) forms. Human IgG allotype is one of the many factors that can contribute to immunogenicity.

The histocompatibility 60 (H60) was originally identified as a transplant rejection antigen and it is a family of murine cell surface glycoproteins contains three members: H60a, H60b, H60c. The genes encoding these proteins are located on murine chromosome 10. H60 family members are related to MHC class I. H60a and H60b consist of external α1α2 domain, a transmembrane segment, and a cytoplasmic domain. H60c is made up of α1α2 domain which is linked to the cell membrane by GPI anchor.

Studies using murine macrophages have shown that TCT encourages cytokine secretion, probably through the Nod1 receptor. As a pleiotropic toxin, TCT also acts as a pyrogen and as a stimulant of slow-wave sleep.

Murine models of HER2 overexpression in conjunction with PTPN1 knockout resulted in delayed tumor growth and with fewer observed metastases to the lung suggesting that PTPN1 may have an oncogenic role in breast cancer.

Leptomys is a genus of rodent from New Guinea. It is considered part of the New Guinea Old Endemics, meaning it was part of the first wave of murine rodents to colonize the island.

Paraleptomys is a genus of rodent from New Guinea. It is considered part of the New Guinea Old Endemics, meaning it was part of the first wave of murine rodents to colonize the island.

In the 2015 taxonomic update to the polyomavirus group, the International Committee on Taxonomy of Viruses classified NJPyV as a member of the genus Alphapolyomaviridae, whose type species is murine polyomavirus (Mus musculus polyomavirus 1).

1(4): 373-80. De Giovanni C, Nicoletti G, Landuzzi L, Palladini A, Lollini PL, Nanni P. "Bioprofiling TS/A Murine Mammary Cancer for a Functional Precision Experimental Model". Cancers (Basel). 2019 Nov 27;11(12).

Vaccination with irradiated tumor cells engineered to secrete murine granulocyte-macrophage colony-stimulating factor stimulates potent, specific, and long-lasting anti-tumor immunity. Proceedings of the National Academy of Sciences, 90(8), pp.3539-3543.

FEBS Lett. 582: 510-516. and cancer.Increase in mitochondrial biogenesis, oxidative stress, and glycolysis in murine lymphomas Enrique Sampera, E., Morgadob, L., Estradab, J.C., Bernadb, A., Hubbarda, A., Susana Cadenas, S. and Melova S., 2009.

Y1 adrenocortical cell is a murine tumor cell line used for biomedical research as a model systems for adrenal cortex studies. Y1 adrenocortical cell was generated from an adrenocortical tumor of a male LAF1 mouse.

HAS2 is a member of the vertebrate gene family encoding putative hyaluronan synthases, and its amino acid sequence shows significant homology to glycosaminoglycan synthetase (DG42) from Xenopus laevis, and human and murine hyaluronan synthase 1.

However, its use is limited by the body's eventual development of human anti-murine antibody, which neutralizes the effects. The Band of Parents raised $2–$3 million to fund the genetic engineering of the murine cell line that produces 3F8 so that it would produce a new antibody, Hu3F8, using human genes. Hu3F8 has the same benefits as 3F8, but because it is 98% human, it does not cause a neutralizing immune response. In theory, this should allow patients to be treated with it indefinitely.

XMRV is a recombinant virus created in a laboratory accident in the mid-1990s. Although it can infect human tissue, no known disease is associated with the infection via EBSCO login and it is unlikely to exist outside laboratories. Alleged discovery of XMRV in blood cells of patients with chronic fatigue syndrome in 2009 caused a controversy and eventual retraction. There were over 50 human cancer cell lines that were claimed to be linked to murine leukemia virus-related virus or murine leukemia virus.

Proto-oncogene serine/threonine-protein kinase Pim-1 is an enzyme that in humans is encoded by the PIM1 gene. Pim-1 is a proto-oncogene which encodes for the serine/threonine kinase of the same name. The pim-1 oncogene was first described in relation to murine T-cell lymphomas, as it was the locus most frequently activated by the Moloney murine leukemia virus. Subsequently, the oncogene has been implicated in multiple human cancers, including prostate cancer, acute myeloid leukemia and other hematopoietic malignancies.

Glypican 3 immunostaining has utility for differentiating hepatocellular carcinoma (HCC) and dysplastic changes in cirrhotic livers; HCC stains with glypican 3, while liver with dysplastic changes and/or cirrhotic changes does not. Using the YP7 murine monoclonal antibody, GPC3 protein expression is found in HCC, not in normal liver and cholangiocarcinoma. The YP7 murine antibody has been humanized and named as 'hYP7'. GPC3 is also expressed to a lesser degree in melanoma, ovarian clear-cell carcinomas, yolk sac tumors, neuroblastoma, hepatoblastoma, Wilms' tumor cells, and other tumors.

Sendai virus position in Paramyxoviridae phylogenetic tree Murine respirovirus, formerly Sendai virus (SeV) and previously also known as murine parainfluenza virus type 1 or hemagglutinating virus of Japan (HVJ), is an enveloped,150-200 nm in diameter, a negative sense, single-stranded RNA virus of the family Paramyxoviridae. It typically infects rodents and it is not pathogenic for humans or domestic animals. Sendai virus (SeV) is a member of genus Respirovirus. The virus was isolated in the city of Sendai in Japan in the early 1950s.

CKK represents a domain that has evolved with the metazoa. The structure of this domain in murine hypothetical protein has shown the domain to adopt a mainly beta barrel structure with an associated alpha-helical hairpin.

The nonessential genes, lysA and lysB, seem to play a role in controlling the correct timing of lysis.Zimecki, M., et al., Bacteriophages provide regulatory signals in mitogen-induced murine splenocyte proliferation. Cell Mol Biol Lett, 2003.

50:627Klochendler-Yeivin A, et al., « The murine SNF5/INI1 chromatin remodeling factor is essential for embryonic development and tumor suppression. », EMBO Rep, 2000, 1, p. 500Yaniv M., « Chromatin remodeling: from transcription to cancer », Cancer Genet.

Increase in mitochondrial biogenesis, oxidative stress, and glycolysis in murine lymphomas. Free Radical Biology and Medicine 46(3): 387-396. Other fields of application are e.g. sports science and the connection between mitochondrial function and aging.

The next year, murine neuroglobin was determined at a higher resolution. A practical treatment for carbon monoxide poisoning based on binding of CO by neuroglobin (Ngb) with a mutated distal histidine (H64Q) appears to be possible.

Myricetin has been seen to demonstrate antiviral activity against a number of viruses including Moloney murine leukemia virus, Rauscher murine leukemia virus, and the human immunodeficiency virus. Its effects against the proliferation of viruses is thought to be a consequence of myricetin’s ability to inhibit the proper functioning of reverse transcriptase. Myricetin was identified as a competitive inhibitor of the reverse transcriptase of Rauscher murine leukemia virus and a partial competitor with respect to the human immunodeficiency virus. Investigations into the activity of the HIV-1 strain when introduced to myricetin suggest the antiviral effects are derived from the inhibition of HIV-1 integrase, however, there are suspicions that the inhibition is non-specific. Structural analysis of myricetin and other flavonoids with observed antiviral effects indicate that the 3,4’ free hydroxyl groups likely are responsible for inhibition.

The life cycle of ameloblasts consists of six stages: # Morphogenic stage # Organizing stage # Formative (secretory) stage (Tomes' processes appear) # Maturative stages # Protective stage # Desmolytic stage The murine ALC (ameloblast like cell) cell line is of ameloblastic origin.

In murine models, two distinct transcripts are produced from opposite strands of the il14 gene that are called IL-14α and IL-14β. The il14 locus is near the gene for LCK on chromosome 1 in humans.

In 1991, three groups reported discovering CD154, which is the molecular basis of T cell helper function. Seth Lederman at Columbia University generated a murine monoclonal antibody, 5c8 that inhibited contact-dependent T cell helper function in human cells which characterized the 32 kDa surface protein transiently expressed on CD4+ T cells. Richard Armitage at Immunex cloned a cDNA encoding CD154 by screening an expression library with CD40-Ig. Randolph Noelle at Dartmouth Medical School generated an antibody that bound a 39 kDa protein on murine T cells and inhibited helper function.

Abrogation of anti-tumor immunity in CD4-knockout mice or mice depleted of CD4+ T cells has been demonstrated in cases of cell-based vaccines, recombinant viral vaccines and recombinant bacterial vaccines. While most adoptive transfer experiments have been performed with tumor-specific CD8+ T cells, activated CD4+ T cell clones specific for the murine leukemia virus have been demonstrated to confer systemic anti-tumor immunity upon transfer into tumor-bearing hosts.Greenberg, P.D., Kern, D.E. and Cheever, M.A., 1985. Therapy of disseminated murine leukemia with cyclophosphamide and immune Lyt-1+, 2-T cells.

In 1991, three groups reported discovering CD154. Seth Lederman, Michael Yellin, and Leonard Chess at Columbia University generated a murine monoclonal antibody, 5c8, that inhibited contact-dependent T cell helper function in human cells and which characterized a 32 kDa surface protein transiently expressed on activated CD4+ T cells. Richard Armitage at Immunex cloned a cDNA encoding CD154 by screening an expression library with CD40-Ig. Randolph Noelle at Dartmouth Medical School generated an antibody that bound a 39 kDa protein on murine T cells and inhibited helper function.

The α/β hydrolase domain including lipase motif and catalytic triad is conserved between murine and human ABHD12. Based on the observation of ABHD12 mutation in PHARC affected subjects, PHARC cell lines have been considered as human models of ABHD12 knockout. Mouse knockout (ABHD12 -/-) models demonstrate cerebellar microgliosis, motor and auditory impairment, alongside elevated neuroinflammation with progression associated with age. These characteristics are considered PHARC-like phenotypes as a murine model for human PHARC, however the mouse knockout model doesn’t demonstrate ocular or myelination defects, or early onset typical of PHARC.

Mammalian TRAP is encoded by one gene, which is localized on chromosome 19 (19p13.2–13.3) in humans, and on chromosome 9 in mice. TRAP DNA is, as expected from protein sequencing, highly conserved throughout the class mammalia. The TRAP gene has been cloned and sequenced in porcine, rat, human, and murine species. Human, murine, and porcine TRAP genes all contain 5 exons, and have the ATG codon at the beginning of exon 2, with exon 1 being non-coding. Within the exon 1 promoter, there are three distinct “tissue-specific” promoters: 1A, 1B, and 1C.

USP18 is stabilized by ISG15, but independently of the ubiquitin-like conjugation. Without ISG15-mediated stabilization, USP18 is degraded at the proteasome. This relationship exists in human, canine and porcine USP18/ISG15, but is absent in murine systems.

After a 2000 PhD titled 'Immunological responses to live and live recombinant BCG in a murine model ' at the University of Otago, and a post-doc at Cancer Research UK, Young returned to Otago rising to full professor.

STING is expressed broadly in numerous tissue types, of both immune and non-immune origin. STING was identified in murine embryonic fibroblasts, and is required for the type 1 interferon response in both immune and non-immune cells.

3F8 is a murine IgG3 monoclonal antibody which binds to GD2. It has been used in the detection and treatment of neuroblastoma. For imaging neuroblastoma, it is labelled with one of the radioisotopes iodine-124 and iodine-131.

Human models for cystinosin are typically derived from cystinotic renal tubular cell lines. Non-human protein homologs for cystinosin include ERS1 in Saccharomyces cerevisiae (yeast cells) and the Caenorhabditis elegans protein, C41C4.7. Murine ctns has also been used.

It also releases betulinic acid and lupeol from the stem bark. All of those compounds are used as anti-inflammatory, and are protecting plants from protozoan parasites. The plants are also effective against blood platelet aggregation and murine tumors.

S180 is a murine Sarcoma cancer cell line. It has been commonly used in cancer research due to its rapid growth and proliferation in mice. The cell line was initially harvested from a soft tissue tumor in a Swiss mouse.

Barbigerone from S. globosus is validated to have significant antioxidant property. Barbigerone exhibits profound antiplasmodial activity against the malarial parasite Plasmodium falciparum. It is also demonstrated that it has anti-cancer potential as it causes apoptosis of murine lung-cancer cells.

Murine Epo Receptor truncations and known functions. Erythroid differentiation depends on transcriptional regulator GATA1. EpoR is thought to contribute to differentiation via multiple signaling pathways including the STAT5 pathway. In erythropoiesis, EpoR is best known for inducing survival of progenitors.

The information collected from these studies is vital so that safe human testing can begin. Typically, in drug development studies animal testing involves two species. The most commonly used models are murine and canine, although primate and porcine are also used.

The murine leukemia viruses (MLVs) cause cancer in mouse hosts.Coffin JM, Hughes SH, Varmus HE, eds. (1997). Retroviruses. Cold Spring Harbor Laboratory. . Retroviruses are valuable research tools in molecular biology, and they have been used successfully in gene delivery systems.

Activity of murine magnus raphe cells predicts tachypnea and on-going nociceptive responsiveness. Journal of Neurophysiology Volume 98, Issue 6, December 2007, Pages 3121-33.Hellman, Kevin et al., Opioid microinjection into raphe magnus modulates cardiorespiratory function in mice and rats.

Avian diversity increased after the dams were built, but there was probably once a greater diversity. For some families of birds the number of individuals also increased. There are approximately 75 species of mammals in the Durance catchment area, including: Eurasian beaver, southwestern water vole, Eurasian water shrew, many species of bat (barbastelle (Barbastella barbastellus, large murine (Myotis myotis), large rhinolophe (Rhinolophus ferrumequinum), minioptère of Schreibers (Miniopterus schreibersi), small murine (Myotis blythii), small rhinolophe (Rhinolophus hipposideros), vespertilion with indented ears (Myotis emarginatus), and vespertilion of Capaccini (Myotis capaccinii)). invasive are becoming more problematic including coypu and the recently arrived muskrat.

The Vps10p domain receptor family was based on the discovery of SorLA in 1996 and sortilin in 1997, and has since been expanded with the SorCS subfamily with SorCS2 being described in 2001 SorCS2 was first found from isolated cDNA in murine floor plate samples of the central nervous system (CNS) as well as in regions of the brain. The cDNA contained the characteristic Vps10p domain enabling its classification as a SorCS protein. Not long after, a corresponding partial cDNA was found in human samples, and it was possible to determine the missing N-terminal by homology to murine SorCS2.

Francis Sargent Cheevers, Joan B. Daniels, Alwin M. Pappenheimer and Orville T. Bailey investigated the case of brain disease (murine encephalitis) at the Department of Bacteriology and Immunology of Harvard Medical School in Boston in 1949. Two laboratory mice (Schwenktker strains) of 17 and 18 days old had flaccid paralysis and died. By then it was known that murine encephalitis was caused by a picornavirus, called Theiler's virus, which was discovered by Max Theiler at the Rockefeller Foundation in New York in 1937. But the Harvard scientists found that the two mice had unusual symptoms other than brain damage (demyelination).

Treatment with LXR agonists (hypocholamide, T0901317, GW3965, or N,N-dimethyl-3beta-hydroxy- cholenamide (DMHCA)) lowers the cholesterol level in serum and liver and inhibits the development of atherosclerosis in murine disease models. Synthetic LXR agonist GW3965 improves glucose tolerance in a murine model of diet-induced obesity and insulin resistance by regulating genes involved in glucose metabolism in liver and adipose tissue. GW3965 inhibits the expression of inflammatory mediators in cultured macrophage and inflammation in mice. Aberrant LXR signaling in macrophages due to the oxidized cholesterol 7-ketocholesterol promotes the inflammation that leads to atherosclerosis.

KLF2 is now believed to play an important role in embryonic erythropoiesis, specifically in regulating embryonic and fetal β-like globin gene expression. In a murine KLF2-deficient embryo, expression of β-like globin genes normally expressed in primitive erythroid cells was significantly decreased, although adult β-globin gene expression was unaffected. The role of KLF2 in human β-like globin gene expression was further elucidated by transfection of a murine KLF2-deficient embryo with the human β-globin locus. It was found that KLF2 was important for ε-globin (found in embryonic hemoglobin) and γ-globin (found in fetal hemoglobin) gene expression.

Murine studies point to IL-6 whereas human studies have shown IL-21. Foxp3 is the major transcription factor controlling T-regulatory cells (Treg or CD4+ cells). CD4+ cells are leukocytes responsible for protecting animals from foreign invaders such as bacteria and viruses.

Treatment also had to be tailored to each individual patient, which was impracticable in routine clinical settings. Four major antibody types that have been developed are murine, chimeric, humanised and human. Antibodies of each type are distinguished by suffixes on their name.

The ABHD -/- murine model shows increased long-chain lysoPS accumulation in the brain suggesting lysoPS signalling contributes to PHARC-like pathology. A zebrafish knockdown (+/-) model has been developed which demonstrates ophthalmic defects including microphthalmia, lack of lens clarity, and disrupted retina architecture.

Epidemic typhus generally occurs in outbreaks when poor sanitary conditions and crowding are present. While once common, it is now rare. Scrub typhus occurs in Southeast Asia, Japan, and northern Australia. Murine typhus occurs in tropical and subtropical areas of the world.

Immunoprecipitation of RNA transcripts of murine olfactory cells have identified an enriched pool of odorant receptors activated by TMT, including five receptors (Olfr20, Olfr30, Olfr57, Olfr376, Olfr491 )that localize to the dorsal portion of the olfactory epithelium which can mediate fear behaviour.

The PDZ domain of syntrophin-α1(SNTA1), the most abundant isoform in the heart, has been reported to bind to the C-terminal domain of murine cardiac voltage-gated sodium channels (SkM2) causing altering ion channel activity leading to Long QT syndrome.

The bactericidal properties of arenicin-3 are responsible for its efficacy in inducing a 3-log reduction of E. coli bacterial load within 4 hours in a murine peritonitis model.andvang, D., Neve, S., et al. "NZ17074 - Pharmacokinetic and efficacy in mice" . Novozymes A/S.

Haptoglobin is produced mostly by hepatic cells but also by other tissues such as skin, lung and kidney. In addition, the haptoglobin gene is expressed in murine and human adipose tissue. Haptoglobin had been shown to be expressed in adipose tissue of cattle as well.

Murine (mouse) ASCT1 expressing cells are only susceptible to syncytin-1 and another endogenous retroviral env protein (that of Baboon Endogenous Retrovrius) and human ASCT1 has only been shown to bind syncytin-1. Further research is needed to elucidate ASCT and RDR binding determinants.

HAS1 is a member of the newly identified vertebrate gene family encoding putative hyaluronan synthases, and its amino acid sequence shows significant homology to the hasA gene product of Streptococcus pyogenes, a glycosaminoglycan synthetase (DG42) from Xenopus laevis, and a recently described murine hyaluronan synthase.

Catalase has been shown to interact with the ABL2 and Abl genes. Infection with the murine leukemia virus causes catalase activity to decline in the lungs, heart and kidneys of mice. Conversely, dietary fish oil increased catalase activity in the heart, and kidneys of mice.

Xenotropic murine leukemia virus-related virus (XMRV) is a retrovirus which was first described in 2006 as an apparently novel human pathogen found in tissue samples from men with prostate cancer. Initial reports erroneously linked the virus to prostate cancer and later to chronic fatigue syndrome (CFS), leading to considerable interest in the scientific and patient communities, investigation of XMRV as a potential cause of multiple medical conditions, and public-health concerns about the safety of the donated blood supply. Xenotropic viruses replicate or reproduce in cells other than those of the host species. Murine refers to the rodent family Muridae, which includes common household rats and mice.

To understand the pathogenesis of cancer patients, it is necessary to have model systems that faithfully mimic this condition. The application of a murine cancer cell line, such as 4T1, in a mouse model is of great value for preclinical TNBC studies. The 4T1 cell line is widely used as a syngeneic model for human triple-negative breast cancer, which is responsible for more than 17% of breast cancers diagnosed worldwide each year. 4T1 cells can be transplanted into the fat pad of the murine mammary gland, where they are highly tumorigenic, invasive, and spontaneously metastasize to distant organs such as the lungs, liver, lymph nodes, brain, and bone.

60 amino acids each, plus transmembrane and cytoplasmic regions. Isoform CR2 (1,032 amino acids) is encoded by a shorter transcript (3,096 coding nucleotides) that lacks exons 2-8 encoding SCR1-6. CR1 and CR2 on murine B cells form complexes with a co-accessory activation complex containing CD19, CD81, and the fragilis/Ifitm (murine equivalents of LEU13) proteins. The CR2 gene of primates produces only the smaller isoform, CR2; primate complement receptor 1, which recapitulates many of the structural domains and presumed functions of Cr2-derived CR1 in subprimates, is encoded by a distinct CR1 gene (apparently derived from the gene Crry of subprimates).

MCV is the fifth polyomavirus that infects humans to be discovered. It belongs to the murine polyomavirus group, one of the three main clades of polyomaviruses. (The group is named for murine polyomavirus, the earliest virus of the group to be discovered, and does not imply that MCV is transmitted to humans from rodents.) Although it has been confused with the controversial SV40 virus in some blog postings, it is a completely distinct virus. MCV is genetically most closely related to the African green monkey lymphotropic polyomavirus (formerly known as African green monkey lymphotropic papovavirus), which is consistent with MCV coevolving with human primates.

Lemniscomys, sometimes known as striped grass mice or zebra mice, is a genus of murine rodents from Africa. Most species are from Sub-Saharan Africa; L. barbarus is the only found north of the Sahara.Kingdon, J. (1997). The Kingdon Field Guide to African Mammals. pp. 212-213.

Two prominent murine human commensals have become vital laboratory animals. The brown rat and house mouse are both used as medical subjects. The murines have a distinctive molar pattern that involves three rows of cusps instead of two, the primitive pattern seen most frequently in muroid rodents.

Technetium (99mTc) arcitumomab is an immunoconjugate. Arcitumomab is a Fab' fragment of IMMU-4, a murine IgG1 monoclonal antibody extracted from the ascites of mice. The enzyme pepsin cleaves the F(ab')2 fragment off the antibody. From this, the Fab' fragment is prepared by mild reduction.

On 5 December 2008, orphan designation (EU/3/08/592) was granted by the European Commission to Medimmune Limited, United Kingdom, for murine anti-CD22 antibody variable region fused to truncated Pseudomonas exotoxin 38 for the treatment of hairy cell leukaemia. It was renamed to Moxetumomab pasudotox.

These genes include SOCS2 (i.e. suppressor of cytokine signaling 2), CYP1A1, CYP1A2, CYP1B1, glutathione S-transferase Ya subunit, quinone oxidoreductase, UDP- glucuronosyltransferase and Aldehyde dehydrogenase 3 family, member A1. This LXA4 activity has been demonstrated only in murine cells. LXA4 binds to and activates estrogen receptor alpha.

Dubosiella is a Gram-positive genus from the family of Erysipelotrichidae with one known species (Dubosiella newyorkensis). Dubosiella newyorkensis has been isolated from the intestinal content of a murine from New York City in the United States. Dubosiella is named after the American microbiologist René Dubos.

The polymerase catalytic subunit was identified as the 125 kDa polypeptide by activity staining in 1991. Several groups independently cloned the human and murine POLD1 cDNAs. Following its purification from various sources including calf thymus, human placenta, and HeLa cells, its activity was implicated in DNA repair.

In 2001, two cases of homozygous aniridia patients were reported; the fetuses died prior to birth and had severe brain damage. In mice, homozygous small eye defect (mouse Pax-6) leads to loss of the eyes and nose and the murine fetuses suffer severe brain damage.

Hierarchical perception of stimuli during case construction in the bagworm moth Eumeta crameri. J. Insect Behavior 13, 667-677. Pati AK, Florentin I, Chung V, De Sousa M, Lévi F and Mathé G (1987). Circannual rhythm in natural killer cell activity and mitogen responsiveness of murine splenocytes.

Similarly, unlike the common murine research model, M. coucha can support the complete lifecycle of B. malayi, a parasite that causes lymphatic filariasis. This has made it a key tool in discovering new drugs and vaccines to fight an infection that affects an estimated 130 million people.

Activation of the CAS is associated with hereditary angioedema, a disorder characterised by episodes of swelling. Genetic knockout studies in murine models of cardiovascular disease and genetic linkage studies in humans have implicated the contact factors in contributing to diverse cardiovascular disease processes including thrombosis and stroke.

Shearer, G. M., Rehn, T. G. and Garbarino, C. A., Cell-mediated lympholysis of trinitrophenyl-modified autologous lymphocytes. Effector cell specificity to modified cell surface components controlled by H-2K and H-2D serological regions of the murine major histocompatibility complex. J Exp Med 1975. 141: 1348-1364.

Respirovirus is a genus of viruses in the order Mononegavirales, in the family Paramyxoviridae. Rodents and human serve as natural hosts. There are currently seven species in this genus including the type species Murine respirovirus. Diseases associated with this genus include: croup and other acute febrile respiratory tract infections.

Hepcidin itself is also an anti-inflammatory agent. In the murine model very low levels of iron restrict hepcidin synthesis, worsening the inflammation that is present. Enteral nutrition has been found to be efficient to improve hemoglobin level in patients with inflammatory bowel disease, especially combined with erythropoietin.

Rat coronavirus, or RCV, is a strain or subspecies of Murine coronavirus that infects rats. The earliest discovered strains of Rat coronavirus were Sialodacryoadenitis virus, also known as SDAV, and Parker's Rat Coronavirus (PRC). Four other substrains have since been discovered; CARS, RCV-BCMM, RCV-W and RCV-NJ.

There have also been claimed discoveries of murine gammeretroviruses in lung cancer cell lines. While it was unclear what role these viruses have in the cancer development, it was believed that they are most prevalent during the tumor developing stage of the cancer by inhibiting tumor suppressing genes.

Typhus, also known as typhus fever, is a group of infectious diseases that include epidemic typhus, scrub typhus, and murine typhus. Common symptoms include fever, headache, and a rash. Typically these begin one to two weeks after exposure. The diseases are caused by specific types of bacterial infection.

Sialodacryoadenitis virus (SDAV), which is a strain of the species Murine coronavirus, is highly infectious coronavirus of laboratory rats, which can be transmitted between individuals by direct contact and indirectly by aerosol. Rabbit enteric coronavirus causes acute gastrointestinal disease and diarrhea in young European rabbits. Mortality rates are high.

NKX3-1 plays an essential role in normal murine prostate development. Loss of function of NKX3-1 leads to defects in prostatic protein secretions as well as ductal morphogenesis. Loss of function also contributes to prostate carcinogenesis. NKX3-1 has been established as a marker for identifying metastatic tumors.

Soul Taehakkyo Saengyak Yonguso Opjukjip 18, 30–31. Pokeweed also contains lectins, such as pokeweed mitogenBekeredjian- Ding, I., S. Foermer, C. J. Kirschning, M. Parcina, and K. Heeg. 2012. Poke Weed Mitogen Requires Toll-Like Receptor Ligands for Proliferative Activity in Human and Murine B Lymphocytes. PLoS One 7.

Activin disrupts epithelial branching morphogenesis in developing murine kidney, pancreas, and salivary gland. Mechanisms of Development 50: 229 - 245. After co-authoring an early paper in evolutionary developmental biology,Gilbert, S. F., Opitz, J., and Raff, R. A. 1996. Resynthesizing evolutionary and developmental biology. Developmental Biology 173: 357 - 372.

The potent immunomodulatory activities of BiP/GRP78 have also been demonstrated in animal models of autoimmune disease including collagen- induced arthritis, a murine disease that resembles human rheumatoid arthritis. Prophylactic or therapeutic parenteral delivery of BiP has been shown to ameliorate clinical and histological signs of inflammatory arthritis.

Brothers Robert and Joseph Switzer of Berkeley, California, began investigating fluorescence in the 1930s using a black light to identify naturally occurring fluorescent compounds, hitting first upon Murine eye wash.Ensminger, David. "Black Light Panthers: The Politics of Fluorescence," Art in Print Vol. 5 No. 2 (July–August 2015).

Judy Anne Mikovits (born ) is a former American research scientist who is known for her discredited medical claims, such as that murine endogenous retroviruses are linked to chronic fatigue syndrome. As an outgrowth of these claims, she has engaged in anti-vaccination activism, promoted conspiracy theories, and been accused of scientific misconduct. She has made false claims about vaccines, COVID-19 and chronic fatigue syndrome (CFS), among others. As research director of CFS research organization Whittemore Peterson Institute (WPI) from 2006 to 2011, Mikovits led an effort that reported in 2009 that a retrovirus known as xenotropic murine leukemia virus-related virus (XMRV) was associated with CFS and might have a causal role.

Two independent ClC-5 knock-out mice, the so called Jentsch and Guggino models, provided critical insights into the mechanisms of proximal tubular dysfunction in Dent disease 1. These two murine models recapitulated the major features of Dent disease (low-molecular-weight proteinuria, hypercalciuria and nephrocalcinosis/nephrolithiasis) and demonstrated that ClC-5 inactivation is associated with severe impairment of both fluid phase and receptor-mediated endocytosis, as well as trafficking defects leading to the loss of megalin and cubilin at the brush border of proximal tubules. However, targeted disruption of ClC-5 in the Jentsch model did not lead to hypercalciuria, kidney stones or nephrocalcinosis, while the Guggino model did. The Jentsch murine model produced slightly more acidic urines.

Since the field of genomics takes into account the entire genome of an organism, and not simply its individual genes, the stud of latent viral infection falls into this realm. For example, the DNA of a latent herpesvirus integrates into the host's chromosome and propagates through cell replication, although it is not part of the organism's genome, and was not present at the birth of the individual. An example of this is found in a study published in Nature, which showed that mice with a latent infection of a herpesvirus were less susceptible to bacterial infections. Murine mice were infected with murine gammaherpesvirus 68 and then challenged with the Listeria monocytogenes bacterium.

Since 1987 Bangham has conducted research on the Human T-lymphotropic virus 1 (HTLV-1). His contributions include the discovery of the viral synapse, the mechanism by which viruses including HTLV-1, HIV and murine leukaemia virus (MLV) are transmitted from cell-to-cell, starting a new field in virology.

HPyV9 was reported to have 75% sequence identity to the African green monkey lymphotropic polyomavirus. In the 2015 taxonomic update to the polyomavirus group, the International Committee on Taxonomy of Viruses classified HPyV9 as a member of the genus Alphapolyomaviridae, whose type species is murine polyomavirus (Mus musculus polyomavirus 1).

The mice had no visible illness or diarrhoea, which usually are associated with murine encephalitis. In addition, the causative virus was isolated from different organs including liver, spleen, lungs, and kidneys. This indicated that brain was not the primary target organ. Liver was particularly affected with severe necrosis, indicating hepatitis.

Most polyomaviruses do not infect humans. Of the polyomaviruses cataloged as of 2017, a total of 14 were known with human hosts. However, some polyomaviruses are associated with human disease, particularly in immunocompromised individuals. MCV is highly divergent from the other human polyomaviruses and is most closely related to murine polyomavirus.

It is a non-adjuvant test. In the test, Guinea pigs are exposed to a high dose of the substance. They are then given a challenge dose, which is the highest dose that does not cause irritation. The test has been largely superseded by the murine local lymph node assay.

As cell culture, Chinese hamster ovary cells (CHO) are used in order to acquire proper processing of factor VIII protein, that has demonstrated good efficacy in thrombin generation and clot formation in preclinical evaluations in murine (mouse) and canine (dog) models of hemophilia A and in patient-derived whole blood.

Polycomb complex protein BMI-1 also known as polycomb group RING finger protein 4 (PCGF4) or RING finger protein 51 (RNF51) is a protein that in humans is encoded by the BMI1 gene (B cell-specific Moloney murine leukemia virus integration site 1). BMI1 is a polycomb ring finger oncogene.

Pre-mRNA sequence of miR-712 is generated from the murine ribosomal RN45s gene at the internal transcribed spacer region 2 (ITS2). XRN1 is an exonuclease that degrades the ITS2 region during processing of RN45s. Reduction of XRN1 under d-flow conditions therefore leads to the accumulation of miR-712.

This gene encodes an integral membrane protein. The exact function of this protein is unclear, but studies of a similar murine protein suggest that it is a synaptic vesicle protein that also interacts with the dopamine transporter. The gene product belongs to the synaptogyrin gene family. [provided by RefSeq, Dec 2010].

This indicates a significant interaction between CiRS-7 and miR-7 in vivo. Another notable circular miRNA sponge is SRY. SRY, which is highly expressed in murine testes, functions as a miR-138 sponge. In the genome, SRY is flanked by long inverted repeats (IRs) over 15.5 kilobases (kb) in length.

The cheeks, throat, belly and inner surfaces of legs are yellowish with a median white pectoral area.Tate, G. H. H. 1933. A systematic revision of the marsupial genus Marmosa, with a discussion of the adaptive radiation of the murine opossums (Marmosa). Bulletin of the American Museum of Natural History, 66: 1-250.

Phylogeny and biogeography of African Murinae based on mitochondrial and nuclear gene sequences, with a new tribal classification of the subfamily. BMC Evolutionary Biology2008 8:199 DOI: 10.1186/1471-2148-8-199 which analyzes African murine species based on the mitochondrial cytochrome b gene and two nuclear gene fragments. Lecompte, et al.

E. moshkovskii has been identified in occasionally causing diarrhea with similar severity, duration, and age of onset to diarrhea acquired from E. histolytica. In murine models of mice, E. moshkovskii caused diarrhea, weight loss, and colitis. When children in Bangladesh were tested for intestinal issues, E. moshkovskii infection was associated with diarrhea.

The plant has been used as an herbal medicine for treatment of rheumatism, dengue and fever. The plant is known to contain barbigerone which is validated to have significant antioxidant property, highly effective against the malarial parasite Plasmodium falciparum, and with anti-cancer potential as it causes apoptosis of murine lung-cancer cells.

The WW domain may mediate specific protein–protein interactions. Three alternatively spliced transcript variants encoding distinct isoforms have been found for this gene. In neurons, murine ortholog Wwp2 and its homolog Wwp1 control polarity acquisition, formation, and branching of axons, as well as migration of newly born nerve cells into the cortical plate.

V. Aina, G. Lusvardi, G. Malavasi, L. Menabue, C. Morterra, Fluoride-containing bioactive glasses: surface reactivity in simulated body fluids, Acta Biomaterialia 5 (2009) 3548–3562.Zhang, J., Wang, M., Cha, JM. & Mantalaris, A. (2009). The incorporation of 70s bioactive glass to the osteogenic differentiation of murine embryonic stems cells in 3D bioreactors.

Most LINE copies have variable length at the start because reverse transcription usually stops before DNA synthesis is complete. In some cases this causes RNA polymerase II promoter to be lost so LINEs cannot transpose further. Genetic structure of murine LINE1 and SINEs. Bottom: proposed structure of L1 RNA-protein (RNP) complexes.

PMEG (9-[2-(phosphonomethoxy)ethyl] guanine) is an acyclic nucleoside phosphonate. Acyclic nucleoside phosphonates can have significant antiviral, cytostatic and antiproliferative activities. PMEG can inhibit cell proliferation and cause genotoxicity. PMEG is active against leukemia and melanoma in animal tumor models, and also has antiviral activities against herpes viruses in murine models.

Hybrid resistance was first described by Cudkowic in 1963. In a case of hybrid resistance, the parental bone marrow (BM) graft is rejected by F1 generation in murine model. This rejection is caused by natural killer (NK) cells of the recipient. The model which describes this event is called "The missing self"..

Gorer is credited with the co-discovery of histocompatibility antigens and the elucidation of their genetic regulation. Together with George Snell, he helped discover the murine histocompatibility 2 locus, or H-2, which is analogous to the human leukocyte antigen. Gorer also identified antigen II and determined its role in transplant tissue rejection.

The venom of this species, like most spitting cobras, contains a mixture of neurotoxins and cytotoxins. Bite symptoms include slight pain around the wound and numbness of the lips, fingers and tongue. Although it rarely causes human fatalities, survivors are usually disfigured. The murine IP value for this snake is 2 mg/kg.

NS0 cells are a model cell line derived from the nonsecreting murine myeloma used in biomedical research and commercially in the production of therapeutic proteins. The cell line is a cholesterol-dependent cell line that was generated from a subline of NSI/1 which produced only the light chain but no heavy chain.

The murine leukemia viruses are group/type VI retroviruses belonging to the gammaretroviral genus of the Retroviridae family. The viral particles of replicating MLVs have C-type morphology as determined by electron microscopy. The MLVs include both exogenous and endogenous viruses. Exogenous forms are transmitted as new infections from one host to another.

Blocking PD-L2 has been shown to exacerbate experimental autoimmune encephalomyelitis. Unlike PD-L1, PD-L2 has been shown activate the immune system. PD-L2 triggers IL-12 production in murine dendritic cells leading to T cell activation. Others have shown that treatment with PD-L2 Ig led to T helper cell proliferation.

Cynaropicrin is an inhibitor of TNF-α, a cytokine used in inflammation of tissue. It inhibits the production of TNF-α from lipopolysaccharide-stimulated murine macrophage RAW264.7 cells. It also inhibits the release of nitric oxide from lipopolysaccharide- and interferon-γ-stimulated RAW264.7 cells. Lastly. it also suppressed lymphocyte proliferation from splenocytes.

Neither is known much about the mechanism of the protein misfolding nor its kinetics. Using the known structure of PrPc and the results of the in vitro and in vivo studies described below, Folding@home could be valuable in elucidating how PrPSc is formed and how the infectious protein arrange themselves to form fibrils and amyloid like plaques, bypassing the requirement to purify PrPSc or dissolve the aggregates. The PrPc has been enzymatically dissociated from the membrane and purified, its structure studied using structure characterization techniques such as NMR spectroscopy and X-ray crystallography. Post- translational PrPc has 231 amino acids (aa) in murine. The molecule consists of a long and unstructured amino terminal region spanning up to aa residue 121 and a structured carboxy terminal domain. This globular domain harbours two short sheet-forming anti-parallel β-strands (aa 128 to 130 and aa 160 to 162 in murine PrPc) and three α-helices (helix I: aa 143 to 153; helix II: aa 171 to 192; helix III: aa 199 to 226 in murine PrPc), Helices II and III are anti- parallel orientated and connected by a short loop.

In a recent study conducted at the Hospital for Sick Children in Canada in 2007, researchers found that a ketogenic diet prolonged the lifespan of Aldh5a1-/- mice by greater than 300%, along with the normalization of ataxia and some improvement in various seizure types seen in SSADH deficient murine models. These effects were in conjunction with "...a significant restoration of GABAergic synaptic activity and region-specific restoration of GABAA receptor associated chloride channel binding." Ultimately, the data seen in the study indicated that a ketogenic diet may work in its ability to restore GABAergic inhibition. But further studies on murine models need to be conducted, ultimately leading to the possibility of conducting a controlled study on humans afflicted with the disorder.

The LTag gene is usually encoded in two exons, of which the first overlaps with the gene for STag (and sometimes other tumor antigens as well, such as the murine polyomavirus middle tumor antigen). Polyomavirus STag proteins are usually around 170-200 residues long and consist of two distinct regions as a result of this genetic encoding. STag and LTag share a common N-terminal domain called the J domain, which is around 80-90 residues long, has homology to DnaJ proteins, and functions as a molecular chaperone. The C-terminal portion of the STag protein is distinct from LTag but shares an additional ~100 residues with middle tumor antigen in those viruses that express it, such as murine polyomavirus.

Proc Natl Acad Sci USA 85:8506–8510 (1988) # v-cbl, a new oncogene from a dual-recombinant murine retrovirus that induced early B-lineage lymphomas. Proc Natl Acad Sci USA 86:1168–1172 (1989) # Transformation of murine bone marrow cells with a raf/myc retrovirus yields clonally related mature B cells and macrophages. Mol Cell Biol 10:3562–3568 (1990) # Novel zinc finger gene implicated as myc collaborator by retrovirally accelerated lymphoma genesis in Eμ-myc transgenic mice. Cell 65:1–10 (1991) # Erythropoietin-induced stimulation of differentiation and proliferation in J2E cells is not mimicked by chemical induction. Blood 80:412–419 (1992) # A rapid fatal erythroleukemia caused by J2E cells can be treated ex vivo with erythropoietin.

Lodzki, M., Godin, B., Rakou, L., Mechoulam, R., Gallily, R., Touitou, E. (2003) Cannabidiol Transdermal Delivery and Anti-Inflammatory Effect in a Murine Model. J. Control. Release, 93: 379-389Godin, B., Touitou, E. (2004) Mechanism of Bacitracin Permeation Enhancement through the Skin and Cellular Membranes from an Ethosomal Carrier. J. Control. Release, 94:365-79.

In: J Biol Response Mod. 1984 Oct;3(5), S. 483–490. Since experiments in murine models demonstrated that local production by gene transduced cells produced a stronger and more specific immune response than a systemic application, e.g. of Interleukin-2, this strategy was also pursued by his group in Phase I clinical trials.

Four different mouse models with Col3a1 defects have been reported. Inactivation of the murine Col3a1 gene using homologous recombination technique led to a shorter life span in homozygous mutant mice. The mice died prematurely from a rupture of major arteries mimicking the human vEDS phenotype. These mice also had a severe malformation of the brain.

It has been determined that Y. pestis became so dangerous because of the acquisition of ymt (yersina murine toxin). This gene is present on the pMT1 plasmid and allowed the survival of the bacterium in the flea vector and facilitated colonization of the midgut in arthropod, giving rise to the past millennium large-scale pandemics.

No specific antivenom currently produced against this species' venom. This makes it a very dangerous snake to be trifled with. Venoms of the water cobras, were assayed for lethality, proteolytic activity and protein content. Naja annulata annulata and Naja christyi venoms averaged 89% protein and lacked proteolytic activity. The murine intraperitoneal LD50 of N. a.

Mixl1 is functionally similar to the Xenopus Mix.1.# Cloning, expression analysis, and chromosomal localization of murine and human homologues of a Xenopus Mix gene. Robb, L., Hartley, L., Begley, C. G., Brodnicki, T. C., Copeland, N. G., Gilbert, D. J., Jenkins, N. A. and Elefanty, A. G. Dec. Dyn. 219, 497-504 (2000).

Mice that have had the murine ortholog (see ) of this gene knocked out exhibit an excessive pathologic grooming behavior. This behavior is similar to the behavior of humans suffering from the obsessive-compulsive spectrum disorder trichotillomania. Transplantation of normal (wild-type) bone marrow into a Hoxb8 mutant mouse results in a reduction of compulsive grooming.

Though no known direct link exists between N-RAP mutations and human cardiomyopathies, N-RAP has been shown to be significantly upregulated in murine models of dilated cardiomyopathy. This has been hypothesized to be an adaptive response to correct for disorganized actin thin filament architecture at intercalated disc junctions in cardiomyocytes during dilated cardiomyopathy.

The double stranded DNA is highly stable and easily integrated into a host genome. A few examples of the virus are Moloney murine leukemia virus, xenotropic MuLB-related virus, feline leukemia virus, and feline sarcoma virus. Gammaretroviruses are very popular retroviral vectors in laboratory studies. These vectors are crucial for gene therapy and gene transfer.

In the case of the murine leukemia viruses, a species of viruses capable of causing cancer in murines (mice), the viral life cycle can also be responsible for oncogenesis through a Gag-v-Onc fusion protein called "Mo-MuLV(src)", which is a Gag-v-Src protein capable of inducing oncogenesis in living mice.

The association of SOX-9 and Dax1 actually creates Sertoli cells, another vital process in male development. In the brain development, its murine ortholog Sox-9 induces the expression of Wwp1, Wwp2, and miR-140 to regulate cortical plate entry of newly born nerve cells, and regulate axon branching and axon formation in cortical neurons.

Stoye has worked with the human immunodeficiency virus (HIV), other primate retroviruses, murine leukaemia viruses and retroviruses of pigs, goats, sheep and other animals. His recent publications describe investigations of host restriction factors such as Fv1, TRIM5alpha and other members of the tripartite motif family as well as the lentiviral accessory proteins Vpx and Vpr.

Jurkat J6 cells have been found to produce a xenotropic murine leukemia virus (X-MLV) (referred to as XMRV) that could potentially affect experimental outcomes. There is no evidence that this virus can infect humans. This infection may also change the virulence and tropism of the virus by way of phenotypic mixing and/or recombination.

Mammalian renal inner medullary (IM) cells routinely face and resist hypertonic stress. Such stress causes DNA damage to which IM cells respond with cell cycle arrest. All three GADD45 isoforms GADD45A, GADD45B, and GADD45G are induced by acute hypertonicity in murine IM cells. Maximum induction occurs 16-18 h after the onset of hypertonicity.

The LAG3 protein, which belongs to immunoglobulin (Ig) superfamily, comprises a 503-amino acid type I transmembrane protein with four extracellular Ig-like domains, designated D1 to D4. When human LAG-3 was cloned in 1990 it was found to have approx. 70% homology with murine LAG3. The homology of pig LAG3 is 78%.

When the acquired immune deficiency syndrome (AIDS) epidemic was first identified, Shearer realized that the immune deficiencies occurring in AIDS patients closely resembled the immune deficiencies occurring in experimental murine models of graft versus host disease that he had been studying.Shearer, G., Immune-deficiency syndrome (AIDS) A consequence of allogeneic Ia-antigen recognition. Immunol Today 1983. 4: 181-185.

According to Ernst & Zug et al. the murine SC value is 0.21 mg/kg, making it one of the most venomous true cobra species (genus Naja) in the world. Severe envenomation is likely in case of a bite and envenomation rate is high. The untreated mortality rate is not known, but is thought to be high (~60%).

Initial therapeutic antibodies were murine analogues (suffix -omab). These antibodies have: a short half-life in vivo (due to immune complex formation), limited penetration into tumour sites and inadequately recruit host effector functions. Chimeric and humanized antibodies have generally replaced them in therapeutic antibody applications. Understanding of proteomics has proven essential in identifying novel tumour targets.

VP1 is capable of self-assembly into virus-like particles even in the absence of other viral components. This process requires bound calcium ions and the resulting particles are stabilized by, but do not require, inter-pentamer disulfide bonds. The structure of an individual pentamer of the murine polyomavirus VP1 protein. Each monomer is colored differently.

A fragment of the murine polyomavirus VP2 (yellow) in complex with the major capsid protein VP1 (blue). From . Both VP2 and VP3 are primarily intrinsically unstructured proteins; they have DNA-binding domains and a nuclear localization signal at their C-terminal ends. Both VP2 and VP3 bind to the interior of VP1 pentamers in the assembled capsid.

These virus include flaviviruses (dengue virus and West Nile virus), filoviruses (Marburg virus and Ebola virus) coronaviruses (SARS coronavirus) and lentivirus (Human immunodeficiency virus). However, IFITM proteins did not affect alphaviruses, arenaviruses and murine leukaemia virus infection. Potential mechanisms.IFITM proteins inhibit viral membrane and cellular endosomal or lyso¬somal vesicles membrane fusion by modify lipid components or fluidity.

Research indicates both PIWI proteins and esiRNAs may also play a role in silencing retrotransposons through DNA methylation.Kuramochi-Miyagawa, S., Watanabe, T., Gotoh, K., Totoki, Y., Toyoda, A., Ikawa, M., et al. (2008). DNA methylation of retrotransposon genes is regulated by Piwi family members MILI and MIWI2 in murine fetal testes. [Article]. Genes & Development, 22(7), 908-917.

Fleas are vectors for viral, bacterial and rickettsial diseases of humans and other animals, as well as of protozoan and helminth parasites. Bacterial diseases carried by fleas include murine or endemic typhus and bubonic plague. Fleas can transmit Rickettsia typhi, Rickettsia felis, Bartonella henselae, and the myxomatosis virus. They can carry Hymenolepiasis tapeworms and Trypanosome protozoans.

Murine norovirus (MNV) is a species of norovirus affecting mice. It was first identified in 2003. MNV is commonly used in research to model Human norovirus because the latter is difficult to grow in the laboratory. Standardized cell cultures are used in MNV propagation and the virus naturally infects mice, which allows studies in animal systems.

Adaptor proteins TRAF2 and TRAF5 have been shown to mediate the signaling process of this receptor. CD27-binding protein (SIVA), a proapoptotic protein, can bind to this receptor and is thought to play an important role in the apoptosis induced by this receptor. In murine γδ T cells its expression has been correlated with the secretion of IFNγ.

The GHR gene is used in animals as a nuclear DNA phylogenetic marker. The exon 10 has first been experienced to explore the phylogeny of the major groups of Rodentia. GHR has also proven useful at lower taxonomic levels, e.g., in octodontoid, arvicoline, muroid, murine, and peromyscine rodents, in arctoid and felid carnivores, and in dermopterans.

However, if there is no specific self MHC I (H2 alele in murine model) the inhibition of inhibition comes to pass. It means activation of NK cell. In a case of BM transplantation, where the F1 generation arise from two individuals with H2b/b and H2k/k MHC I phenotype. The F1 generation will be H2b/k.

Genetic structure of human and murine LINE1 and SINEs. Short interspersed nuclear elements (SINEs) are non-autonomous, non-coding transposable elements (TEs) that are about 100 to 700 base pairs in length. They are a class of retrotransposons, DNA elements that amplify themselves throughout eukaryotic genomes, often through RNA intermediates. SINEs compose about 13% of the mammalian genome.

CCL27 is expressed in numerous tissues, including gonads, thymus, placenta and skin. It elicits its chemotactic effects by binding to the chemokine receptor CCR10. The gene for CCL27 is located on human chromosome 9. Studies of a similar murine protein indicate that these protein-receptor interactions have a pivotal role in T cell-mediated skin inflammation.

Genetic structure of murine LINE1 and SINEs. Bottom: proposed structure of L1 RNA-protein (RNP) complexes. ORF1 proteins form trimers, exhibiting RNA binding and nucleic acid chaperone activity. LINE1 (also L1 and LINE-1) are class I transposable elements in the DNA of some organisms and belong to the group of long interspersed nuclear elements (LINEs).

The over expression of GRK2ct has been shown to significantly rescue cardiac function in murine models of heart failure by blocking Gβγ subunit signalling. In another study, biopsies were taken from patients with heart failure and virally induced overexpression of GRK2ct in the heart myocytes. Other tests showed an improvement in cardiac cell contractile function by inhibiting Gβγ.

Alpha/beta hydrolase domain containing 3 (ABHD3; alternative names: lung alpha/beta hydrolase 3, phospholipase ABHD3) is a single pass type II membrane member of the serine hydrolase family of enzymes. The expression of murine ABHD3 is highest in the brain, liver, and kidney. ABHD3 hydrolytic activity is highly specific for medium chain (e.g., dimyristoylphosphatidylcholine) and oxidatively truncated (e.g.

Epidemic typhus is caused by the bacteria Rickettsia Prowazekii; it comes from lice. Murine Typhus is caused by the Rickettsia Typhi bacteria, from the fleas on rats. Scrub Typhus is caused by the Orientia Tsutsugamushi bacteria, from the harvest mites on humans and rodents. Queensland tick typhus is caused by the Rickettsia Australis bacteria, from ticks.

Genetic structure of murine LINE1 and SINEs, including Alu. Two main promoter "boxes" are found in Alu: a 5' A box with the consensus , and a 3' B box with the consensus (IUPAC nucleic acid notation). tRNAs, which are transcribed by RNA polymerase III, have a similar but stronger promoter structure. Both boxes are located in the left arm.

Morin treatment significantly down- regulated expressions of BLT2, NF-κB, and Th2-cytokine (TNF-α, IL-1β, IL-4, IL-6, and IL-13) in lungs of murine model of allergic asthma. Morin can be used to test for the presence of aluminium or tin in a solution, since it forms characteristically fluorescent coordination complexes with them.

Susceptibility to CVID may also be linked to the Major Histocompatibility Complex (MHC) of the genome, particularly to DR-DQ haplotypes. A mutation in the NFKB2 gene has recently been shown to cause CVID-like symptoms in a murine model. The frequency of this NFKB2 mutation in the CVID population is, however, yet to be established.

Upon IFN-γ stimulation, PD-L1 is expressed on T cells, NK cells, macrophages, myeloid DCs, B cells, epithelial cells, and vascular endothelial cells. The PD-L1 gene promoter region has a response element to IRF-1, the interferon regulatory factor. Type I interferons can also upregulate PD-L1 on murine hepatocytes, monocytes, DCs, and tumor cells.

Pheophorbide a is the product of chlorophyll breakdown. It is used as a photosensitizer. Photodynamic therapy (PDT) with several photosensitizers is a promising modality for the treatment of cancer. In this study, the therapeutic effect of PDT using the synthetic photosensitizer pheophorbide a (Pa-PDT) was examined in AT-84 murine oral squamous cell carcinoma (OSCC) cells.

The Oriental rat flea (Xenopsylla cheopis), also known as the tropical rat flea, is a parasite of rodents, primarily of the genus Rattus, and is a primary vector for bubonic plague and murine typhus. This occurs when a flea that has fed on an infected rodent bites a human, although this flea can live on any warm blooded mammal.

She engineered the virus-like particles using yeast as a recombinant system. She has explored the viral genomes of various other viruses, including picornaviruses, noroviruses and coronaviruses. Noroviruses are a common cause of gastroenteritis, but there are no vaccines or specific antivirals. Stonehouse has investigated murine norovirus, the form of norovirus that affects mice, using cryogenic electron microscopy.

Death-associated protein kinase 3 (DAPK3) induces morphological changes in apoptosis when overexpressed in mammalian cells. These results suggest that DAPK3 may play a role in the induction of apoptosis. Unlike most other mammalian genes, murine (rat and mouse) DAPK3 has undergone accelerated evolution and diverged from the tightly conserved consensus that is maintained from fish to human.

These are Theiler's Murine encephalomyelitis virus (TMEV), Vilyuisk human encephalomyelitis virus (VHEV), a Theiler-like rat virus (TRV) (which has yet to be named) and Saffold virus (SAF-V). Of these 4, only VHEV and SAF-V are thought to cause infection in humans. Thus far, cardiovirus C has only been observed in the brown rat.

In addition, inclusion or exclusion of exons 6 and 7 mediate interactions with heparan sulfate proteoglycans (HSPGs) and neuropilin co-receptors on the cell surface, enhancing their ability to bind and activate the VEGF receptors (VEGFRs). Recently, VEGF-C has been shown to be an important inducer of neurogenesis in the murine subventricular zone, without exerting angiogenic effects.

N. brasiliensis provides a valuable lab model in determining the migration pathway through the host. The lifecycle of N. brasiliensis can be passed through lab mice. The availability of inbred and mutant mouse strains can be advantageous when examining the genetic basis of murine susceptibility and resistance to infection.Stadnyk, A.W., P.J. McElroy, J. Gauldie, and A.D. Befus. 1990.

From 1960 to 1974 he taught part-time at Howard University. Rowe and his colleagues showed that retroviruses can cause leukemia in mice. He was among the first "to recognize the role of the immune response in the pathogenesis of murine lymphocytic choriomeningitis." He was a pioneer in research on adenoviruses and their role in human diseases.

The Pho1 phosphate permease family (TC# 2.A.94) is a family of phosphate transporters belonging to the ion transporter (IT) superfamily. Representative members of the Pho1 family include the putative phosphate transporter PHO1 of Arabidopsis thaliana (TC# 2.A.94.1.1), and the xenotropic and polytropic murine-leukemia virus receptor Xpr1 of Culex pipiens (TC# 2.A.94.1.2).

T cells recognise antigens primarily via the T cell receptor. This receptor needs various co-receptors to function, one of which is CD3. The T cell receptor-CD3 complex transduces the signal for the T cell to proliferate and attack the antigen. Muromonab-CD3 is a murine (mouse) monoclonal IgG2a antibody which was created using hybridoma technology.

Active site of CDO, with iron (II) bound to cysteine substrate and key residues highlighted. Generated from 2IC1. CDO is a 22.5 kDa protein that contains 200 amino acid residues and has an isoelectric point (pI) of 5.5. The primary structure is highly conserved between mammalian species, with murine and human CDO differing in only 16 residues.

Human as well murine STAT4 genes lie next to STAT1 gene locus suggesting that the genes arose by gene duplication. STAT proteins have several functional domains, including an N-terminal interaction domain, a central DNA-binding domain, an SH2 domain, and the C-terminal transactivation domain. The length of the protein is 748 amino acids, and the molecular weight is 85 941 Dalton .

The gene that encodes the human EHD3 protein is located in chromosome number 2, most specifically in the 23.1 region. On the other hand, the murine EHD3 gene is located in chromosome 17, in the 21st region. The human gene is formed approximately of 35,438 bases. Both the human and the mouse genes contain a polymorphic (CA) repeat in their 3'UTR.

Glioma 261 (GL261) is a frequently used murine glioma model. It was induced via intracranial injection of methylcholanthrene followed by serial intracranial and subcutaneous transplantations of tumor fragments into syngeneic C57BL/6 mice. By the mid-1990s, multiple groups had established a permanent cell line from the tumor. GL261 tumors resemble ependymoblastomas on histology but show many characteristics of glioblastoma phenotypes.

Most Gram-negative bacteria keep TCT within the cell wall by using a PGN-transporter protein known as AmpG. However, B. pertussis is not capable of recycling PGNs via AmpG and thus, TCT escapes into the surrounding environment. Also, TCT appears to be constitutively expressed by B. pertussis. The first murine-model studies using TCT involved treatment of hamster tracheal cells.

41 The Tylomyinae are characterized by the presence of ungual tufts on their hindfeet.Musser and Carleton, 2005, p. 1186 White ungual tufts are also present in the Philippine murine genus Batomys. B. hamiguitan and B. russatus have short tips, not extending to the tips of the claws, but those of B. granti and B. salomonseni have tufts longer than the claws.

Pvt1 oncogene (non-protein coding), also known as PVT1 or Plasmacytoma Variant Translocation 1 is a long non-coding RNA gene. In mice, this gene was identified as a breakpoint site in chromosome 6;15 translocations. These translocations are associated with murine plasmacytomas. The equivalent translocation in humans is t(2;8), which is associated with a rare variant of Burkitt's lymphoma.

This gene encodes a member of the SLAP family of adapter proteins. The encoded protein may play an important receptor-proximal role in downregulating T and B cell-mediated responses and inhibits antigen receptor- induced calcium mobilization. This protein interacts with Cas-Br-M (murine) ecotropic retroviral transforming sequence c. Two transcript variants encoding distinct isoforms have been identified for this gene.

Scientists Turn Skin Cells into Heart Cells and Brain Cells Using Drugs. Gladstone Institutes. News Center In another study, ischemic cardiomyopathy in the murine infarction model was targeted by iPS cell transplantation. It synchronized failing ventricles, offering a regenerative strategy to achieve resynchronization and protection from decompensation by dint of improved left ventricular conduction and contractility, reduced scarring and reversal of structural remodelling.

Mandelboim, O., Vadai, E., Fridkin, M., Katz- Hillel, A., Feldman, M., Berke, G. and Eisenbach, L., 1995. Regression of established murine carcinoma metastases following vaccination with tumour- associated antigen peptides. Nature medicine, 1(11), pp.1179-1183.Mayordomo, J.I., Zorina, T., Storkus, W.J., Zitvogel, L., Celluzzi, C., Falo, L.D., Melief, C.J., Ildstad, S.T., Kast, W.M., Deleo, A. and Lotze, M.T., 1995.

CTL responses can be enhanced by co-inoculation with co- stimulatory molecules such as B7-1 or B7-2 for DNA vaccines against influenza nucleoprotein, or GM-CSF for DNA vaccines against the murine malaria model P. yoelii. Co-inoculation with plasmids encoding co-stimulatory molecules IL-12 and TCA3 were shown to increase CTL activity against HIV-1 and influenza nucleoprotein antigens.

Moreover, the deficient of M33 also possessed abnormally few nucleated cells in the thymus and spleen, due to the aberrant T-cell expansion. In transiently transfected cells, M33 acts as a transcriptional repressor . Biochemical assays indicate that two murine proteins, Ring1A and Ring1B interact directly with the repressor domain of M33 and that Ring1A can also behave as a transcriptional repressor.

The human TMPO gene maps to chromosome band 12q22 and consists of eight exons. TMPO alpha is present diffusely expressed with the cell nucleus while TMPO beta and gamma are localized to the nuclear membrane. TMPO beta is a human homolog of the murine protein LAP2. LAP2 plays a role in the regulation of nuclear architecture by binding lamin B1 and chromosomes.

Journal of Immunology. 2003 Feb 15;170(4):1625-9. Cited 404 times according to Google Scholar #Dawicki W, Marshall JS. New and emerging roles for mast cells in host defence. Current opinion in immunology. 2007 Feb 1;19(1):31-8. Cited 307 times according to Google Scholar #McCurdy JD, Lin TJ, Marshall JS. Toll‐like receptor 4‐mediated activation of murine mast cells.

Antibodies are produced for the HIV-1 gp41 protein. These antibodies can cross-react with astrocytes within human CNS tissue and act as autoantibodies. This contributes to many CNS complications found in AIDS patients. Theiler's murine encephalomyelitis virus (TMEV) leads to the development in mice of a progressive CD4+ T cell-mediated response after these cells have infiltrated the CNS.

There has been extensive research into its role in antibody-directed immunotherapy through the use of the high-affinity murine monoclonal antibody, mAb5T4, to deliver response modifiers (such as staphylococcus aureus superantigen) accurately to a tumor. 5T4 is also the target of the cancer vaccine TroVax which is in clinical trials for the treatment of a range of different solid tumour types.

100 distinct cell types) of the then visual cortical regions and associated structures (thalamus, colliculus) and their dynamics. The scientists seek to know what the animal sees, how it thinks, and how it decides. They seek to map out the murine mind in a quantitative manner. The Allen Institute for Brain Science currently employs about 300 scientists, engineers, technologists and supporting personnel.

Tuftsin sequence appears in residues 9-12 from the amino terminal of p12 protein of Rauscher murine leukemia virus. The tetrapeptide Thr-Arg-Pro-Lys is in the influenza hemagglutinin virus protein, residues 214–217. The canine analogue is tetrapeptide: Thr-Lys-Pro-Lys. The peptide Thr-Arg-Pro-Arg is biologically active pancreatic polypeptide 32–35 with gastrointestinal functions.

As early as 1865, this position was disputed on the basis of the dental formula. Peters (1865) suggested that the species was unrelated to the dormice and suggested that they should be placed with the murine genera of India. This position in the family Muridae was used in The Fauna of British India (1891). Palmer (1897) placed the subfamily Platacanthomyinae within the Gliridae.

Ciglitazone significantly decreases VEGF production by human granulosa cells in an in vitro study, and may potentially be used in ovarian hyperstimulation syndrome. Ciglitazone is a potent and selective PPARγ ligand. It binds to the PPARγ ligand-binding domain with an EC50 of 3.0 μM. Ciglitazone is active in vivo as an anti-hyperglycemic agent in the ob/ob murine model.

Opn was found highly expressed by a specific dendritic cell (DC) subset derived from murine mesenteric lymph nodes (MLNs) and is highly proinflammatory for colitis. Dendritic cells are important for the development of intestinal inflammation in humans with IBD and in mice with experimental colitis. Opn expression by this inflammatory MLN DC subset is crucial for their pathogenic action during colitis.

The primary sequence of PrP is 253 amino acids long before post- translational modification. Signal sequences in the amino- and carboxy- terminal ends are removed posttranslationally, resulting in a mature length of 208 amino acids. For human and golden hamster PrP, two glycosylated sites exist on helices 2 and 3 at Asn181 and Asn197. Murine PrP has glycosylation sites as Asn180 and Asn196.

The snake tends to bite repeatedly and let go, so there can be multiple puncture wounds. Its bite can deliver about 100–120 mg of venom on average; the maximum recorded dose is 400 mg. The murine median lethal dose (LD50) when administered intravenously has been calculated at 0.32 and 0.33 mg/kg. Bites were often fatal before antivenom was widely available.

The U.S. CDC currently does not mention rickettsialpox or murine typhus on its website about diseases directly transmitted by rodents (in general). Leptospirosis is carried by a variety of wild and domestic animals including dogs, rats, swine, cattle, mice in general, and can be transmitted by the urine of an infected animal and is contagious as long as the urine is still moist.

Epidemic typhus is due to Rickettsia prowazekii spread by body lice, scrub typhus is due to Orientia tsutsugamushi spread by chiggers, and murine typhus is due to Rickettsia typhi spread by fleas. Vaccines have been developed, but none are commercially available. Prevention is achieved by reducing exposure to the organisms that spread the disease. Treatment is with the antibiotic doxycycline.

The virus was then known as infectious bronchitis virus (IBV). Charles D. Hudson and Fred Robert Beaudette cultivated the virus for the first time in 1937. The specimen came to be known as the Beaudette strain. In the late 1940s, two more animal coronaviruses, JHM that causes brain disease (murine encephalitis) and mouse hepatitis virus (MHV) that causes hepatitis in mice were discovered.

The JY cell line is an Epstein–Barr virus (EBV)-immortalised B cell lymphoblastoid line. JY cells express HLA class-I A2 and class-II DR. JY is a suspension cell line, although the cells are known to grow in clumps. The growth medium is RPMI 1640, 10% fetal calf serum and 1% L-glutamine. JY cells are positive for murine leukemia virus.

This persistent, low-level inflammation was later shown to confer enhanced resistance to a wide array of viruses. This phenotype results from a previously-unrecognized function of ISG15 to negatively regulate IFN signaling, which is absent in murine systems. Other higher-order mammals (e.g. pig and dog), however, have achieved this negative regulatory function of ISG15, seemingly by convergent evolution.

It also appears to play a role in liver invasion by Plasmodium species. CD81 is required for Plasmodium vivax sporozoite entry into human hepatocytes and for Plasmodium yoelii sporozoite entry into murine hepatocytes. HIV gag proteins use tetraspanin enriched microdomains (containing minimally CD81, CD82, CD63) as a platform for virion assembly and release. Purified HIV produced by MOLT\HIV cells contains CD81.

These processes happen in a Mg2+ dependent fashion. Retroviral RNases H cleave their substrates through 3 different modes: #sequence-specific internal cleavage of RNA [1-4]. Human immunodeficiency virus type 1 and Moloney murine leukemia virus enzymes prefer to cleave the RNA strand one nucleotide away from the RNA-DNA junction. #RNA 5'-end directed cleavage 13-19 nucleotides from the RNA end.

Both Slit1 and Slit2 are found in the murine postnatal septum as well as in the neocortex. Further, Slit2 participates in inhibiting leukocyte chemotaxis. In rats, Slit1 was found in the neurons of adult and fetal forebrains. This shows that Slit proteins in mammals most likely contribute to the process of forming and maintaining the endocrine and nervous systems through interactions between proteins.

GPC3 is a promising therapeutic target for treating liver cancer. Several therapeutic anti-GPC3 antibodies have been developed, including GC33 and YP7. The laboratory of Dr. Mitchell Ho at the National Cancer Institute, NIH (Bethesda, Maryland, US) has generated YP7 and other murine monoclonal antibodies that recognize the C-lobe of GPC3 by hybridoma technology. These antibodies have been humanized (e.g.

MTA2 was initially recognized as an MTA1 like 1 gene, named MTA1-L1, from a large scale sequencing of randomly selected clones from human cDNA libraries in 1999. Clues about the role of MTA2 in gene expression came from the association of MTA2 polypeptides in the NuRD complex in a proteomic study This was followed by targeted cloning of murine Mta2 in 2001.

In 1937, Max Theiler discovered a filterable agent that was a known cause for paralysis in mice. He found the virus was not transmittable to rhesus macaques, and that only some mice developed symptoms. The virus is now referred to as Theiler's murine encephalomyelitis virus. The virus has been well characterized, and now serves as a standard model for studying multiple sclerosis.

This SPX-dependent inhibition is mediated by a physical interaction with Spl2. NUC-2 contains several ankyrin repeats. Several members of this family are annotated as XPR1 proteins: the xenotropic and polytropic retrovirus receptor confers susceptibility to infection with xenotropic and polytropic murine leukaemia viruses (MLV). Infection by these retroviruses can inhibit XPR1-mediated cAMP signaling and result in cell toxicity and death.

Tyrosine-protein kinase ABL1 also known as ABL1 is a protein that, in humans, is encoded by the ABL1 gene (previous symbol ABL) located on chromosome 9. c-Abl is sometimes used to refer to the version of the gene found within the mammalian genome, while v-Abl refers to the viral gene, which was initially isolated from the Abelson murine leukemia virus.

Cynaropicrin shows a reduction in parasitemia in murine models and has potent antitrypanosomal activity. It lowers intracellular GSH and trypanothione levels and inhibits trypanosomal ornithine decarboxylase with its α,β-unsaturated methylene moiety which acts as Michael acceptor. This leads to apoptosis of parasites. The 2-hydroxymethyl-2-propenoyl moiety was found to play an important role in the toxicity.

ICI-118,551 has been used in pre-clinical studies using murine models. When dissolved in saline, the compound crosses the blood–brain barrier. Common systemic doses used in rodent research are 0.5 or 1 mg/kg although efficacy has been demonstrated at doses as low as 0.0001 mg/kg in rhesus monkeys. Doses up to 20 mg/kg have been used without toxicity.

Modern knowledge of the impact of these diseases on populations with no prior exposure suggests that 33–50% of the population of the highlands perished. Population levels in the Guatemalan Highlands did not recover to their pre-conquest levels until the middle of the 20th century.Lovell 2005, p. 71. In 1666 pestilence or murine typhus swept through what is now the department of Huehuetenango.

Casein kinase 1 epsilon and delta are known to phosphorylate a tumor suppressor protein, p53 in vivo in both humans and murine, or old world rats. CK1 phosphorylates p53 on its N-terminus to induce its activation, which subsequently increases cell cycle arrest and apoptosis. Damage to DNA has been shown to activate p53 through enhanced CK1 activation. Inactivation of CK1 leads to decreased resistance to apoptosis.

In molecular biology mir-202 microRNA is a short RNA molecule. MicroRNAs function to regulate the expression levels of other genes by several mechanisms. The pre-miR-202 in the mouse genome is located fully within an exon, whereas in human it lies across a splice junction. This implies that human miR-202 is exposed to a negative regulation by splicing, whereas murine miR-202 is not.

Mouse studies utilizing Ffar2 gene deletions have implicated the receptor in the regulation of energy metabolism and immune responses. Short Chain Fatty Acids (SCFA's) generated in the processing of fiber by intestinal microbiota act as ligands for the receptor and can affect neutrophil chemotaxis. However, discrepancies between the pathways activated by FFAR2 agonists in human cells and the equivalent murine counterparts have been observed.

Thy1 expression varies between species. Amongst the cells reported to generally express Thy-1 are thymocytes (precursor of T cells in the thymus) & CD34(+) prothymocytes; neurons, mesenchymal stem cells, hematopoietic stem cells, NK cells, murine T-cells, endothelium (mainly in high endothelial venules or HEVs where diapedesis takes place), renal glomerular mesangial cells, circulating metastatic melanoma cells, follicular dendritic cells (FDC), a fraction of fibroblasts and myofibroblasts.

Another approach to DNA vaccination is expression library immunization (ELI). Using this technique, potentially all the genes from a pathogen can be delivered at one time, which may be useful for pathogens that are difficult to attenuate or culture. ELI can be used to identify which genes induce a protective response. This has been tested with Mycoplasma pulmonis, a murine lung pathogen with a relatively small genome.

Synaptogyrin-1 is a protein that in humans is encoded by the SYNGR1 gene. This gene encodes an integral membrane protein associated with presynaptic vesicles in neuronal cells. The exact function of this protein is unclear, but studies of a similar murine protein suggest that it functions in synaptic plasticity without being required for synaptic transmission. The gene product belongs to the synaptogyrin gene family.

During his time in Philadelphia, Levy conducted research on Epstein-Barr virus (EBV) with Gertrude and Werner Henle at Children's Hospital and on B lymphocyte biology at the Wistar Institute with Dr. Vittorio Defendi. While studying tumor viruses, particularly retroviruses, at NIH, he discovered xenotropic viruses Levy, J.A., Xenotropic viruses: murine leukemia viruses associated with NIH Swiss, NZB, and other mouse strains. Science, 1973. 182: p.

The Friend virus (FV) is a strain of murine leukemia virus identified by Charlotte Friend in 1957. The virus infects adult immunocompetent mice and is a well-established model for studying genetic resistance to infection by an immunosuppressive retrovirus. The Friend virus has been used for both immunotherapy and vaccines. It is a member of the retroviridae group of viruses, with its nucleic acid being ssRNA.

Bone morphogenetic protein 8B is a protein that in humans is encoded by the BMP8B gene. The protein encoded by this gene is a member of the TGF-β superfamily. It has close sequence homology to BMP7 and BMP5 and is believed to play a role in bone and cartilage development. It has been shown to be expressed in the hippocampus of murine embryos.

Development was shelved after it proved biologically inert in mice. In 1974, Wolfram Ostertag of the Max Planck Institute for Experimental Medicine in Göttingen, Germany reported that AZT specifically targeted Friend virus (strain of murine leukemia virus). This report attracted little interest from other researchers as the Friend leukemia virus is a retrovirus, and at the time, there were no known human diseases caused by retroviruses.

Telfer is currently a reproductive biologist and Professor of Reproductive Biology at the University of Edinburgh. She is a former Associate Editor of Molecular Human Reproduction journal. From 1987-1989, Telfer worked in the Department of Physiology at the University of Edinburgh. Here, she worked with the physiologist Roger Gosden to develop a culture systems to support murine follicle development, one of the first of its kind.

The became known as infectious bronchitis virus (IBV), but later officially renamed as Avian coronavirus. A new brain disease of mice (murine encephalomyelitis) was discovered in 1947 at Harvard Medical School in Boston. The virus causing the disease was called JHM (after Harvard pathologist John Howard Mueller). Three years later a new mouse hepatitis was reported from the National Institute for Medical Research in London.

The venom of this cobra is a postsynaptic neurotoxin and bites result in severe neurotoxicity. Ernst and Zug et al. 1996 list a value of 0.225 mg/kg SC. According to Brown and Fry of the Australian Venom and Toxin Database, the murine intraperitoneal value is 0.324 mg/kg. The average venom yield per bite is 571 mg and the maximum venom yield is 1102 mg.

CYR61 promotes the apoptotic functions of inflammatory cytokines such as TNFα, FasL, and TRAIL. It also reprograms macrophages towards M1 polarization through αMβ2-mediated activation of NF-κB. CYR61 is upregulated in patients with Crohn's disease and ulcerative colitis. CYR61 supports the patrolling behavior of murine resident Ly6Clow monocytes along the endothelial in the steady state and is required for their accumulation under viral-mimicking vascular inflammation.

Murine Mta1 contains three protein coding transcripts and three non-coding RNA transcripts. Among human MTA1 variants, only two spliced variants are characterized: ZG29p variant is derived from the c-terminal MTA1, with 251 amino acids and 29-kDa molecular weight; and MTA1s variant generated from alternative splicing of a middle exon followed by a frame-shift, is 430 amino acids and 47-kDa molecular weight.

Immunology 13.2 (2013): 145. They participate in effective antimicrobial defence through the production of IL-17 and IL-22. The role of IL-22 in humans and mice is somewhat different. In the murine model, IL-22 was found to play a role in improving the course of inflammatory bowel disease and epithelial restoration in the loss of the protective mucin barrier in the large intestine.

Roy obtained a Bachelor of Science degree in microbiology, with a minor in South Asian studies at the University of Toronto. She then pursued a Master of Science, studying the photo sensitivity of murine fibrosarcoma cells, at McMaster University. Under the supervision of Denise Belsham, Roy completed her PhD in reproductive neuroendocrinology and molecular biology at the University of Toronto's Institute of Medical Sciences.

Eculizumab is a recombinant humanized monoclonal antibody against the complement protein C5. It is an immunoglobulin G-kappa (IgGκ) consisting of human constant regions and murine complementarity- determining regions grafted onto human framework light and heavy chain variable regions. The compound contains two 448-amino acid heavy chains and two 214-amino acid light chains, and has a molecular weight of approximately 148 kilodaltons (kDa).

Known mutations in AIRE include Arg139X, Arg257X, and Leu323SerfsX51. Disruption of AIRE results in the development of a range of autoimmune diseases, the most common clinical conditions in the syndrome are hypoparathyroidism, primary adrenocortical failure and chronic mucocutaneous candidiasis.OMIM A gene knockout of the murine homolog of Aire has created a transgenic mouse model that is used to study the mechanism of disease in human patients.

In 1990 an oncogene, v-mpl, was identified from the murine myeloproliferative leukemia virus that was capable of immortalizing bone marrow hematopoietic cells from different lineages. In 1992 the human homologue, named, c-mpl, was cloned. Sequence data revealed that c-mpl encoded a protein that was homologous with members of the hematopoietic receptor superfamily. Presence of anti-sense oligodeoxynucleotidesu of c-mpl inhibited megakaryocyte colony formation.

This gene has also been shown to encourage the growth of granulocytes and monocytes, but at the cost of other blood cells. HOXB6 has the ability to cause the indefinite proliferation of murine marrow cells, as well as expand hematopoietic stem cells. When expressed abnormally, HOXB6 displays many characteristics of a potent oncoprotein. An oncoprotein can cause the transformation of a normal cell into a tumor cell.

This gene is one of the fifteen kallikrein subfamily members located in a cluster on chromosome 19. In some tissues its expression is hormonally regulated. The expression pattern of a similar mouse protein in murine developing teeth supports a role for the protein in the degradation of enamel proteins. Alternate splice variants for this gene have been described, but their biological validity has not been determined.

Other causes or associations of disease are: a compromised immune system, environmental toxins, radiation exposure, diet and other lifestyle choices, stress, and genetics. Diseases may also be multifactorial, requiring multiple factors to induce disease. For example: in a murine model, Crohn's disease can be precipitated by a norovirus, but only when both a specific gene variant is present and a certain toxin has damaged the gut.

John B. Hibbs Jr. is an American physician-scientist and educator. He is Distinguished Professor Emeritus in the Department of Medicine at the University of Utah. He is known for the discovery of the direct synthesis of L-citrulline and nitrogen oxides from L-arginine by murine activated macrophages, published in January 1987. This reaction was inhibited strongly by the non-toxic NG-monomethyl-L-arginine molecule.

The gray tree rat was first described by the American zoologist Gerrit Smith Miller as Lenothrix canus in 1903. Molecular data suggests that it is closely related to the white-bellied rats Niviventer, but is widely diverged from Maxomys, and its phylogenetic affinities are unclear. It has many primitive morphological, cranial and dental features and may have diverged from the core murine lineage at an early stage.

The red rock rat is a rat-sized murine rodent. Adults have a head-body length of , with a long, , tail, and weigh from . Males are not significantly larger than females. The fur on the upper body and flanks is mostly reddish-brown, but mixed with dark brown or black hairs, producing an overall colour that varies from orange-yellow or cinnamon to medium brown.

Deletion of murine ortholog Ube3b leads to severe developmental delay in mice. The conventional knockout of Ube3b leads to a growth retardation, decreased grip strength, and loss of vocalization associated with the metabolic disease with nucleotide metabolism and the tricarboxylic acid cycle being the most affected. Such metabolic disturbances were also found in KOS patients. In this context, UBE3B ubiquitinated α-ketoacid dehydrogenase kinase (BCKDK).

In vivo testing of mice that developed murine colon carcinoma tumour cells. They were injected with the solution of AuNPs that were allowed to spread after 6 hours. Surrounding cells were swabbed with PEG and exposed to laser treatment for detection of abnormal heating indicating areas where Au nanoshells may have gathered. The injected area was also swabbed with PEG to maximize light penetration.

Yanai R, Nishida R, Chikama T, Morishige N, Yamada N, Sonoda KH, Potential New Modes of Treatment of Neurotrophic Keratopathy. Cornea 34 Suppl 11 (2015) S121-7 Nerve Growth Factor (NGF) play a role in the epithelial proliferation and differentiation and in the survival of corneal sensory nerves. Topical treatment with murine NGF showed to promote recovery of epithelial integrity and corneal sensitivity in NK patients.

IL-38 concentrations correlated with IL-1β. The overexpression of IL-38 in murine model of arthritis and serum transfer-induced arthritis ameliorate these diseases but not in case of antigen-induced arthritis. TNF production and IL-17 responses were decreased in these models. These data shows that IL-38 could have anti-inflammatory properties in rheumatoid arthritis and probably could be use in a therapeutic strategy.

Mice without cones or without both photoreceptive cells (rd/rd cl allele) still entrained to light. Meanwhile, mice with eyes removed could not entrain to light. Foster concluded that rods and cones are unnecessary for entrainment to light, and that the murine eye contains additional photoreceptive cell types. Later studies showed that melanopsin expressing photoreceptive retinal ganglion cells (pGRCs) were accountable for non-rod, non-cone entrainment to light.

The nucleoside diphosphate (NDP) kinases (EC 2.7.4.6) are ubiquitous enzymes that catalyze transfer of gamma-phosphates, via a phosphohistidine intermediate, between nucleoside and dioxynucleoside tri- and diphosphates. The enzymes are products of the nm23 gene family, which includes NME4. The first nm23 gene, nm23-H1 (NME1), was isolated based on its reduced expression in a highly metastatic murine melanoma cell line and was proposed to be a metastasis suppressing gene.

This gene encodes a component of BLOC-1 (biogenesis of lysosome-related organelles complex 1). Components of this complex are involved in the biogenesis of organelles such as melanosomes and platelet- dense granules. A mouse model for Hermansky–Pudlak syndrome is mutated in the murine version of this gene. Some transcripts of the downstream gene TXNDC5 overlap this gene, but they do not contain an open reading frame for this gene.

Putative trace amine-associated receptor 3 (TAAR3) is a human pseudogene with the gene symbol TAAR3P. Retrieved 28 November 2019 In other species such as mice, TAAR3 is a functional protein-coding gene that encodes a trace amine- associated receptor protein. Ligands: Isobutylamine is a known ligand of TAAR3 in mice associated with sexual behaviour in male mice. Isopentylamine was identified as a ligand for murine TAAR3 eliciting aversive behavior.

Red-bellied black snake (Pseudechis porphyriacus) The Red-bellied black snake (Pseudechis porphyriacus) is a venomous species native to Australia. The venom of the red-bellied black snake consists of myotoxins, coagulants and also has haemolytic and cytotoxic properties. It also contains weak pre-synaptic neurotoxins. The murine is 2.52 mg/kg SC. Average venom yield per bite is 37 mg and a maximum yield of 97 mg.

MAIT cells are most common in the liver, where they usually comprise 20-40% of the T lymphocyte population. The total murine MAIT cell population is roughly ten times smaller than the human MAIT cell population. While MAIT cells display effector characteristics immediately out of the thymus, they may also undergo clonal expansion in the periphery and establish antigen memory. In this way, MAIT cells display both innate and adaptive characteristics.

Murine polyomavirus VP1 in complex with the GT1a glycan. GT1a is shown in yellow and the VP1 monomer with a white surface and a blue protein backbone. A complex network of hydrogen bonds, many water-mediated, is shown at the binding surface by orange lines, with participating protein residues shown as sticks. Mutations of the two residues shown in cyan at the bottom of the figure can significantly affect pathogenicity.

GITR was identified as a new member of the TNF receptor superfamily, by comparing gene expression in untreated and DEX-treated murine T-cell lines. GITR can T cells are activated. Although mouse GITR is induced by either GC engagement or T-cell activation, its human homologue (hGITR/AITR) is upregulated only by activation. Therefore, the requirements for GR signaling in inducing GITR expression by T cells remain moot .

This gene is the human homolog of murine plunc, and like the mouse gene, is specifically expressed in the airways and nasopharyngeal regions. Plunc inhibits the epithelial sodium channel (ENaC), and also has anti-microbial functions.6 As such, plunc is believed to play a role in innate immune defense in the airways. PLUNC's ability to regulate ENaC is pH- sensitive and fails in acidic cystic fibrosis airways.

PDE4 hydrolyzes cyclic adenosine monophosphate (cAMP) to inactive adenosine monophosphate (AMP). Inhibition of PDE4 blocks hydrolysis of cAMP thereby increasing levels of cAMP within cells. cAMP suppresses the activity of immune and inflammatory cells. PDE4 inhibition in an induced chronic lung disease murine model was shown to have anti-inflammatory properties, attenuate pulmonary fibrin deposition and vascular alveolar leakage, and prolong survival in hyperoxia- induced neonatal lung injury.

In 2001, the company acquired Knoll, the pharmaceutical division of BASF. In 2002, it divested the Selsun Blue brand to Chattem. Later in 2002, the company sold Clear Eyes and Murine to Prestige Brands. In 2004, the company acquired TheraSense, a diabetes-care company, which it merged with its MediSense division to become Abbott Diabetes Care. In 2006, Abbott assisted Boston Scientific in its purchase of Guidant Corporation.

Polycomb genes in Drosophila mediate changes in higher-order chromatin structure to maintain the repressed state of developmentally regulated genes . M33 deficiency interferes with steps upstream of the Y-chromosome-specific SRY gene may cause sex reversal. It may also involved in the campomelic syndrome and neoplastic disorders linked to allele loss in this region. Disruption of the murine M33 gene, displayed posterior transformation of the sternal ribs and vertebral columns .

There are notable differences between the hereditary dilated cardiomyopathy in DMD and acute coxsackieviral-mediated cardiomyopathy. #The amount of virally infected cardiomyocytes varies in different stages of the disease. In a mouse model, at the acute stage (7 days after infection with coxsackievirus B3) approximately 10% of the myocytes are infected and could affect overall cardiac function. In chronic murine infection, the percentage of infected cardiomyocytes are much lower.

Magnetite and maghemite are preferred in biomedicine because they are biocompatible and potentially non-toxic to humans. Iron oxide is easily degradable and therefore useful for in vivo applications. Results from exposure of a human mesothelium cell line and a murine fibroblast cell line to seven industrially important nanoparticles showed a nanoparticle specific cytotoxic mechanism for uncoated iron oxide. Solubility was found to strongly influence the cytotoxic response.

Cell-based aAPCs have been produced by transfecting murine fibroblasts to express specific peptide-loaded HLA molecules with co-stimulatory signal B7.1, and cell adhesion molecules ICAM-1 and LFA-3. Many microparticle systems have been developed as microparticles represent physiologically similar sizes to cells. Microparticle curvature and shape has also been shown to play an important role in effective T cell stimulation. Nanoparticles have also been used.

Follistatin also is implicated in prostate cancers where mutations in its gene may preventing it from acting on activin which has anti- proliferative properties. Lefty is a regulator of TGFβ and is involved in the axis patterning during embryogenesis. It is also a member of the TGF superfamily of proteins. It is asymmetrically expressed in the left side of murine embryos and subsequently plays a role in left-right specification.

Dock4 was discovered as a gene product which was disrupted during tumour progression in a murine cancer model-derived osteosarcoma cell line. Subsequent Northern blot analysis revealed high levels of Dock4 expression in skeletal muscle, prostate and ovary as well as lower levels in the heart, placenta and colon. A separate study has reported expression of a Dock4 splice variant (Dock4-Ex49) in the brain, inner ear and eye.

CD8.4 is a murine chimeric coreceptor. The extracellular and transmembrane part of the coreceptor is from wild-type CD8 coreceptor, whereas the intracellular domain from CD4 coreceptor. This model was created to examine role of coreceptor coupling to Lck (lymphocyte-specific protein tyrosine kinase) as the CD4 and CD8 coreceptors have an Lck-binding site in their intracellular domain. CD4 coreceptor has higher coupling to Lck in thymocytes than CD8 coreceptor.

CidA and LrgA are homologous holin and anti-holin proteins, each with 4 putative transmembrane segments (TMSs). Members of the CidA/LrgA holin family also include putative murine hydrolase exporters from a wide range of Gram-positive and Gram-negative bacteria as well as archaea. Most CidA/LrgA holin family proteins vary in size between 100 and 160 amino acyl residues (aas) in length although a few are larger.

Genes encoding human Ly6 family members are located in clusters on chromosomes 6, 8, 11 and 19. In the murine genome family members are located on chromosomes 17, 15, 9 and 7, respectively. Genes encoding Ly6 proteins with one LU domain consist of 3 exons and 2 introns. The first exon encodes the signal peptide, Exons 2 and 3 encode the LU domain, and exon 3 also encodes the GPI anchor.

Venoms of species in the Elapidae are mainly neurotoxic for immobilizing prey and defense. The main group of toxins are PLA2 and Three finger toxins (3FTx). Other toxic components in some species comprise cardiotoxins and cytotoxins, which cause heart dysfunctions and cellular damage, respectively. All members are venomous to varying extents, and some are considered among the world's most venomous snakes based upon their murine values, such as the taipans.

Cat fleas can transmit other parasites and infections to dogs and cats and also to humans. The most prominent of these are Bartonella, murine typhus, and apedermatitis. The tapeworm Dipylidium caninum can be transmitted when an immature flea is swallowed by pets or humans. In addition, cat fleas have been found to carry Borrelia burgdorferi, the etiologic agent of Lyme disease, but their ability to transmit the disease is unclear.

XMRV is closely related to several known xenotropic mouse viruses. These viruses recognize and enter cells of non- rodent species by means of the cell-surface xenotropic and polytropic murine leukemia virus receptor (XPR1). Only fractionated plasma is heat treated, blood for transfusion is not. A United States federal consortium is now working to determine the prevalence of XMRV in the blood supply and the suitability of different detection methods.

Raf kinases found in retroviruses (such as murine v-Raf) are secondarily derived from the corresponding vertebrate genes of their hosts. These Raf genes encode severely truncated proteins, that lack the entire N-terminal autoinhibitory domain, and the 14-3-3 binding motifs. Such severe truncations are known to induce an uncontrolled activity of Raf kinases: that is just exactly what a virus may need for efficient reproduction.

His work also showed that the bZIP transcription factor: XBP1 forms a hetero-dimer with c-Fos. This has turned out to be relevant to the developmental control of B cell differentiation. His lab also discovered the NFX1 transcription factor and cloned both the human and murine cDNAs. This factor can bind DNA, RNA and protein via a reiterated RING finger motifs in the central domain of the polypeptide.

Infusion of decorin into experimental rodent spinal cord injuries has been shown to suppress scar formation and promote axon growth. Decorin has been shown to have anti-tumorigenic properties in an experimental murine tumor model and is capable of suppressing the growth of various tumor cell lines. The decorin-deficient knockout mouse shows reduced inflammatory reactions during contact dermatitis due to a defect in leukocyte recruitment and altered interferon gamma function.

Using a reverse transcriptase enzyme and purified RNA templates, one strand of cDNA is produced (first-strand cDNA synthesis). The M-MLV reverse transcriptase from the Moloney murine leukemia virus is commonly used due to its reduced RNAse H activity suited for transcription of longer RNAs. The AMV reverse transcriptase from the avian myeloblastosis virus may also be used for RNA templates with strong secondary structures (i.e. high melting temperature).

Besides causing respiratory infections, human coronavirus OC43 is also suspected of playing a role in neurological diseases. In the 1950s, the human coronavirus OC43 began to diverge into its present genotypes. Phylogentically, mouse hepatitis virus (Murine coronavirus), which infects the mouse's liver and central nervous system, is related to human coronavirus OC43 and bovine coronavirus. Human coronavirus HKU1, like the aforementioned viruses, also has its origins in rodents.

Human, murine and rat Pim-1 contain 313 amino acids, and have a 94 – 97% amino acid identity. The active site of the protein, ranging from amino acids 38-290, is composed of several conserved motifs, including a glycine loop motif, a phosphate binding site and a proton acceptor site. Modification of the protein at amino acid 67 (lysine to methionine) results in the inactivation of the kinase.

Knockout mice have been generated for FANCA. However, both single and double knockout murine models are healthy, viable, and do not readily show the phenotypic abnormalities typical of human Fanconi anaemia sufferers, such as haematological failure and increased susceptibility to cancers. Other markers such as infertility however still do arise. This can be seen as evidence for a lack of functional redundancy in the FANCA gene-encoded proteins.

Loss of CD47 allows sustained proliferation of primary murine endothelial cells and enables these cells to spontaneously reprogram to form multipotent embryoid body-like clusters. Expression of several stem cell markers, including c-Myc, is elevated in CD47-null endothelial cells and a human T cell line lacking CD47. Activation of CD47 with TSP-1 in wild-type cells inhibits proliferation and reduces expression of stem cell transcription factors.

IAS proteins were originally identified in studies that were aimed to decipher the Janus Kinase (JAK)/STAT signaling pathway. Originally, PIAS3 was found to interact specifically with phosphorylated STAT3 in Interleukin -6 (IL-6) activated murine myeloblast M1 cells. This interaction is mediated via PIAS3 binding to the STAT3 DNA binding domain. Hence, STAT3 transcriptional activity is inhibited by the physical prevention of its binding to target genes.

Activation of NLRP1B-dependent inflammasome responses appears in host defense with mechanism like IL-1β and neutrophils. NLRP1B can function as a sensor of bacterial proteases, immune responses are specifically activated by virulence factors. It is not clear what stimuli might activate NLRP1A, the other known functional murine NLRP1 paralog. The study identified a mouse carrying a missense gain-of-function mutation in NLRP1A (Q593P) that active inflammasome responses.

In molecular biology, Six3OS1 is a long non-coding RNA. It was originally identified in the murine embryonic and postnatal retina. It is located in the distal promoter region of the gene encoding Six3, a homeodomain transcription factor. It regulates the activity of Six3 in the developing mouse retina, by binding to transcriptional co-regulators of Six3 and to histone modification enzymes and acting as a transcriptional scaffold.

Autosomal recessive NOS2 deficiency has been described in mice. They lack the gene encoding nitric oxide synthase 2 (Nos2) and are susceptible to murine CMV infection. In February 2020, the same autosomal recessive, complete NOS2 deficiency was described in a human. A 51-year-old previously healthy person died after 29 months of progressive CMV infection due to respiratory failure secondary to CMV pneumonitis, CMV encephalitis, and hemophagocytic lymphohistiocytosis.

Murine microRNA-712 is a potential biomarker (i.e. predictor) for atherosclerosis, a cardiovascular disease of the arterial wall associated with lipid retention and inflammation. Non-laminar blood flow also correlates with development of atherosclerosis as mechanosenors of endothelial cells respond to the shear force of disturbed flow (d-flow). A number of pro- atherogenic genes including matrix metalloproteinases (MMPs) are upregulated by d-flow, mediating pro-inflammatory and pro-angiogenic signals.

The coastal taipan (Oxyuranus scutellatus), or common taipan, is a species of large, extremely venomous snake in the family Elapidae. The species is native to the coastal regions of northern and eastern Australia and the island of New Guinea. According to most toxicological studies, this species is the third- most venomous land snake in the world after the Inland taipan and Eastern brown snake based on its murine .

The 25-kDa core protein (excluding the heavy glycosylation) of rodent Thy-1 is 111 or 112 amino acids in length, and is N-glycosylated at three sites (In contrast to only two glycosylation sites for human Thy-1). The 162aa (murine, 161 for human) Thy1 precursor has 19 amino acid (aa 1-19) signal sequence and 31 amino acid (aa 132-162) C-terminal transmembrane domain that is present in pro form but removed when transferring the 112 amino acid (aa 20-131) mature peptide to GPI anchor which would attach through the aa 131. Some of the common monoclonal antibodies used to detect this protein are clones OX7, 5E10, K117 and L127. There have been some reports of Thy1 monoclonal antibodies cross reacting with some cytoskeletal elements: anti Thy-1.2 with actin in marsupial, murine, and human cells and anti Thy-1.1 with vimentin, and were suggested to be due to sequence homology by studies done more than 20 years back.

Papular urticaria has been suggested as developing in some people. No human disease has been definitively found to be naturally vectored by this mite. Lab demonstrations have proved that the mite is at least capable of vectoring murine typhus, rickettsialpox, tularemia, plague, coxsackievirus, and Q fever, although it has not been known to do so outside the lab. The mite was reported as capable of vectoring human typhus, but these reports are not generally accepted.

Coiled-coil domain-containing protein 181 (CCDC181) is a protein that in human is encoded by C1orf114, which is located at the Chromosome 1 at 1q24.2. The accession is Q5T1D7. Researches have recently revealed that CCDC 181 is a microtubule-binding protein that interacts with murine Hook1 in haploid male germ cells and localizes to the sperm tail and motile cilia. The disruption of Hook1 may lead to inappropriate function of spermatogenesis.

They contain activating mutations of the K-ras as well as mutations of p53, resulting in high expression of c-myc. GL261 tumors also highly express MHC I, explaining their partial immunogenicity and have limited expression of MHC II, B7-1, and B7-2. The tumors are invasive, are not known to be metastatic, and do not spontaneously regress. Other immunocompetent murine models used to study GBM include GL26, CT-2A, SMA-560, and 4C8.

Micromys is a genus of small rodents in the subfamily Murinae. The genus, which is not closely related to any other murine genus, contains two living species: the widespread Eurasian harvest mouse (Micromys minutus) of much of Europe and Asia; and the more restricted Micromys erythrotis of Vietnam, southern China, and perhaps nearby regions. Fossils of Micromys date back to the Late Miocene and include at least 10 extinct species, which form several lineages.

Nucleoplasmin-3 is a protein that in humans is encoded by the NPM3 gene. The protein encoded by this gene is related to the nuclear chaperone phosphoproteins, nucleoplasmin and nucleophosmin. It is highly homologous to the murine Npm3 gene. Based on the structural similarity of the human NPM3 gene product to nucleoplasmin and nucleophosmin, NPM3 may represent a new member of this gene family, and may share basic functions with the molecular chaperones.

The design incentive behind aerosol delivery is to target the lungs rapidly, easily and painlessly in contrast to intradermal immunization. In murine studies, intradermal vaccination caused localized inflammation at the site of injection whereas MVA85A did not cause unfavourable effects. A correlation has been found between the mode of delivery and vaccine protection efficacy. Research data suggests aerosol delivery has not only physiological and economic advantages, but also the potential to supplement systemic vaccination.

They are central to the pathogenesis of sterile inflammatory and autoimmune diseases such as systemic lupus erythematosus.Christensen, S.R., et al. Toll-like receptor 7 and TLR9 dictate autoantibody specificity and have opposing inflammatory and regulatory roles in a murine model of lupus. Immunity 25(3):417-28, 2006 The research on TLRs won him the Nobel Prize in 2011.Jules A. Hoffmann (background) and BeutlerThe positional cloning of Lps was completed in 1998.

Egyptian cobra (Naja haje) The Egyptian cobra (Naja haje) is another species of cobra which causes a significant number of bites and human fatalities throughout its range. The venom of the Egyptian cobra consists mainly of neurotoxins and cytotoxins. The average venom yield is 175 to 300 mg in a single bite, and the murine subcutaneous value is 1.15 mg/kg. This species has large fangs and can produce large quantities of venom.

Mali cobra (Naja katiensis) The Mali cobra (Naja katiensis) is a venomous species of spitting cobra native to western Africa. The venom of this species consists of postsynaptic neurotoxins and cardiotoxins with cytotoxic (necrotizing) activity. An average wet venom yield of 100 mg has been reported for this species. The average murine value of this species is 1.15 mg/kg IV, but there is an IV range of 0.97 mg/kg-1.45 mg/kg.

However, incompatibilities between the human and murine systems hamper clinical evaluation of these agents. Moreover, urokinase is used by normal cells for tissue remodeling and vessel growth, which necessitates distinguishing cancer-associated urokinase features for specific targeting. uPA breakdown of the extracellular matrix is crucial for initiating the angiogenesis which is associated with cancer growth. uPA antigen is elevated in breast cancer tissue, which correlates with poor prognosis in breast cancer patients.

In keeping with the stem cell hypothesis, the more undifferentiated daughter typically inherited the chromatids with the older DNA, while the more differentiated daughter inherited the younger DNA. Experimental evidence against the immortal strand hypothesis is sparse. In one study, researchers incorporated tritiated thymidine into dividing murine epidermal basal cells. They followed the release of tritiated thymidine after various chase periods, but the pattern of release was not consistent with the immortal strand hypothesis.

Halmaheramys bokimekot, or the spiny Boki Mekot rat, is a rodent found on the island of Halmahera in the Molucca archipelago, whose discovery was announced in 2013. This is the only locality where this particular species has been found. H. bokimekot was confirmed as a new species through probabilistic methodologies applied to morphological and molecular data. Named after its geographical provenance in the North Moluccas, Halmaheramys is the only known murine species endemic to Halmahera.

The murine homolog of human 15(S)-lipoxygenase-2 (ALOX15B), 8(S)-lipoxygenase, while preferring arachidonic acid over linoleic acid, metabolizes linoleic acid predominantly to (9(S)-HpODE, which in tissues and cells is rapidly reduced to 9(S)-HODE.Mol Carcinog. 1999 Feb;24(2):108-17Oncogene. 2005 Feb 10;24(7):1174-87 However, ALOX15B, similar to human 15-lipoxygenase-1 (ALOX15), metabolizes linoleic acid to 13(S)-HODE but not to 9(S)-HODEs.Eur.

Protein fosB, also known as FosB and G0/G1 switch regulatory protein 3 (G0S3), is a protein that in humans is encoded by the FBJ murine osteosarcoma viral oncogene homolog B (FOSB) gene. The FOS gene family consists of four members: FOS, FOSB, FOSL1, and FOSL2. These genes encode leucine zipper proteins that can dimerize with proteins of the JUN family (e.g., c-Jun, JunD), thereby forming the transcription factor complex AP-1.

The venom of this species is not well studied, but it is believed that the venom is dangerously neurotoxic, like that of most elapids. A study listed the intraperitoneal (IP) of this species at 0.143 mg/kg. Venoms of the water cobras, were assayed for lethality, proteolytic activity and protein content. Naja annulata annulata and Naja christyi venoms averaged 89% protein and lacked proteolytic activity. The murine intraperitoneal LD50 of N. a.

It is an ATP- competitive Bcr-Abl tyrosine-kinase inhibitor with an additional inhibitory effect on SRc family kinases (including Src, Lyn and Hck). It has also shown activity against the receptors for platelet derived growth factor and vascular endothelial growth factor. Bosutinib inhibited 16 of 18 imatinib-resistant forms of Bcr-Abl expressed in murine myeloid cell lines, but did not inhibit T315I and V299L mutant cells. Bosutinib is metabolized through CYP3A4.

Activating receptors have lower affinity for their ligands than do inhibitory receptors. Although the purpose of this difference in affinity is unknown, it is possible that the cytolysis of target cells occurs preferentially under conditions in which the expression of stimulating MHC class I molecules on target cells is high, which may occur during viral infection. This difference, which is also present in Ly49, the murine homolog to KIR, tips the balance towards self-tolerance.

NeutroSpec was approved by the U.S. Food and Drug Administration (FDA) in June 2004 for imaging of patients with symptoms of appendicitis. It consisted of an intact murine (mouse) IgM monoclonal antibody against human CD15, labeled with technetium-99m so as to be visible on a gamma camera image. Since anti-CD15 antibodies bind selectively to white blood cells such as neutrophils, it could be used to localize the site of an infection.

They also induce the synthesis and release of other pro-inflammatory cytokines such as interleukin 1 (IL-1), IL-6 and TNF-α from fibroblasts and macrophages. The genes for CCL3 and CCL4 are both located on human chromosome 17 and on murine chromosome 11. They are produced by many cells, particularly macrophages, dendritic cells, and lymphocytes. MIP-1 are best known for their chemotactic and proinflammatory effects but can also promote homeostasis.

Combination therapy experiments with sirolimus (rapamycin) and doxorubicin have shown promise in treating Akt-positive lymphomas in mice. In 2006, animal research coupling a murine monoclonal antibody with doxorubicin has created an immunoconjugate that was able to eliminate HIV-1 infection in mice. Current treatment with antiretroviral therapy (ART) still leaves pockets of HIV within the host. The immunoconjugate could potentially provide a complementary treatment to ART to eradicate antigen-expressing T cells.

Halichondria produces the eribulin precursor halichondrin B Lacking any protective shell or means of escape, sponges have evolved to synthesize a variety of unusual compounds. One such class is the oxidized fatty acid derivatives called oxylipins. Members of this family have been found to have anti-cancer, anti-bacterial and anti-fungal properties. One example isolated from the Okinawan plakortis sponges, plakoridine A, has shown potential as a cytotoxin to murine lymphoma cells.

Myotonia can be achieved in preparations of intact isolated muscle by the administration of 9-Anthracenecarboxylic acid, a blocker of chloride channels. It is also possible to achieve myotonia in preparations of intact isolated muscle by greatly lowering or removing the extracellular content of chloride in the bathing medium. During the 1970s several murine models of myotonia appeared. One in particular has been used widely, the adr mouse or "arrested development of righting response".

As a result, cells such as neurons are very resistant to infection and transduction by retroviruses. There is concern that insertional mutagenesis due to integration into the host genome might lead to cancer or leukemia. This concern remained theoretical until gene therapy for ten SCID-X1 patients using Maloney murine leukemia virus resulted in two cases of leukemia caused by activation of the LMO2 oncogene due to nearby integration of the vector.

Runx1 was purified as a sequence-specific DNA-binding protein that regulated the disease specificity of the Moloney murine Leukemia virus. Furthermore, Ito et al. purified Runx2, the homolog of Runx1. Purified transcription factors consisted of two subunits, a DNA binding CBFα chain (RUNX1 or RUNX2) and a non-DNA-binding subunit called core binding factor β (CBFβ); the binding affinity of RUNX1 and RUNX2 was significantly increased by association with CBFβ.

In the fields of molecular biology and genetics, c-Fos is a proto-oncogene that is the human homolog of the retroviral oncogene v-fos.Curran, T: The c-fos proto-oncogene. In: Reddy EP, Skalka AM, Curran T (eds.). The Oncogene Handbook 1988 Elsevier, New York, pp 307–327, It was first discovered in rat fibroblasts as the transforming gene of the FBJ MSV (Finkel–Biskis–Jinkins murine osteogenic sarcoma virus) (Curran and Tech, 1982).

The murine local lymph node assay (LLNA) is an in vivo test for skin sensitisation. LLNA has largely superseded the guinea pig maximisation test and the Buehler test. It is considered more scientific and less cruel (lower number of animals; less suffering) and has found broad scientific and regulatory acceptance. The principle underlying the LLNA is that skin sensitizers induce growth of lymphocytes in the lymph nodes draining the site of application.

The role of OSM as an inflammatory mediator was clear as early as 1986. Its precise effect on the immune system, as with any cytokine, is far from clear. However, two schools of thought are emerging: The first proposes that OSM is pro-inflammatory; whilst the other holds the opposite view, claiming OSM is anti-inflammatory. It is important to note that before 1997 differences in human and murine OSM receptor usage were unknown.

Despite a small modicum of successes, transfer factor generated from human blood (human-derived), cow spleen (bovine- derived), or mouse spleen (murine derived) is not in routine clinical use today. A trial investigating its ability to immunize children with leukemia against shingles showed promise in a small number of patients, but represents only one of two placebo-controlled studies. Instead, transfer factors derived from cow colostrum and/or chicken eggs yolks are used predominantly today.

Studies have shown that the loss of PLK1 expression can induce pro-apoptotic pathways and inhibit growth. Based on yeast and murine studies of meiosis, human PLK1 may also have a regulatory function in meiosis. S. cerevisiae polo kinase CDC5 is required to phosphorylate and remove meiotic cohesion during the first cell division. In CDC5 depleted cells, kinetochores are bioriented during meiosis I, and Mam1, a protein essential for coorientation, fails to associate with kinetochores.

Early settlers feared the red-bellied black snake, though it turned out to be much less dangerous than many other species. The murine median lethal dose (LD50) is 2.52 mg/kg when administered subcutaneously. A red-bellied black snake yields an average of 37 mg of venom when milked, with the maximum recorded being 94 mg. It accounted for 16% of identified snakebite victims in Australia between 2005 and 2015, with no deaths recorded.

The murine MKK7 protein is encoded by 14 exons which can be alternatively spliced to yield a group of protein kinases. This results in six isoforms with three possible N-termini (α, β, and γ isoforms) and two possible C-termini (1 and 2 isoforms). The molecular mass of the isoforms spans from 38 to 52 kDa, with between 345 and 467 amino acids. The physiological relevance of the different MKK7 isoforms is still unclear.

In addition, NT5E functions as an adhesion and signaling molecule and can regulate cellular signaling with extracellular matrix components such as fibronectin and laminin. This can mediate the metastatic and invasive properties of cancer. In mouse breast and prostate cancer tumor models as well as in breast cancer xenograft model, NT5E was confirmed to support tumor angiogenesis. His expression promotes invasion and metastasis of murine and human melanoma cells and human breast cancer cells.

The upstream 2.5 kilobases of the perlecan promoter region were studied by CAT activation in cell lines of various histological origins. This study concluded that there existed a TGF-β responsive element in the promoter just 285 base pairs upstream of the transcriptional start site. This result has been corroborated in such tissues as human colon carcinoma cells. and murine uterine epithelium by in vitro addition of the cytokine to cell culture medium.

Development of murine neoplasms started with work with the BALB/c mice to isolate the IgG1 secreting MOPC21 tumor. From this tumor, the P3K cells were isolated and developed into two cell lines, 289-16 and P3-X63. The 289-16 cell line secreted only light chain and no heavy chain and was renamed NSI/1. Clones from that cell line were isolated and a nonsecreting cell line was identified and was named NS0/1.

M. coucha has been used frequently in medical research. Unlike the common murine research model, M. coucha has been maintained as an outbred line so it has maintained the genetic heterogeneity necessary for many studies involving immune response. M. coucha also has a naturally occurring papillomavirus that mimics the infection cycle and symptoms seen in humans with HPVs. These two traits have made it a good model to study vaccines against HPV infections.

CD45 is a pan- leukocyte protein with tyrosine phosphatase activity involved in the regulation of signal transduction in hematopoiesis. CD45 does not colocalize with lipid rafts on murine and human non-transformed hematopoietic cells, but CD45 positioning within lipid rafts is modified during their oncogenic transformation to acute myeloid leukemia. CD45 colocalizes with lipid rafts on AML cells, which contributes to elevated GM-CSF signal intensity involved in proliferation of leukemic cells.

Mice that are genetically engineered to lack orexin genes demonstrate many similarities to human narcolepsy. During nocturnal hours, when mice are normally present, those lacking orexin demonstrated murine cataplexy and displayed brain and muscle electrical activity similar to the activity present during REM and NREM sleep. This cataplexy is able to be triggered through social interaction, wheel running, and ultrasonic vocalizations. Upon awakening, the mice also display behavior consistent with excessive daytime sleepiness.

The Band of Parents' first project was the development of a humanized antibody, Hu3F8. In addition to surgery, chemotherapy and radiation, many neuroblastoma patients at MSKCC were treated with a murine (mouse-derived) monoclonal antibody called 3F8. Given intravenously, 3F8 binds specifically to neuroblastoma cells and triggers an immune response, which destroys the cancerous cells. Because the antibody also binds to peripheral nerve cells, the treatment is painful, but it is generally without long-term complications.

CD72 (Cluster of Differentiation 72), also known in murine biology as Lyb-2, is a protein active in the immune system of animals. It consists of two identical halves, each of about 39-43 kD, and is a C-type lectin. Its primarily locus of expression is B-cells (from the pro-B through the mature B-cell stage), where it appears to mediate aspects of B-cell - T-cell interaction. It is a ligand for CD5.

The chemical structure of hoiamide D. p53 protein is a well known tumor suppressor that regulates the cell cycle, DNA repair, and apoptosis by acting as a transcription factor. MDM2 is a murine ubiquitin ligase that downregulates p52 by various mechanisms. The binding surface of the two proteins is small, and the interaction is hydrophobic. Through an assay that made available the p53/MDM2 complex, hoiamide D was found to inhibit the activity of the interaction.

The HPyV12 genome follows the typical organization for a polyomavirus, containing a small and large tumor antigen and three viral capsid proteins; it has no open reading frame corresponding to an agnoprotein. In the 2015 taxonomic update to the polyomavirus group, the International Committee on Taxonomy of Viruses classified HPyV12 as a member of the genus Alphapolyomaviridae, whose type species is murine polyomavirus (Mus musculus polyomavirus 1). In 2018, it was renamed to Sorex araneus polyomavirus 1.

It is suggested that these G protein-coupled receptors redundantly activate phospholipase C in basolateral amygdala. One effect of the activation of phospholipase C is deactivation of KCNQ channels. Since KCNQ channels conduct M current that raises the threshold for action potential, deactivation of these channels leads to increased neuronal excitability and enhanced memory consolidation. D5 receptors may be required for long-term potentiation at the synapse between medial perforant path and dentate gyrus in murine hippocampal formation.

Chemokine like receptor 1 also known as ChemR23 ( _Chem_ erin _R_ eceptor _23_ ) is a protein that in humans is encoded by the CMKLR1 gene. Chemokine receptor-like 1 is a G protein-coupled receptor for the chemoattractant adipokine chemerin and the omega-3 fatty acid eicosapentaenoic acid-derived specialized pro-resolving molecule, resolvin E1 (see Specialized proresolving mediators#EPA-derived resolvins (i.e. RvE)). The murine receptor that shares almost 80% homology with the human receptor, is called Dez.

IL-33 is constitutively located in the nucleus of structural cells of humans and mice and has a helix-turn-helix domain presumably allowing it to bind to DNA. There is a paucity of research into the nuclear role of IL-33 but amino acids 40-58 in human IL-33 are sufficient for nuclear localisation and histone binding. IL-33 also interacts with the histone methyltransferase SUV39H1 and murine appears to IL-33 interact to NF- κB.

Z-DNA-binding protein 1, also known as DNA-dependent activator of IFN- regulatory factors (DAI) and DLM-1, is a protein that in humans is encoded by the ZBP1 gene. ZBP1 is also an abbreviation for chicken or rat β-actin zipcode-binding protein 1, a homolog of the human insulin-like growth factor 2 mRNA-binding protein 1 (IMP-1) and murine CRD-BP, the proteins involved in mRNA transport (RNA-binding proteins, RBPs).

Average venom yield is 80–120 mg and the murine is 1.1-1.6 mg/kg SC with an estimated lethal dose for humans of 50–60 mg. Actual bites from this species are fairly rare, and deaths in modern times are so far unheard of. Local symptoms of swelling and bruising is reported in about 25% of cases. General symptoms of drowsiness, nausea, vomiting, violent abdominal pain and vertigo often occur, as does a mild pyrexial reaction.

Dugite (Pseudonaja affinis) The Dugite (Pseudonaja affinis) is a highly venomous Australian brown snake species. The venom of this species contains highly potent presynaptic and postsynaptic neurotoxins and procoagulants. The murine is 0.66 mg/kg SC. The average venom yield per bite is 18 mg (dry weight of milked venom) according to Meier and White (1995). Rate of envenomation is 20-40% and the untreated mortality rate is 10–20 %by cardiac arrest, kidney failure, or cerebral hemorrhage.

Thus, Tregs are being investigated as targets for HIV cure research. Some Treg depletion strategies have been tested in SIV infected nonhuman primates, and shown to cause viral reactivation and enhanced SIV specific CD8+ T cell responses. Regulatory T cells have a large role in the pathology of visceral leishmaniasis and in preventing excess inflammation in patients cured of visceral leishmaniasis. CD4+ regulatory T cells are often associated with solid tumours in both humans and murine models.

SEMA7A promotes axonal growth and is involved in mesoderm derived somite formation. Murine embryonic Sema7A expression is highest on day 7, which is indicative of its role on the differentiation of germ layer structure. Embryonic Sema7A expression is noticeable at all developmental stages as well as in the newborn and adult thymus, indicative of a development T-cell role. In wild type neurons, addition of Sema7A under in vitro conditions promotes elongation and branching in a dose dependent manner.

In normal breast tissue, mRNA expression of SEMA7A is low or not expressed, but activation to re-express SEMA7A occurs in these adult tissues to cause pleiotropic effects which increase tumorigenesis. Tumor cell growth, EMT, lung metastasis and angiogenesis have been linked to increased Sema7a expression in murine models. Increased SEMA7A expression correlates with poor prognosis in breast cancer patients. Tumors increase SEMA7A expression in an involuting environment, but knockout of SEMA7a in mouse models undergoing involution decreases lymphangiogenesis.

Interleukin 34 (IL-34) is a protein belonging to a group of cytokines called interleukins. It was originally identified in humans, by large scale screening of secreted proteins; chimpanzee, murine, rat and chicken interleukin 34 orthologs have also been found. The protein is composed of 241 amino acids, 39 kilodaltons in mass, and forms homodimers. IL-34 increases growth or survival of immune cells known as monocytes; it elicits its activity by binding the Colony stimulating factor 1 receptor.

The researchers concluded that hyperubiquitination and saturation of the proteasome system results due to the accumulation of misfolded protein, which induces stress. The accumulation of misfolded proteins induced by ER stress has also been observed in human DCM. A murine DCM study found an increase in apoptosis due to the high levels of CHOP expression. CHOP is a transcription factor that is elevated during ER stress and causes apoptosis of cells during the process of an unfolded protein response.

Not only have artificial ovaries shown the ability to restore fertility, they have further been linked to the complete restoration of hormone production leading to puberty. Transplantation of a human decellularized artificial ovary containing murine primary follicles has been shown to induce puberty in mice without oocytes by promoting oestradiol and inhibin B production. Mice were then shown to be able to produce viable offspring suggesting that artificial ovaries could be useful in women who have not undergone puberty.

The ectodomain of FAT1 can also be shed from the cell surface by the sheddase ADAM10, with release of this ectodomain a possible new biomarker in pancreatic cancer. FAT1 has also been found to undergo alternative splicing in breast cancer cells undergoing epithelial-to-mesenchymal (EMT) transition with the addition of 12 amino acids in the cytoplasmic tail. Similar splice variants have also been described for murine Fat1 where alternative splicing of the cytoplasmic tail regulated cell migration.

EsiRNA and its protein complex may also function to promote the creation of heterochromatin, protein around which DNA is very tightly coiled, near retrotransposon sites, silencing the DNA by making it difficult for transcription related proteins to access it.Kuramochi-Miyagawa, S., Watanabe, T., Gotoh, K., Totoki, Y., Toyoda, A., Ikawa, M., et al. (2008). DNA methylation of retrotransposon genes is regulated by Piwi family members MILI and MIWI2 in murine fetal testes. [Article]. Genes & Development, 22(7), 908-917.

In 1817 at the age of 28 years Ann married William Thwaytes (1749–1834) who was aged 67. During her marriage, Ann accused her husband of attempting to poison her with mercury. In 1832, during her husband's last illness, Ann developed a mental disorder which began with "low fever" (a 19th- century term for murine typhus) and a subsequent nervous state in which she remained for ten weeks facing the wall whilst believing she was blind.

Many mammalian serpins have been identified that share no obvious orthology with a human serpin counterpart. Examples include numerous rodent serpins (particularly some of the murine intracellular serpins) as well as the uterine serpins. The term uterine serpin refers to members of the serpin A clade that are encoded by the SERPINA14 gene. Uterine serpins are produced by the endometrium of a restricted group of mammals in the Laurasiatheria clade under the influence of progesterone or estrogen.

Elevated levels of galectin-3 have been found to be significantly associated with higher risk of death in both acute decompensated heart failure and chronic heart failure populations. In normal human, murine, and rat cells galectin-3 levels are low. However, as heart disease progresses, significant upregulation of galectin-3 occurs in the myocardium. Galectin-3 also may be used as a biomarker to identify at risk individuals, and predict patient response to different drugs and therapies.

These antibodies are combined with an adjuvant and given as a vaccine. The murine immune system essentially "amplifies" a small mass of TAA antibodies into a much larger mass used to vaccinate humans. Because the antibody produced using the "anti-idiotypic" process closely resembles the original epitope of the antigen, these antibodies can be used to induce immune responses from cellular to antibody-antigen for a given antigen, e. g., TAA, when administered as a vaccine to a human.

This bridge is a shorter distance for axonal growth than the original route. Once the axon has innervated both sites, it continues growing in a retrograde direction (toward the injury site) to innervate other affected NMJs. PSCs have a large role in creating growth scaffolds from one injured NMJ to another. These PSC bridges are seen in vivo following complement-mediated injury in a murine model, showing that this role of PSCs are present in mammalian NMJs.

Understanding how the interaction between virus and cell alters the viral particle and how virus entry is facilitated by the interaction has helped elucidate the means by which poliovirus infection is initiated. Humans are the only known natural host for poliovirus. The study of viral disease is therefore only feasible with the generation of a small animal model. Though not susceptible to poliovirus infection, murine cells do allow for efficient replication of poliovirus RNA introduced into the cytoplasm.

Retroviruses are one of the mainstays of current gene therapy approaches. The recombinant retroviruses such as the Moloney murine leukemia virus have the ability to integrate into the host genome in a stable fashion. They contain a reverse transcriptase to make a DNA copy of the RNA genome, and an integrase that allows integration into the host genome. They have been used in a number of FDA-approved clinical trials such as the SCID-X1 trial.

The first Raf gene, v-Raf was found in 1983. It was isolated from the murine retrovirus bearing the number 3611. It was soon demonstrated to be capable to transform rodent fibroblasts to cancerous cell lines, so this gene was given the name Virus-induced Rapidly Accelerated Fibrosarcoma (V-RAF). A year later, another transforming gene was found in the avian retrovirus MH2, named v-Mil - that turned out to be highly similar to v-Raf.

ConA was found to partially inhibit tumor nodule growth independent of its lymphocyte activation; the eradication of the tumor in the murine in-situ hepatoma model in this study was additionally attributed to the mitogenic/lymphoproliferative action of ConA that may have activated a CD8+ T-cell-mediated, as well as NK- and NK-T cell-mediated, immune response in the liver. ConA intravitreal injection can be used in the modeling of proliferative vitreoretinopathy in rats.

SRP RNA was first detected in avian and murine oncogenic RNA (ocorna) virus particles. Subsequently, SRP RNA was found to be a stable component of uninfected HeLa cells where it associated with membrane and polysome fractions. In 1980, cell biologists purified from canine pancreas an 11S "signal recognition protein" (fortuitously also abbreviated "SRP") which promoted the translocation of secretory proteins across the membrane of the endoplasmic reticulum. It was then discovered that SRP contained an RNA component.

She and her colleagues first described IgD on the surface of murine B cells and she was the co-discoverer of Interleukin-4. Her group demonstrated that IL-4 was a “switch” factor for Ig on B cells. Over the past two decades, she has developed antibody-based “biological missiles” to destroy cancer cells and cells infected with HIV. These novel therapeutics have been evaluated in tissue culture, in animals and, since 1988, in over 300 humans.

Because of these mechanisms, AgRP may be linked to increased body mass and obesity in both humans and mice. Over-expression of AgRP has been linked to obesity in males, while certain polymorphisms of AgRP have been linked to eating disorders like anorexia nervosa. The mechanism underlying hyperinsulinemia in humans is consistent with murine agouti, as insulin secretion is heightened through calcium sensitive signaling in pancreatic beta cells. The mechanism for ASP induced tumorigenesis remains unknown in humans.

The Arctic fox contains advantageous genes to overcome extreme cold and starvation periods. Transcriptome sequencing has identified two genes that are under positive selection: Glycolipid transfer protein domain containing 1 (GLTPD1) and V-akt murine thymoma viral oncogene homolog 2 (AKT2). GLTPD1 is involved in the fatty acid metabolism, while AKT2 pertains to the glucose metabolism and insulin signaling. The average mass specific BMR and total BMR are 37% and 27% lower in the winter than the summer.

Harvey Whittemore and his wife, Annette, were frustrated by lack of answers for myalgic encephalomyelitis/Chronic fatigue syndrome (CFS) patients, including their daughter. In an effort to solve the CFS problem, they created the Whittemore Peterson Institute in 2005; Mikovits became the research director in 2006. Attempts to find a viral cause of CFS were unsuccessful. In 2007, Mikovits met a co-discoverer of xenotropic murine leukemia virus-related virus (XMRV), Robert Silverman, at a conference.

The genus Rattus is a member of the giant subfamily Murinae. Several other murine genera are sometimes considered part of Rattus: Lenothrix, Anonymomys, Sundamys, Kadarsanomys, Diplothrix, Margaretamys, Lenomys, Komodomys, Palawanomys, Bunomys, Nesoromys, Stenomys, Taeromys, Paruromys, Abditomys, Tryphomys, Limnomys, Tarsomys, Bullimus, Apomys, Millardia, Srilankamys, Niviventer, Maxomys, Leopoldamys, Berylmys, Mastomys, Myomys, Praomys, Hylomyscus, Heimyscus, Stochomys, Dephomys and Aethomys. The genus Rattus proper contains 64 extant species. A subgeneric breakdown of the species has been proposed, but does not include all species.

The PAK2 gene is about 92.7-kb long. The gene contains 15 exons and generates three alternatively spliced transcripts - two of which code proteins of 524 amino acids and 221 amino acids, while the third one is a 371-bp non-coding RNA transcript(Gene from review) There are two transcripts generated from the murine PAK2 gene, a 5.7-kb transcript coding a 524 amino acids long polypeptide and a 1.2-kb long non-coding RNA transcript.

BRAF is a human gene that encodes a protein called B-Raf. The gene is also referred to as proto-oncogene B-Raf and v-Raf murine sarcoma viral oncogene homolog B, while the protein is more formally known as serine/threonine- protein kinase B-Raf. The B-Raf protein is involved in sending signals inside cells which are involved in directing cell growth. In 2002, it was shown to be faulty (mutated) in some human cancers.

This gene encodes a protein tyrosine phosphatase which is expressed primarily in lymphoid tissues. This enzyme is involved in several signalling pathways associated with the immune response. Based on models of the murine phosphatase, structural identification, and human genetics the phosphatase forms complexes with C-src tyrosine kinase (Csk), associated with the control of Src family members. The mutation Arg620Trp disrupts binding to Csk, alters the responsiveness of T and B cell receptors, and is associated with autoimmune diseases.

Isoforms CR1 and CR2 derived from the non-primate Cr2 locus possess the same C-terminal sequence, such that association with and activation through CD19 should be equivalent. CR1 can bind to C4b and C3b complexes, whereas CR2 (murine and human) binds to C3dg-bound complexes. CR1, a surface protein produced primarily by follicular dendritic cells, appears to be critical for generation of appropriately activated B cells of the germinal centre and for mature antibody responses to bacterial infection.

The miR-17-92 cluster containing miR-19 miRNA family is also involved into control endothelial cell functions and neo- vascularization. MiRNA cluster (miR-17, miR-18, miR-19 and miR-20) increased during the induction of endothelial cell differentiation in embryonic stem cells (tested on murine) or induce pluripotent stem cells. Even though this cluster regulates vascular integrity and angiogenesis, none of each members has a significant impact on the endothelial differentiation of pluripotent stem cells.

RanGAP1, is a homodimeric 65-kD polypeptide that specifically induces the GTPase activity of RAN, but not of RAS by over 1,000-fold. RanGAP1 is the immediate antagonist of RCC1, a regulator molecule that keeps RAN in the active, GTP-bound state. The RANGAP1 gene encodes a 587-amino acid polypeptide. The sequence is unrelated to that of GTPase activators for other RAS-related proteins, but is 88% identical to Rangap1 (Fug1), the murine homolog of yeast Rna1p.

Her research career began in Prague, where she studied the lifecycle of the murine polyomavirus. She became interested in attending Western universities and began her preparation, but did not have the funding to cover her fees. After learning that University College London offered full scholarships to students from Central European countries, Kečkéšová joined University College London in 2003, where she worked toward a doctoral degree in infectious diseases. Her thesis considered retroviral infections and was awarded the Qiagen Award.

Mutation of the PDE6b gene leads to the dysfunction of PDE, which results in failure of hydrolysis of cGMP. The rd1 mouse is a well-characterized animal model of retinitis pigmentosa caused by the mutation of Pde6b gene. The phenotype was first discovered in rodless mice in the 1920s by Keeler. An insertion of Murine leukemia provirus is present near the first exon combined with a point mutation, which introduces a stop codon in exon 7.

In a murine model of a self-limiting pulmonary allergic reaction, MaR1 reduced lung inflammation. It appeared to act at least in part by augmenting the generation of regulatory T cells which interacted with Group 2 innate lymphoid cells (i.e. Helper T cell lymphocytes, see Innate lymphoid cell#GroupILC) to markedly suppress the production of two cytokines, Interleukin-5 and Interleukin-13, implicated in mediating allergic reactions. MaR1 accelerated tissue regeneration in experimentally injured planaria worms.

The venom has a murine median lethal dose () has been measured at 41 μg/kg—when using 0.1% bovine serum albumin in saline rather than saline alone—to 53 μg/kg when administered subcutaneously. The composition of venom of captive snakes did not differ from that of wild snakes. The eastern brown snake's venom contains coagulation factors VF5a and VF10, which together form the prothrombinase complex pseutarin-C. This cleaves prothrombin at two sites, converting it to thrombin.

TRAF-interacting protein is a protein that in humans is encoded by the TRAIP gene. This gene encodes a protein that contains an N-terminal RING finger motif and a putative coiled-coil domain. A similar murine protein interacts with TNFR-associated factor 1 (TRAF1), TNFR-associated factor 2 (TRAF2), and cylindromatosis. The interaction with TRAF2 inhibits TRAF2-mediated nuclear factor kappa-B, subunit 1 activation that is required for cell activation and protection against apoptosis.

The protein encoded by this gene is homologous to the murine protein MCAP, which associates with chromosomes during mitosis, and to the human BRD2 (RING3) protein, a serine/threonine kinase. Each of these proteins contains two bromodomains, a conserved sequence motif which may be involved in chromatin targeting. This gene has been implicated as the chromosome 19 target of translocation t(15;19)(q13;p13.1), which defines the NUT midline carcinoma. Two alternatively spliced transcript variants have been described.

Until recently it was believed that during muscle wasting (atrophy) muscle cells lost nuclei by a nuclear self-destruct mechanism called apoptosis, but recent observations using time laps in vivo imaging in mice do not support this model. Direct observation indicated that no nuclei are lost under such conditions,Bruusgaard JC & Gundersen K. (2008). In vivo time-lapse microscopy reveals no loss of murine myonuclei during weeks of muscle atrophy. J Clin Invest 118, 1450-1457.

In most well-studied polyomaviruses, STag improves the efficiency of viral proliferation but is not essential. SV40 and murine polyomavirus STags appear to have a role in promoting host cell expression of genes under the control of certain types of promoters. This function is mediated by the J domain, presumably indirectly as STag has no DNA-binding ability of its own. Both STag and LTag interact through their J domains with Hsc70 to increase its ATPase activity.

Muegge in October 1995 As a principal investigator at the Frederick National Laboratory for Cancer Research she investigates in the Laboratory of Cancer Prevention chromatin organization during embryonic development and in tumor progression. She is a senior investigator in the mouse cancer genetics program and head of the epigenetics section. Muegge studies molecular mechanisms that alter chromatin structure and function during murine development. She discovered several links between chromatin modifiers, including nucleosomal remodeling and DNA methylation.

Forebrain-specific conditional Ube3b knockout mice showed impaired spatial learning, altered social interactions, and repetitive behaviors. Ube3b knockout neurons exhibited decreased dendritic branching, increased density and aberrant morphology of dendritic spines, altered synaptic physiology, and changes in hippocampal circuit activity. Dendritic and spine phenotype was regulated by Ube3b in a cell-autonomous manner. Murine Ube3b ubiquitinated the catalytic γ-subunit of calcineurin, Ppp3cc, the overexpression of which phenocopied Ube3b loss with regard to dendrite branching and dendritic spine density.

Viral promoters are often used for constitutive expression in plasmids and in viral vectors because they normally force constant transcription in many cell lines and types reliably. Inducible expression depends on promoters that respond to the induction conditions: for example, the murine mammary tumor virus promoter only initiates transcription after dexamethasone application and the Drosophilia heat shock promoter only initiates after high temperatures. Some vectors are designed for transcription only, for example for in vitro mRNA production. These vectors are called transcription vectors.

Such research has included targeting the European rabbit (Oryctolagus cuniculus) in Australia by engineering rabbit zona pellucida glycoproteins into a recombinant myxoma virus. This approach has induced marginal reduction of fertility in laboratory rabbits with some of the glycoproteins. Further improvement of efficacy is necessary before such an approach is ready for field trials. Research has also targeted the house mouse (Mus domesticus) in Australia by engineering murine zona pellucida antigens into a recombinant ectromelia virus and a recombinant cytomegalovirus.

There is evidence that the change is selective, and DNMT1 is overexpressed in reelin-secreting GABAergic neurons but not in their glutamatergic neighbours. Methylation inhibitors and histone deacetylase inhibitors, such as valproic acid, increase reelin mRNA levels, while L-methionine treatment downregulates the phenotypic expression of reelin. One study indicated the upregulation of histone deacetylase HDAC1 in the hippocampi of patients. Histone deacetylases suppress gene promoters; hyperacetylation of hystones was shown in murine models to demethylate the promoters of both reelin and GAD67.

The inland taipan (Oxyuranus microlepidotus) is considered the most venomous snake in the world with a murine value of 0.025 mg/kg SC. Ernst and Zug et al. 1996 list a value of 0.01 mg/kg SC, which makes it the most venomous snake in the world in their study too. They have an average venom yield of 44 mg. Bites from this species have a mortality rate of 80% if left untreated, although it is very rare for this species to bite.

Plasmodium berghei is a species in the genus Plasmodium subgenus Vinckeia. It is a protozoan parasite that causes malaria in certain rodents. Originally, isolated from thicket rats in Central Africa, P. berghei is one of four Plasmodium species that have been described in African murine rodents, the others being Plasmodium chabaudi, Plasmodium vinckei, and Plasmodium yoelii. Due to its ability to infect rodents and relative ease of genetic engineering, P. berghei is a popular model organism for the study of human malaria.

Iron is a necessary cofactor for many enzymes, and can act as a catalyst in the electron transport system. A. fumigatus has two mechanisms for the uptake of iron, reductive iron acquisition and siderophore-mediated. Reductive iron acquisition includes conversion of iron from the ferric (Fe+3) to the ferrous (Fe+2) state and subsequent uptake via FtrA, an iron permease. Targeted mutation of the ftrA gene did not induce a decrease in virulence in the murine model of A. fumigatus invasion.

The insertion of one or more base pairs, resulting in DNA mutations, is also known as insertional mutagenesis. Engineered mutations such as these can provide important information in cancer research, such as mechanistic insights into the development of the disease. Retroviruses and transposons are the chief instrumental tools in insertional mutagenesis. Retroviruses, such as the mouse mammory tumor virus and murine leukemia virus, can be used to identify genes involved in carcinogenesis and understand the biological pathways of specific cancers.

When tested against B16 murine melanoma it was found to be active in the low micromolar range. It also proved to be an effective antimicrobial agent against the Gram-positive bacteria (Bacillus megaterium) and the Gram-negative bacteria (Escherichia coli) and was found to be antifungal against (Microbotryum violaceum) and antialgal against (Chlorella fusca). Secalonic acid D (SAD) is a toxic and teratogenic metabolite. Teratogenic effects were observed in the development of rats that were exposed to SAD injected during fetal development.

The tin (IV) purpurins are more active when compared with analogous zinc (II) purpurins, against human cancers. Sulphonated benzochlorin derivatives demonstrated a reduced phototherapeutic response against murine leukemia L1210 cells in vitro and transplanted urothelial cell carcinoma in rats, whereas the tin (IV) metallated benzochlorins exhibited an increased photodynamic effect in the same tumour model. Copper octaethylbenzochlorin demonstrated greater photoactivity towards leukemia cells in vitro and a rat bladder tumour model. It may derive from interactions between the cationic iminium group and biomolecules.

The human PAK6 gene consists of 16 exons of which 8 exons are used for 5’-UTR splicing to generating 17 transcripts by alternative splicing, and the gene is about 38-kb long. Among PAK6 transcripts, 14 are protein coding RNAs to code four proteins of 681 and 636 amino acids while remaining PAK6 transcripts are non- coding RNAs. There are five transcripts in murine PAK6 gene, of which two transcripts are protein coding and other two non-coding RNAs(Gene from review).

It is typically derived from bovine, porcine and murine sources. As these are all animal sources, cellular agriculture overcomes this through the use of transgenic organisms which are capable of producing the amino acid repeats which make up the collagen. Collagen naturally exists as Collagen type I and has been produced as porous hydrogels, composites and substrates with topographical cues and biochemical properties. Synthetic kinds of collagen have also been produced through recombinant protein production — Collagen type II and III, tropoelastin and fibronectin.

In the 1960s, lymphocytes were discovered to be the mediators of allograft rejection in animals. Attempts to use T cells to treat transplanted murine tumors required cultivating and manipulating T cells in culture. Syngeneic lymphocytes were transferred from rodents heavily immunized against the tumor to inhibit growth of small established tumors, becoming the first example of ACT. Description of T cell growth factor interleukin-2 (IL-2) in 1976 allowed T lymphocytes to be grown in vitro, often without loss of effector functions.

STAT3-deficient mouse embryos cannot develop beyond embryonic day 7, when gastrulation begins. It appears that at these early stages of development, STAT3 activation is required for self-renewal of embryonic stem cells (ESCs). Indeed, LIF, which is supplied to murine ESC cultures to maintain their undifferentiated state, can be omitted if STAT3 is activated through some other means. STAT3 is essential for the differentiation of the TH17 helper T cells, which have been implicated in a variety of autoimmune diseases.

Retinoic acid early inducible 1 (RAE-1) family of murine cell surface glycoproteins is composed of at least five members (RAE-1α-ε). Genes encoding these proteins are located on mouse chromosome 10. RAE-1 proteins are related to MHC class I, they are made up of external α1α2 domain which is linked to the cell membrane by the GPI anchor. They function as stress-induced ligands for NKG2D receptor and their expression is low or absent on normal cells.

Tabin was educated at the University of Chicago where he was awarded a BS in physics in 1976. He went on to graduate school at Massachusetts Institute of Technology and was awarded a PhD in 1984 for work on the regulation of gene expression in the Ras subfamily of oncogenes supervised by Robert Weinberg based in the MIT Department of Biology. In Weinberg's lab, Tabin constructed murine leukemia virus, the first recombinant retrovirus that could be used as a eukaryotic vector.

Onyx-015 (dl1520) underwent trials in conjunction with chemotherapy before it was abandoned in the early 2000s. The combined treatment gave a greater response than either treatment alone, but the results were not entirely conclusive. Vaccinia virus GL-ONC1 was studied in a trial combined with chemo- and radiotherapy as Standard of Care for patients newly diagnosed with head & neck cancer. Herpes simplex virus, adenovirus, reovirus and murine leukemia virus are also undergoing clinical trials as a part of combination therapies.

While rat fleas are the most common vectors, cat fleas and mouse fleas are less common modes of transmission."A previous study [1943] reported house mice naturally infected with R. typhi in the state of Georgia; however, no PCR-positive mice were detected in our study. Eruptions of mouse populations in the absence of rats have been implicated in several outbreaks of murine typhus; however, these observations were not supported by laboratory data." Endemic typhus is highly treatable with antibiotics.

Ectopic expression of CDX2 was reported in more than 85% of the human patients with acute myeloid leukemia (AML). Ectopic expression of Cdx2 in murine bone marrow induced AML in mice and upregulate Hox genes in bone marrow progenitors. CDX2 is also implicated in the pathogenesis of Barrett's esophagus where it has been shown that components from gastroesophageal reflux such as bile acids are able to induce the expression of an intestinal differentiation program through up-regulation of NF-κB and CDX2.

Sticky mouse is a murine mutant possessing a defective alanyl-tRNA synthetase (AARS) and therefore used in investigational studies into mechanisms of neuronal degeneration. Its most immediately obvious symptom is a sticky secretion on the mouse's fur (thus the name); however, it is accompanied by lack of muscle control, ataxia, alopecia, loss of Purkinje cells in the cerebellum, and eventually, death. Sticky mouse is one of several animal mutants that are known to have problems in mRNA translation and are used in studies.

Loss of CD47 promotes proliferation and increases asymmetric division of primary murine endothelial cells. Additionally, activation of CD47 with TSP-1 in wild-type primary mouse cerebral endothelial cells induces cytotoxicity, which is significantly decreased in cerebral endothelial cells derived from CD47 knockout mice. CD47 signaling may suppress angiogenesis as TSP-1 activation significantly inhibited endothelial cell migration and tube formation in vitro. In vivo, injections of TSP-1 in mice after hindlimb ischemia induces a significant decrease of blood flow recovery.

Interactions between endothelial cell CD47 and leukocyte SIRPγ regulate T cell transendothelial migration (TEM) at sites of inflammation. CD47 knockout mice show reduced recruitment of blood T cells as well as neutrophils and monocytes in areas of inflammation. CD47 also functions as a marker of self on murine red blood cells which allows RBC to avoid phagocytosis. Red blood cells that lack CD47 are rapidly cleared from the bloodstream by macrophages, a process that is mediated by interaction with SIRPα.

Pyoverdine has been reported to be required for virulence in a variety of disease models, including C. elegans and various models of murine infection (e.g., burn models, pneumonia models, etc.). As noted above, pyoverdine contributes in several fashions to general virulence, including regulating the production of itself, exotoxin A (which stalls translation), and the protease PrpL. There is also evidence that, although not essential for its formation, pyoverdine contributes to the production and development of biofilms that are important for virulence.

ABL2 has been shown to interact with three proteins: Abl gene, catalase, and SORBS2. The protein Abl gene is also known as abelson murine leukemia viral oncogene homolog 1 and is a protein that is encoded by the human ABL1 gene. Catalase is a common enzyme that catalyzes the decomposition of hydrogen peroxide to water and oxygen. SORBS2 is also known as Sorbin and SH3 domain-containing protein 2 and is a protein encoded by the SORBS2 gene in humans.

While the murine caspase-11 is mainly expressed in macrophages, human caspase-4 is also expressed at high levels in intestinal epithelial cells. Similar to what was observed for the epithelial NAIP/NLRC4 inflammasome, human epithelial cells were shown to undergo caspase-4-dependent, caspase-1-independent cell death and extrusion in response to infection with the enteropathogens such as Salmonella, Shigella flexneri or Escherichia coli. Furthermore, secretion of IL-18 could be triggered by cytosolic LPS in epithelial cells.

FICZ likewise suppresses pulmonary Th2-type cytokine production in a mouse model of ovalbumin-induced allergic asthma. The key roles played by dynamic AHR signaling in skin immunity have been emphasized by Stockinger and coworkers (Di Meglio et al. 2014). When full-thickness biopsies from the lesional skin of patients with psoriasis was exposed to FICZ, 29 genes belonging to the psoriasis transcriptome were down-regulated. A later murine study confirmed that FICZ decreased IL-17 expression and lessened the severity of psoriasis.

The induction of ANGPTL4 in exercising muscle likely is counteracted via AMP-activated protein kinase (AMPK)-mediated down-regulation, promoting the use of plasma triglycerides as fuel for active muscles. High-throughput RNA sequencing of lung tissue samples from the 1918 and 2009 influenza pandemic revealed that ANGPTL4 was one of the most significantly upregulated gene. Murine influenza infection of the lungs stimulated the expression of ANGPTL4 via a STAT3-mediated mechanism. ANGPTL4 enhanced pulmonary tissue leakiness and exacerbated inflammation-induced lung damage.

Increasing evidence has implicated Wnt5a in chronic inflammatory disorders. In particular Wnt5a has been implicated in atherosclerosis. It has been previously reported that there is an association between Wnt5a mRNA and protein expression and histopathological severity of human atherosclerotic lesions as well as co-expression of Wnt5a and TLR4 in foam cells/macrophages of murine and human atherosclerotic lesions. However, the role of Wnt proteins in the process and development of inflammation in atherosclerosis and other inflammatory conditions is not yet clear.

These granules usually appear regular (but some can be irregularly shaped), and they grow in size and number until approximately 2 weeks of gestation. Granules differ between species, with rat uNK cells displaying an increased number of small granules than murine cells. Rat uNK morphology also differs from the mouse due to the common occurrence of myelin within the granules. In all species, as active cells, they have numerous prominent organelles including mitochondria, well-developed golgi apparatus, free ribosomes and rough endoplasmic reticulum.

The transmission of Y. pestis by fleas is well characterized. Initial acquisition of Y. pestis by the vector occurs during feeding on an infected animal. Several proteins then contribute to the maintenance of the bacteria in the flea digestive tract, among them the hemin storage system and Yersinia murine toxin (Ymt). Although Ymt is highly toxic to rodents and was once thought to be produced to ensure reinfection of new hosts, it is important for the survival of Y. pestis in fleas.

Several scientists have developed murine models of SSADH (Aldh5a1-/-) by typical gene methodology to create a uniform absence of the SSADH enzyme activity as well as accumulations of GHB and GABA in tissues and physiological fluids. The mice are born at the expected Mendelian frequencies for an autosomal recessive disorder. Most of the models include distinctive neurological phenotypes and exhibit hypotonia, truncal ataxia, generalized tonic-clonic seizures associated with 100% mortality. The mice uniformly die at 3-4 postnatal weeks.

The first microprotein (miP) discovered was during a research in the early 1990s on genes for basic helix–loop–helix (bHLH) transcription factors from a murine erythroleukaemia cell cDNA library. The protein was found to be an inhibitor of DNA binding (Id), and it negatively regulate transcription factor complex. The Id protein was 16 kDa and consisted of a helix-loop-helix (HLH) domain. The microprotein formed bHLH/HLH heterodimers which disrupted the functional basic helix–loop–helix (bHLH) homodimers.

Muromonab-CD3 is a murine anti-CD3 monoclonal antibody of the IgG2a type that prevents T-cell activation and proliferation by binding the T-cell receptor complex present on all differentiated T cells. As such it is one of the most potent immunosuppressive substances and is administered to control the steroid- and/or polyclonal antibodies-resistant acute rejection episodes. As it acts more specifically than polyclonal antibodies it is also used prophylactically in transplantations. The muromonab's mechanism of action is only partially understood.

In 1910, Ricketts became interested in a strain of murine-carried typhus known as tabardillo due to a major outbreak in Mexico City, and the apparent similarity of the disease to spotted fever. Days after isolating the organism that he believed caused typhus, he himself died of the disease. Ricketts was survived by his wife, Myra Tubbs Ricketts, and children. His family established an annual student research prize, the Howard Taylor Ricketts Prize, at the University of Chicago in 1912.

When used as a food additive, ractopamine added to feed can be distributed by the blood to the muscle tissues, where it serves as a full agonist to murine TAAR1 (not necessarily human). It is also an agonist to beta-adrenergic receptors. A cascade of events will then be initiated to increase protein synthesis, which results in increased muscle fiber size. Ractopamine is known to increase the rate of weight gain, improve feed efficiency, and increase carcass leanness in finishing swine.

Eschar due to O. tsutsugamushi infection on the shoulder (a, b) of a female and on the penis (c, d) of a male. The main symptom of O. tsutsugamushi infection is high (febrile) fever; however, the symptom is similar to other vector-borne tropical diseases such as malaria, leptospirosis, typhoid, murine typhus, chikungunya, and dengue fever. This makes precise clinical diagnosis difficult, which often leads to misdiagnosis. The initial indications are fever with chills, associated with headache, muscle pain (myalgia), sweating and vomiting.

He and his team utilized an infectious disease model using Bacillus Calmette–Guérin (BCG), a mycobacteria that is a potent inducer of interferon (IFN)-gamma. Using this model, they found both BCG and IFN-gamma activate an enzyme in the brain, known as indole 2,3-dioxygenase, that catabolizes tryptophan along the kynurenine pathway rather than serotonin.O’Connor, J.C., M.A. Lawson, C. André, E.M. Briley, S.S. Szegedi, et al. 2009. Induction of IDO by Bacille Calmette-Guérin is responsible for development of murine depressive-like behavior.

On a higher level, increased maternal care was found to correlate with reelin expression in rat pups; such correlation was reported in hippocampus and in the cortex. According to one report, prolonged exposure to corticosterone significantly decreased reelin expression in murine hippocampi, a finding possibly pertinent to the hypothetical role of corticosteroids in depression. One small postmortem study has found increased methylation of RELN gene in the neocortex of persons past their puberty compared with those that had yet to enter the period of maturation.

The S100 calcium-binding protein mS100a7a15 is the murine ortholog of human S100A7 (Psoriasin) and human S100A15 (Koebnerisin). mS100a7a15 is also known as S100a15, mS100a7 and mS100a7a and is encoded by the mS100a7a gene (alias: S100a15) S100 proteins are a diverse calcium-binding family that mediate fundamental cellular and extracellular processes including cell proliferation and differentiation, cell migration, and the antimicrobial host defense as antimicrobial peptides. mS100a7a15 was first cloned as mS100a15 from adult mouse skin (FVB/N mice, clone RP1-128L15, accession no.: AL591704).

Furthermore, transplantation of cardiac transcription factors into injured murine hearts resulted in poor cell survival and minimal expression of cardiac genes. Meanwhile, advances in the methods of obtaining cardiac myocytes in vitro occurred. Efficient cardiac differentiation of human iPS cells gave rise to progenitors that were retained within infarcted rat hearts and reduced remodeling of the heart after ischemic damage. The team of scientists, who were led by Sheng Ding, used a cocktail of nine chemicals (9C) for transdifferentiation of human skin cells into beating heart cells.

Current research has revealed an association between seasonal affective disorder (SAD) and general mood disorder related to NPAS2, ARNTL, and CLOCK polymorphisms. These genes may influence seasonal variations through metabolic factors such as body weight and appetite. Associated with a connection to mood disorders, NPAS2 has been found to be involved with dopamine degradation. This was first suggested by the observation that the clock components BMAL1 and NPAS2 transcriptionally activated a luciferase reporter driven by the murine monoamine oxidase A (Maoa) promoter in a circadian fashion.

Ofranergene obadenovec, also known as VB-111, is an anti-angiogenic gene therapy. The vector is a non-replicating adenovirus 5. The payload is a chimeric gene encoding a fusion protein that combines the extracellular and intramembrane domains of the human TNF receptor 1 and the intracellular domain of the Fas receptor, under the control of a modified version of the murine promoter for endothelin-1, which is called PPE-1. PPE-1 drives tissues specific expression and also has a hypoxia responsive element.

This gene is the cellular homolog of the fox sequence in the Finkel-Biskis-Reilly murine sarcoma virus (FBR-MuSV). It encodes a fusion protein consisting of the ubiquitin-like protein fubi at the N-terminus and ribosomal protein S30 at the C-terminus. It has been proposed that the fusion protein is post-translationally processed to generate free fubi and free ribosomal protein S30. Fubi is a member of the ubiquitin family, and ribosomal protein S30 belongs to the S30E family of ribosomal proteins.

The enzyme encoded by this gene catalyzes the activation of Neu5Ac to Cytidine 5-prime-monophosphate N-acetylneuraminic acid (CMP-Neu5Ac), which provides the substrate required for the addition of sialic acid. Sialic acids of cell surface glycoproteins and glycolipids play a pivotal role in the structure and function of animal tissues. The pattern of cell surface sialylation is highly regulated during embryonic development, and changes with stages of differentiation. Studies of a similar murine protein suggest that this protein localizes to the nucleus.

The IL-5Rα chain is exclusively expressed by eosinophils, some basophils and murine B1 cells or B cell precursors. Like many other cytokine receptors, alternative splicing of the α-chain gene results in expression of either a membrane bound or soluble form of the bα-chain. The soluble form does not lead to signal transduction and therefore has an antagonistic effect on IL-5 signaling. Both monomeric forms of IL-5Rα are low affinity receptors, while dimerization with the β-chain produces a high affinity receptor.

Hephaestin was first identified by Dr. Christopher D. Vulpe of the University of California, Berkeley in 1999. They named the newfound protein after Hephaestus, the Greek god of metal working. Much of what is known about hephaestin comes from studying heritable mutants of murine iron metabolism. The protein was discovered and identified through the study of mice with sex-linked anemia, or sla mice, in which there is normal mucosal uptake of dietary iron but impaired transport of iron from the intestinal enterocytes into the circulation.

Ertumaxomab (trade name Rexomun) is a rat-murine hybrid monoclonal antibody designed to treat some types of cancer. It is a trifunctional antibody which works by linking T-lymphocytes and macrophages to the cancer cells.Fresenius Phase II clinical trial evaluating the treatment of breast cancer was terminated due to change in Fresenius' development plans.ClinicalTrials.gov: Phase II Study With the Trifunctional Antibody Ertumaxomab to Treat Metastatic Breast Cancer After Progression on Trastuzumab Therapy (So they could concentrate on their other product catumaxomab (trade name Removab).

Based on the extracellular face of the ABHD12 active site and its ability to act on multiple isomeric substrates, ABHD12 has been suggested to act as a guard to the extracellular 2-AG-CB2R signalling pathway in microglia, and peripheral 2-AG signalling, however this has not been confirmed. ABHD12 transcription is abundant in the brain, specifically microglia, but has also been identified in peripheral cell types like macrophages and osteoclasts. Murine models have shown ABHD12 plays a role in regulation of lysophosphatidylserine pathways in the brain.

Hepatic stellate cells can be selectively stained with gold chloride, but their distinguishing feature in routine histological preparations is the presence of multiple lipid droplets in their cytoplasm. Cytoglobin expression has been shown to be a specific marker with which hepatic stellate cells can be distinguished from portal myofibroblasts in the damaged human liver. In murine liver, reelin expressed by Ito cells has been shown to be a reliable marker in discerning them from other myofibroblasts. The expression of reelin is increased after liver injury.

Genetically engineered L. lactis may produce murine IL-10 in the lumen, and the protein may diffuse to responsive cells in the epithelium or the lamina propria. Another route involves L. lactis taken up by M cells because of its bacterial size and shape, and the major part of the effect may be due to recombinant IL-10 production in situ in intestinal lymphoid tissue. Both routes may involve paracellular transport mechanisms that are enhanced in inflammation. After transport, IL-10 may directly down- regulate inflammation.

The antihyperalgesic effects of AM-1241 were investigated in a murine bone cancer model. Sarcoma cells were injected into the femur of a mouse, and then mice were injected twice daily with AM-1241. Treatment with AM-1241 reduced both spontaneous and evoked pain, as well as reducing the bone loss and subsequent fractures due to the tumor. Pretreatment with the CB2 antagonist SR-144,528 reversed the acute effects of AM-1241 on both spontaneous and evoked pain, while having no effect on its own.

Strains of M. ulcerans used in laboratores are less standardized than their murine hosts, with different laboratories using different strains based on convenience and accessibility. Three M. ulcerans strains are particularly common: "Cu001", isolated from a person in Adzopé, Côte d'Ivoire in 1996; "Mu1615", from a person in Malaysia in the 1960s; and "S1013" from someone in Cameroon in 2010. Most Buruli ulcer research is focused on testing new antibiotics against the bacteria, testing vaccine candidates, and better understanding how M. ulcerans infection causes disease.

The hemocyanin found in the blood of the Chilean abalone, Concholepas concholepas, has immunotherapeutic effects against bladder cancer in murine models. Mice primed with C. concholepas before implantation of bladder tumor (MBT-2) cells. Mice treated with C. concholepas hemocyanin showed antitumor effects: prolonged survival, decreased tumor growth and incidence, and lack of toxic effects and may have a potential use in future immunotherapy for superficial bladder cancer. Keyhole limpet hemocyanin (KLH) is an immune stimulant derived from circulating glycoproteins of the marine mollusk Megathura crenulata.

TdTL1 is broadly expressed in lymphoid cell lines while TdTL2 is predominantly expressed in normal small lymphocytes. Both localize in the nucleus when expressed and both possess 3'->5' exonuclease activity. In contrast, TdTS isoforms do not possess exonuclease activity and perform the necessary elongation during V(D)J recombination. Since a similar exonuclease activity hypothesized in murine TdTL is found in human and bovine TdTL, some postulate that bovine and human TdTL isoforms regulate TdTS isoforms in a similar manner as proposed in mice.

Although the RT structures from human, murine and avian retroviruses display different subunits, the relative sizes, orientation and connection of the DNA polymerase and RNase H domains are strikingly similar. The RNase H domain occupies ~25% of the RT protein C-terminal. The DNA polymerase domain occupies ~55% of the RT protein N-terminal. The RNase H domains of MMLV and HIV-1 RT enzymes are structural very similar to the Escherichia coli and Bacillus halodurans RNases H as well as to human RNaseH1.

As Type C retroviruses, replicating murine leukemia viruses produce a virion containing a spherical nucleocapsid (the viral genome in complex with viral proteins) surrounded by a lipid bilayer derived from the host cell membrane. The lipid bilayer contains integrated host and viral proteins studded with carbohydrate molecules. The viral particle is approximately 90 nanometres (nm) in diameter. The viral glycoproteins are expressed on the membrane as trimer of a precursor Env, which is cleaved into SU and TM by host furin or furin-like proprotein convertases.

Whilst MERS has a viral reservoir in camels and may have been transmitted to humans via camel handlers, SARS does not have such a specific reservoir. Coronaviruses that occur in humans are primarily viruses of the respiratory tract. Weiss began to work on coronaviruses in the 1980s, when the field was relatively new. She makes use of the murine coronavirus (known as mouse hepatitis virus or MHV) to develop mouse models that allow the study of various pathologies, including viral encephalitis and demyelinating disease.

Murine caspase-11, and its human homologs caspase-4 and caspase-5, are mammalian intracellular receptor proteases activated by TLR4 and TLR3 signaling during the innate immune response. Caspase-11, also termed the non- canonical inflammasome, is activated by TLR3/TLR4-TRIF signaling and directly binds cytosolic lipopolysaccharide (LPS), a major structural element of Gram- negative bacterial cell walls. Activation of caspase-11 by LPS is known to cause the activation of other caspase proteins, leading to septic shock, pyroptosis, and often organismal death.

Lilotomab (formerly tetulomab, HH1) is a murine monoclonal antibody against CD37, a glycoprotein which is expressed on the surface of mature human B cells. It was generated at the Norwegian Radium Hospital. As of 2016 it was under development by the Norwegian company Nordic Nanovector ASA as a radioimmunotherapeutic in which lilotomab is conjugated to the beta radiation- emitting isotope lutetium-177 by means of a linker called satetraxetan, a derivative of DOTA. This compound is called 177Lu-HH1 or lutetium (177Lu) lilotomab satetraxetan (trade name Betalutin).

These are solutions containing FSL Kode constructs where the construct will exist as a clear micellular dispersion. FSL-GB3 as a solution/gel has been used to inhibit HIV infection and to neutralise Shiga toxin. FSL blood group A as a solution has been used to neutralise circulating antibodies in a mouse model and allow incompatible blood group A (murine kodecytes) transfusion. This model experiment was used to demonstrate the potential of FSLs to neutralise circulating antibody and allow for incompatible blood transfusion or organ transplantation.

Herbert W. "Skip" Virgin was the Edward Mallinckrodt Professor and Chair of the Department of Pathology & Immunology at the Washington University School of Medicine and a member of the National Academy of Sciences. He is best known for establishing murine norovirus as a model system for studying norovirus biology, for identifying host phenotypes associated with persistent viral infections, for defining alterations to the human virome in the context of different diseases, and for elucidating the roles of autophagy and interferon- stimulated genes during viral infection.

In swine, Bischoff et al. compared transcriptional profiles using DNA microarrays to survey differentially expressed genes between parthenotes (2 maternal genomes) and control fetuses (1 maternal, 1 paternal genome). An intriguing study surveying the transcriptome of murine brain tissues revealed over 1300 imprinted gene loci (approximately 10-fold more than previously reported) by RNA-sequencing from F1 hybrids resulting from reciprocal crosses. The result however has been challenged by others who claimed that this is an overestimation by an order of magnitude due to flawed statistical analysis.

Werner H. Kirsten Werner H. Kirsten (1925 in Leipzig — December 24, 1992 in Hyde Park, Chicago)DR. WERNER H. KIRSTEN, 67, by Kenan Heise, in the Chicago Tribune; published January 1, 1993; retrieved April 10, 2020 was a German- American cancer researcher, known as the discoverer and namesake of Kirsten Rat Sarcoma Virus,also known as Kirsten Mouse Sarcoma Virus and Kirsten Murine Sarcoma Virus30 Years Later, WHK Program Remains a Singular Opportunity, by Chris Worthington, at NCI Frederick; published July 10, 2019; retrieved April 10, 2020 and consequently of the KRAS oncogene.

These were originally thought to be scattered only around the centrosomes, but further studies proved that PCM1 was also found throughout the cytoplasm. PCM1 was shown to be essential for cell division because PCM1 antibodies cause cell-cycle arrest when microinjected into fertilized murine eggs. Targeting of centrin, pericentrin and ninein was also dramatically reduced after PCM1 depletion using siRNA, overexpression of PCM1 deletion mutants and PCM1 antibody microinjection. As a result of this depletion, the radial organization of the microtubules was found to be disrupted, but did not appear to effect microtubule nucleation.

Protein tyrosine phosphatase non-receptor type 5 is an enzyme that in humans is encoded by the PTPN5 gene. Protein tyrosine phosphatase (PTP), non-receptor type 5, also known as STEP (STriatal-Enriched protein tyrosine Phosphatase), was the first brain-specific PTP discovered. The human STEP locus maps to chromosome 11p15.2-p15.1 and the murine STEP gene to chromosome 7B3-B5. The single STEP gene is alternatively spliced to produce several isoforms, the best characterized of which are the cytosolic STEP46 protein and the membrane- associated STEP61 protein.

The human equivalent was obtained by cDNA library screening using the murine gene as a probe and found to be homologous to the Drosophila awd gene. A second human gene, nm23-H2 (NME2), encoding a protein 88% identical to nm23-H1, was subsequently isolated. Both genes were localized on 17q21.3 and their gene products were formerly identified as the A and B subunits of NDP kinases. In mammals, functional NDP kinases are heterohexamers of the A and B monomers, which can combine at variable ratios to form different types of hybrids.

The human and the murine GPR84 ORFs both encode proteins of 396 amino acid residues length with 85% identity and are therefore considered as orthologs. The hgpr84 was found by Northern blot analysis as a transcript of about 1.5 kb in brain, heart, muscle, colon, thymus, spleen, kidney, liver, intestine, placenta, lung, and leukocytes. In addition, a 1.2 kb transcript in heart and a strong band at 1.3 kb in muscle were detected. A Northern blot from different brain regions revealed strongest expression of the 1.5 kb transcript in the medulla and the spinal cord.

This allele, identified by deep sequencing of GWAS loci, results in a protein with a C-terminal truncation. In a functional follow-up study, using re-expressed human CARD9 isoforms in murine Card9−/− bone marrow-derived dendritic cells (BMDCs) were assessed for cytokine production. BMDCs expressing the predisposing variant CARD9 S12N showed increased TNFα and IL-6 production compared to BMDCs expressing wild-type CARD9. In contrast, CARD9 Δ11 and CARD9 S12NΔ11, as well as the C-terminal truncated variant CARD9 V6, showed significant impairment in TNFα and IL-6 production.

Forest cobra (Naja melanoleuca), Kakamega Forest, Kenya The Forest cobra (Naja melanoleuca) is the largest true cobra of the genus Naja and is a very bad-tempered, aggressive, and irritable snake when cornered or molested as handled in captivity. According to Brown (1973) this species has a murine IP value of 0.324 mg/kg, while the IV value is 0.6 mg/kg. Ernst and Zug et al. 1996 list a value of 0.225 mg/kg SC. The average venom yield per bite is 571 mg and the maximum venom yield is 1102 mg.

However, in murine models, novel genetic methods have allowed for in vivo Rb reactivation experiments. Rb loss induced in mice with oncogenic KRAS-driven tumors of lung adenocarcinoma negates the requirement of MAPK signal amplification for progression to carcinoma and promotes loss of lineage commitment as well as accelerate the acquisition of metastatic competency. Reactivation of Rb in these mice rescues the tumors towards a less metastatic state, but does not completely stop tumor growth due to a proposed rewiring of MAPK pathway signaling, which suppresses Rb through a CDK-dependent mechanism.

Prior to the discovery of SARS-CoV, M-CoV (MHV, specifically) had been the best-studied coronavirus both in vivo and in vitro as well as at the molecular level. Some strains of M-CoV cause a progressive demyelinating encephalitis in mice which has been used as a murine model for multiple sclerosis. Significant research efforts have been focused on elucidating the viral pathogenesis of these animal coronaviruses, especially by virologists interested in veterinary and zoonotic diseases. A feature of the MHV is that many strains have the hemagglutinin-esterase gene turned into a pseudogene.

250px Modified from: Sun J, Ramnath RD, Tamizhselvi R, Bhatia M."Neurokinin A engages neurokinin-1 receptor to induce NF-kappaB-dependent gene expression in murine macrophages: implications of ERK1/2 and PI 3-kinase/Akt pathways." Am J Physiol Cell Physiol. 2008 Sep;295(3):C679-91 Like Substance P [SP], Neurokinin A is present in excitatory neurons and secretory cells of the hypothalamic–pituitary–adrenal axis. Additionally both SP neurokinin A is found in the neurosensory system and modulates a wide range of inflammatory and tissue repairing processes .

Additionally, one of the most significant results of this expression analysis was the discovery of more than 200 previously unknown genes whose expression was temporally regulated during the response of fibroblasts to serum. These results revealed the importance of viewing the immune response as a collaborative physiological program and begged for further study of the immune system as a network, and not just as individual pieces. In 2006, Moutaftsi et al. demonstrated that epitope-mapping tools could accurately identify the epitopes responsible for 95% of the murine T-cell response to vaccinia virus.

After position 399, three different general structures can be observed. The first variant consists of 415 amino acids across all three organisms and is called TV1 in human and rat, while the murine counterpart is named CRAa. The shortest group of sequences consists of 409 amino acids: TV2 in humans and rats, CRAc in mice. The longest variant consists of 428 amino acids in rat (TV3) and mice (CRAb), while the human (TV3) variant is missing the second to last amino acid (threonine), resulting in a protein of a length of 427 amino acids.

Although venom toxicity values can vary greatly even among specimens of the same species, the Philippine cobra is considered to possess one of the most toxic venom among all of the Naja (cobra) species based on murine , according to most toxinology studies. The average subcutaneous for this species is 0.20 mg/kg (lowest value 0.14 mg/kg) and the average venom yield per bite is 90–100 mg. Only the Caspian cobra (Naja oxiana) has produced a more potent venom, producing an average of 0.18 mg/kg (lowest value 0.1 mg/kg).

In addition to its association with HDL, SAA1 interacts with a number of mammalian proteins, mostly cell surface proteins such as receptors. SAA1 binding to the αvβ3 integrin produces an inhibitory effect on the growth of nasopharyngeal carcinoma. Several receptors for SAA1 have been identified using an SAA1 hybrid protein containing two amino acid substitutions from SAA2. These receptors include the G protein-coupled chemoattractant receptor FPR2 (formyl peptide receptor 2), believed to mediate the chemotactic activity of the recombinant SAA1; the murine scavenger receptor SR-BI and the human equivalent CLA-1.

Thus, CC1 mainly acts as a chemoattractant for monocytes/macrophages, T lymphocytes, specially Th2-differentiated T cells and a subset of T regulatory cells in vitro into inflammatory siter. It can also attract NK cells, immature B cells but do not attracts neutrophils. CCL1 stimulates a transient increase in the concentration of cytoplasmic free calcium in monocytes but not in other type of cells. Futhermore, CCL1 inhibits apoptosis in thymic cell lines by the RAS/MAPK pathway but can prevent dexamethasone-induced apoptosis in cultured murine thymic lymphoma cells.

The Chinese cobra is a highly venomous member of the true cobras (genus Naja). Its venom consists mainly of postsynaptic neurotoxins and cardiotoxins. Four cardiotoxin-analogues I, II, III, and IV, account for about 54% of the dry weight of the crude venom and have cytotoxic properties. The murine values of its venom are 0.29 mg/kg IV and 0.53 mg/kg—0.67 mg/kg SC. The average venom yield from a snake of this species kept at a snake farm was about 250.8 mg (80 mg dry weight).

However, this is only possible when the host cell is co-infected with a helper virus which provides functions it needs to be able to replicate which it does not code for in its own genome such as a reverse transcriptase and some major structural proteins. As such, A-MuLV can be described as a dependovirus. A highly efficient helper virus commonly used when growing A-MuLV in vitro is Moloney murine leukemia virus (M-MuLV). It causes leukemia directly by interfering with the normal growth and differentiation processes of lymphocytes.

VSV entered a host cell as a single negative strand of RNA, but brought with it RNA polymerase to stimulate the processes of transcription and replication of more RNA. Baltimore extended this work and examined two RNA tumor viruses, Rauscher murine leukemia virus and Rous sarcoma virus. He went on to discover reverse transcriptase (RTase or RT) – the enzyme that polymerizes DNA from an RNA template. In doing so, he discovered a distinct class of viruses, later name retroviruses, that use an RNA template to catalyze synthesis of viral DNA.

After winning the Nobel Prize, Baltimore reorganized his laboratory, refocusing on immunology and virology, with immunoglobulin gene expression as a major area of interest. He tackled new problems such as the pathogenesis of Abelson murine leukemia virus (AMuLV), lymphocyte differentiation and related topic in immunology. In 1980, his group isolated the oncogene in AMuLV and showed it was a member of a new class of protein kinases that used the amino acid tyrosine as a phosphoacceptor. This type of enzymatic activity was also discovered by Tony Hunter, who has done extensive work in the area.

Increased formation of brown or beige/brite fat has been shown to have anti-obesity, anti-diabetic effects in multiple murine models, and adult humans have significant deposits of UCP1-positive brown fat. (Our data show) that even relatively short treatments of obese mice with irisin improves glucose homeostasis and causes a small weight loss. Whether longer treatments with irisin and/or higher doses would cause more weight loss remains to be determined. The worldwide, explosive increase in obesity and diabetes strongly suggests exploring the clinical utility of irisin in these and related disorders.

As many of the protein components necessary for alpha globin stability complex appear to be widely expressed across species and cell types this mechanism of mRNA stabilisation is likely to be a general one. However, in the mouse the cis and trans determinants have diverged to some extent. The mouse sequence requirements are equally C and U-rich compared to the predominantly C-rich human element. Despite this shift the murine alpha globin mRNA is still as stable due to a complementary change in the specificity of the poly(C)-binding protein.

Through testing in mouse models, it has been shown that activation of the CB-1 receptor helps reduce reactions associated with acute pain, indicating that it alleviates bone pain. Thus, a new target for potential treatments is activation of the CB-1 receptor.Furuse, S. Kawamata, T. Yamamoto, J. Niiyama, Y. Omote, K. Watanabe, M. Namiki, A.(2009). Reduction of Bone Cancer Pain by Activation of Spinal Cannabinoid Receptor 1 and Its Expression in the Superficial Dorsal Horn of the Spinal Cord in a Murine Model of Bone Cancer Pain. Anesthesiology.

Murine embryoid bodies in suspension culture after 24 hours of formation from embryonic stem cells. Embryoid bodies are a common in vitro pluripotency test for stem cells and their size needs to be controlled to induce directed differentiation to specific lineages. High throughput formation of uniform sized embryoid bodies with microwells and microfluidics allows easy retrieval and more importantly, scale up for clinical contexts. Actively controlling embryoid body cell organization and architecture can also direct stem cell differentiation using microfluidic gradients of endoderm-, mesoderm- and ectoderm-inducing factors, as well as self-renewal factors.

Elevated levels of IL-17A have been found in the sputum and in bronchoalveolar lavage fluid of patients with asthma and a positive correlation between IL-17A production and asthma severity has been established. In murine models, treatment with dexamethasone inhibits the release of Th2-related cytokines but does not affect IL-17A production. Furthermore, Th17 cell-mediated airway inflammation and airway hyperresponsiveness are steroid resistant, indicating a potential role for Th17 cells in steroid-resistant asthma. However, a recent trial using anti- IL-17RA did not show efficacy in subjects with asthma.

Mouse model studies using the IL-17RA knock out mice and the IL-17A knock out mice with the murine adapted influenza strain (PR8) as well as the 2009 pandemic H1N1 strain [93] both support that IL-17A plays a detrimental role in mediating the acute lung injury. The role of adaptive immune responses mediated by antigen specific Th17 has been investigated more recently. Antigen specific Th17 cells were also shown to recognize conserved protein antigens among different K. pneumoniae strains and provide broad-spectrum serotype-independent protection.

Natural killer cell cytolysis of target cells and cytokine production is controlled by a balance of inhibitory and activating signals, which are facilitated by NK cell receptors. NK cell inhibitory receptors are part of either the immunoglobulin- like (IgSF) superfamily or the C-type lectin-like receptor (CTLR) superfamily. Members of the IgSF family include the human killer cell immunoglobulin-like receptor (KIR) and the Immunoglobulin-like transcripts (ILT). CTLR inhibitory receptors include the CD94/NKG2A and the murine Ly49, which is probably analogous to the human KIR.

Activated STAT6 molecules form dimers which translocate to the nucleus to bind responsive elements (e.g. CD23 promoter in B cells,Keegan AD, Conrad DH. The murine lymphocyte receptor for IgE. V. Biosynthesis, transport, and maturation of the B cell Fc epsilon receptor. J Immunol (1987) 139:1199–205 arginase1 enhancer in macrophages ) The binding affinity of IL-4 for IL-4Rα is much higher than IL-13 for the IL-13Rα1, hence IL-4 would out- compete IL-13 for receptor availability within IL4R2 at parity of concentration.

Hephaestin has not yet been linked to a human disease. However, when the protein was ablated in murine models, both intestine-specific and whole-body hephaestin knockout (KO) strains exhibited similarly severe accumulation of iron in the duodenal enterocytes and suffered from microcytic, hypochromic anemia, indicative of systemic iron deficiency. The shared phenotype between the two strains suggests that intestinal hephaestin plays an important role in maintaining whole-body iron homeostasis. However, since both strains were viable, it is likely that hephaestin is not essential and other compensatory mechanisms exist to keep these mice alive.

Piezo1 has been implicated in extrusion of epidermal cells when a layer becomes too confluent to preserve normal skin homeostasis. This acts to prevent excess proliferation of skin tissue, and has been implicated in cancer biology as a contributing factor to metastases by assisting living cells in escaping from a monolayer. Expression of murine PIEZO1 in mouse innate immune cells is essential for their function, a role mediated by sensing mechanical cues. Deficiency in PIEZO1 in mice lead to increased susceptibility of myeloid cells to infection by Pseudomonas aeruginosa.

Xu, W, S R Presnell, J Parrish-Novak, W Kindsvogel, S Jaspers, Z Chen, S R Dillon, et al. « A soluble class II cytokine receptor, IL-22RA2, is a naturally occurring IL-22 antagonist ». Proceedings of the National Academy of Sciences of the United States of America 98, nᵒ. 17 (août 14, 2001): 9511-951 Weiss, B, K Wolk, B H Grünberg, H-D Volk, W Sterry, K Asadullah, et R Sabat. « Cloning of murine IL-22 receptor alpha 2 and comparison with its human counterpart ». Genes and Immunity 5, nᵒ.

Experimental research, for example, often focuses on creating environments that isolate and identify the role of "niche-specific virulence genes". These are genes that perform specific tasks within specific tissues/places at specific times; the sum total of niche-specific genes is the virus' virulence. Genes characteristic of this concept are those that control latency in some viruses like herpes. Murine gamma herpesvirus 68 (γHV68) and human herpesviruses depend on a subset of genes that allow them to maintain a chronic infection by reactivating when specific environmental conditions are met.

The role that inhibition of GSK-3 might play across its other signaling roles is not yet entirely understood. GSK-3 inhibition also mediates an increase in the transcription of the transcription factor Tbet (Tbx21) and an inhibition of the transcription of the inhibitory co-receptor programmed cell death-1 (PD-1) on T-cells. GSK-3 inhibitors increased in vivo CD8(+) OT-I CTL function and the clearance of viral infections by murine gamma-herpesvirus 68 and lymphocytic choriomeningitis clone 13 as well as anti-PD-1 in immunotherapy.

Although functional studies of radial glia are increasing, it is difficult to distinguish them from neuroprogenitors and astrocytes. Like neuroprogenitors, radial glia express intermediate filament proteins nestin as well as the transcription factor PAX6 that is expressed in some neuroprogenitors in the ventral half of the neural tube. Radial glia also express proteins characteristic of astrocytes, including the widely used glial fibrillar acidic protein (GFAP), among others. Cytological markers that might be unique to radial glia include modified forms of nestin identified by the RC1 and RC2 antibodies that recognize the murine antigens.

They successfully identified eight putative SCEs in the murine (mouse) embryonic stem (meS) cell line with resolution up to 23 bp. This methodology has also been shown to hold great utility in discerning patterns of non-random chromatid segregation, especially in stem cell lineages. Furthermore, SCEs have been implicated as diagnostic indicators of genome stress, information that has utility in cancer biology. Most research on this topic involves observing the assortment of chromosomal template strands through many cell development cycles and correlating non-random assortment with particular cell fates.

Mouse mammary tumor virus (MMTV) is a milk-transmitted retrovirus like the HTL viruses, HI viruses, and BLV. It belongs to the genus Betaretrovirus. MMTV was formerly known as Bittner virus, and previously the "milk factor", referring to the extra-chromosomal vertical transmission of murine breast cancer by adoptive nursing, demonstrated in 1936, by John Joseph Bittner while working at the Jackson Laboratory in Bar Harbor, Maine. Bittner established the theory that a cancerous agent, or "milk factor", could be transmitted by cancerous mothers to young mice from a virus in their mother's milk.

XMRV is a murine leukemia virus (MLV) that formed through the recombination of the genomes of two parent MLVs known as preXMRV-1 and preXMRV-2. MLVs belong to the virus family Retroviridae and the genus gammaretrovirus and have a single-stranded RNA genome that replicates through a DNA intermediate. The name XMRV was given because the discoverers of the virus initially thought that it was a novel potential human pathogen that was related to but distinct from MLVs. The XMRV particle is approximately spherical and 80 to 100 nm in diameter.

SLP-76 was originally identified as a substrate of the ZAP-70 protein tyrosine kinase following T cell receptor (TCR) ligation in the leukemic T cell line Jurkat. The SLP-76 locus has been localized to human chromosome 5q33 and the gene structure has been partially characterized in mice. The human and murine cDNAs both encode 533 amino acid proteins that are 72% identical and composed of three modular domains. The NH2-terminus contains an acidic region that includes a PEST domain and several tyrosine residues that are phosphorylated following TCR ligation.

AgRP is a paracrine signalling molecule made up of 112 amino acids (the gene product of 132 amino acids is processed by removal of the N-terminal 20-residue signal peptide domain). It was independently identified by two teams in 1997 based on its sequence similarity with agouti signalling peptide (ASIP), a protein synthesised in the skin that controls coat colour. AgRP is approximately 25% identical to ASIP. The murine homologue of AgRP consists of 111 amino acids (precursor is 131 amino acids) and shares 81% amino acid identity with the human protein.

Klas Kärre (born January 12, 1954 in Strasbourg, France) is a Swedish immunologist. Kärre received his doctorate in 1981 at Karolinska InstitutetKärre, Klas (1981): On the immunobiology of natural killer cells: studies of murine NK-cells and their interactions with T-cells and T-lymphomas, Diss., Stockholm and is a professor of molecular immunology at Karolinska Institutet since 1993. In the mid-1980s Kärre discovered one of the mechanisms for how cells of the immune system, natural killer cells (NK cells), identify their target cells and kill them.

Selection of biological targets on the basis of their combinatorial effects on the leukemic lymphoblasts can lead to clinical trials for improvement in the effects of ALL treatment. Tyrosine-kinase inhibitors (TKIs), such as imatinib, are often incorporated into the treatment plan for people with Bcr-Abl1+ (Ph+) ALL. However, this subtype of ALL is frequently resistant to the combination of chemotherapy and TKIs and allogeneic stem cell transplantation is often recommended upon relapse. Blinatumomab, a CD19-CD3 bi-specific monoclonal murine antibody, currently shows promise as a novel pharmacotherapy.

Citrinin can also act synergistically with Ochratoxin A to depress RNA synthesis in murine kidneys. Ergot Alkaloids are compounds produced as a toxic mixture of alkaloids in the sclerotia of species of Claviceps, which are common pathogens of various grass species. The ingestion of ergot sclerotia from infected cereals, commonly in the form of bread produced from contaminated flour, causes ergotism, the human disease historically known as St. Anthony's Fire. There are two forms of ergotism: gangrenous, affecting blood supply to extremities, and convulsive, affecting the central nervous system.

Sensitivity to acute thermal stimulation is the most common test used in live species pain research. The behavioral reflex evoked by noxious heat stimuli is a relatively good predictor of pain sensitivity and its reduction through various analgesics. One significant limitation of thermal assays lies in the specificity and validity of results in animals as models of human pain. Very little is known about the functional mechanics of nociceptive afferents in murine subjects, thus the translation of any pain response observed from these animals to humans is questionable.

Fear of mice and rats is one of the most common specific phobias. It is sometimes referred to as musophobia (from Greek μῦς "mouse") or murophobia (a coinage from the taxonomic adjective "murine" for the family Muridae that encompasses mice and rats), or as suriphobia, from French souris, "mouse". The phobia, as an unreasonable and disproportionate fear, is distinct from reasonable concern about rats and mice contaminating food supplies, which may potentially be universal to all times, places, and cultures where stored grain attracts rodents, which then consume or contaminate the food supply.

Expression in various retinal cell types can be determined by the promoter sequence. In order to restrict expression to a specific cell type, a tissue-specific or cell-type specific promoter can be used. For example, in rats the murine rhodopsin gene drive the expression in AAV2, GFP reporter product was found only in rat photoreceptors, not in any other retinal cell type or in the adjacent RPE after subretinal injection. On the other hand, if ubiquitously expressed immediate-early cytomegalovirus (CMV) enhancer-promoter is expressed in a wide variety of transfected cell types.

Therefore, they were suggested to take part in schistosomula destruction either alone or in cooperation with macrophages and T-cells. Hypertrophied astrocytes are located in the migratory tracks and in the proximity of the schistosomula which implies their role in immune response and tissue reparation. Murine astrocytes and microglia were shown to produce pro- inflammatory cytokines (IL-6 and TNF-α) and nitric oxide after in vitro exposure to parasite antigens, which supports their role in host immune response. IgM antibody response targets mainly carbohydrate epitopes of parasite molecules.

If this occurs the infection can develop into pneumonia. Several diseases, like Rat Coronavirus Infection (RCI), Sendai virus, and Murine Respiratory Mycoplasmosis (MRM, Mycoplasma pulmonis), are prevalent simply because their highly contagious natures work in tandem with the way rats are kept in laboratories, pet stores, and by breeders. MRM is far less likely to occur in laboratory rats than in those kept as pets. Pet rats can also develop pituitary tumors if they are given high-calorie diets, and ringtail if they are placed in areas with low humidity or high temperatures.

There is also a strong correlation (with a correlation coefficient of 0.93) between the antiproliferative effects of taxifolin derivatives on murine skin fibroblasts and human breast cancer cells. Taxifolin has shown to have anti-proliferative effects on many types of cancer cells by inhibiting cancer cell lipogenesis. By inhibiting the fatty acid synthase in cancer cells, taxifolin is able to prevent the growth and spread of cancer cells. The capacity of taxifolin to stimulate fibril formation and promote stabilization of fibrillar forms of collagen can be used in medicine.

C/EBPβ and δ are transiently induced during the early stages of adipocyte differentiation (adipogenesis), while C/EBPα is upregulated during the terminal stages of adipogenesis. In vitro and in vivo studies have demonstrated that each plays an important role in this process. For example, Murine Embryonic Fibroblasts (MEFs) from mice lacking both C/EBPβ and C/EBPδ show impaired adipocyte differentiation in response to adipogenic stimuli. In contrast, ectopic expression of C/EBPβ and δ in 3T3-L1 preadipocytes promotes adipogenesis, even in the absence of adipogenic stimuli.

The most widely studied allele variants are the lethal yellow mutation (Ay) and the viable yellow mutation (Avy) which are caused by ectopic expression of agouti. These mutations are also associated with yellow obese syndrome which is characterized by early onset obesity, hyperinsulinemia and tumorigenesis. The murine agouti gene locus is found on chromosome 2 and encodes a 131 amino acid protein. This protein signals the distribution of melanin pigments in epithelial melanocytes located at the base of hair follicles with expression being more sensitive on ventral hair than on dorsal hair.

The first IL-1 receptor-associated kinase (IRAK) was observed in 1994 through experiments with murine T helper cell lines D10N and EL-4. Two years later the first experimental member of this family of kinases, IRAK1, was cloned. In 2002, through database searches at the National Center for Biotechnology Information in an attempt to recognize novel members of the IRAK family, a human cDNA sequence which encoded a peptide sharing significant homology with IRAK1 was identified. This cDNA sequence was found to have five amino acid substitutions compared to IRAK1 and was termed IRAK4.

Since then, he has tried to demonstrate that thymocyte-thymocyte (or, T cell-T cell, so called T-T) interaction is really present and T cells can be developed by the interaction in vivo. After almost 15 years, he finally established a delicately engineered mouse system in which T cells including thymocytes could expressed MHC class II molecules mimicking human T cells and successfully demonstrated that the T-T interaction occurred in the engineered murine thymus, resulting in the generation of functional CD4+ helper T cells (Immunity. 23:387-96, 2005).

To date not much hard evidence has been found to support a strong correlation between HERV-W transcripts and schizophrenia (SZ). One study found 10 out of 35 individuals with recent onset schizophrenia had retroviral pol gene HERV-W transcripts and murine leukemia virus gene transcripts in cell-free CSF and 1 in 20 patients with chronic schizophrenia. This was significant when compared to the 22 non-inflammatory patients and the 30 healthy patients that had no retroviral transcripts. Contrasting this data a micro-array was performed to analyze HERV transcription activity in human brains.

This led to the publication of a joint report in which the term "chronic fatigue syndrome" was found to be most representative. This was followed in 2002 by a further report by the new CMO, Liam Donaldson. The U.S. Centers for Disease Control & Prevention (CDC) recognize CFS as a serious illness, and launched a campaign in June 2006 to raise public and medical awareness about it. A 2009 study published in the journal Science reported an association between a retrovirus xenotropic murine leukemia virus-related virus (XMRV) and CFS.

PTP1B has clinical implications in the treatment of type 2 diabetes as well as cancer. Gene knockout studies conducted in murine models has provided substantial evidence for the role PTP1B plays in the regulation of insulin signalling and the development of obesity. PTPN1 knockout mice kept on high fat diets showed a resistance to obesity and an increased degree of insulin sensitivity as compared to their wild-type counterparts. As such, the design and development of PTP1B inhibitors is a growing field of research for the treatment of type 2 diabetes and obesity.

The protein interacts with Cas-Br-M (murine) ectropic retroviral transforming sequence, and can function as a bimodal regulator of epidermal growth factor receptor/mitogen-activated protein kinase signaling. This protein may play a role in alveoli branching during lung development as shown by a similar mouse protein. SPRY2 is a negative feedback regulator of multiple receptor tyrosine kinases (RTKs) including receptors for fibroblast growth factor (FGF), epidermal growth factor (EGF), and hepatocyte growth factor (HGF). Antagonization of growth factor mediated pathways, cell migration, and cellular differentiation occurs through the ERK pathway.

The EP4 receptor is over- expressed in human prostate cancer tissue and a selective EP4-receptor antagonist inhibits the growth and metastasis of human prostate cancer cell xenografts. An EP4 receptor antagonist as well EP4 Gene knockdown inhibit the in vitro proliferation and invasiveness of human breast cancer cells. And, gene knockdown of EP4 inhibit the metastasis of murine breast cancer cells in a mouse model of induced breast cancer. PGE2 stimulates the in vitro growth of human non-small cell lung cancer while an antagonist of EP4 or EP4 gene knockdown inhibits this growth.

Murine models instead require induction of typical anaemic phenotypes by elevated dosing with MMC that does not affect wild-type animals, before they can be used experimentally as preclinical models for bone marrow failure and potential stem cell transplant or gene therapies. Both female and male mice homozygous for a FANCA mutation show hypogonadism and impaired fertility. Homozygous mutant females exhibit premature reproductive senescence and an increased frequency of ovarian cysts. In spermatocytes, the FANCA protein is ordinarily present at a high level during the pachytene stage of meiosis.

Is it possible to devise immunopreventive strategies for tumors not caused by infectious agents? The challenge is to predict in each individual the risk of specific cancer types and to design immune strategies targeting these cancer types. This is not yet feasible in humans, thus immunoprevention of non-infectious tumors is at a preclinical stage of development. Effective immunoprevention of various types of cancer was obtained in murine models of cancer risk, in particular in transgenic mice harboring activated oncogenes, thus demonstrating that activation of the immune system in healthy hosts can indeed prevent carcinogenesis.

Furthermore, downregulation of PSMB8 also inhibited the differentiation of murine and human adipocytes in vitro, while an injection of siRNA against Psmb8 in mouse skin could reduce adipocyte tissue volume. Thus, PSMB8 may be an essential component and regulator not only for inflammation, but also in the differentiation of adipocytes, hereby indicating that immunoproteasomes may have pleiotropic functions to maintain the homeostasis of a variety of cell types. Subsequently, in addition to autoimmune diseases the PSMB8 protein also has been linked in the diagnosis of lipodystrophy syndrome. Glycosylation disorders are sometimes involved.

The canonical Cr2/CD21 gene of subprimate mammals produces two types of complement receptor (CR1, ca. 200 kDa; CR2, ca. 145 kDa) via alternative mRNA splicing. The murine Cr2 gene contains 25 exons; a common first exon is spliced to exon 2 and to exon 9 in transcripts encoding CR1 and CR2, respectively. A transcript with an open reading frame of 4,224 nucleotides encodes the long isoform, CR1; this is predicted to be a protein of 1,408 amino acids that includes 21 short consensus repeats (SCR) of ca.

Unexpectedly, when PAI-1 deficient mice were challenged with cancer cells on a collagenous matrix, angiogenesis and vascular stabilization was inhibited, hampering tumor growth. This finding was credited to the protective properties PAI-1 imparts against excessive degradation of the surrounding ECM by plasmin. Without this protection the footholds used by endothelial cells to migrate and form capillary structures are destroyed. Uncontrolled proteolysis also is attributed to the disruption of vascular development and premature deaths in murine embryos deficient of the inhibitor reversion-inducing-cysteine-rich protein with kazal motifs (RECK).

The group II PAKs have less coding exons compared with group I PAKs, highlights the potential structural and functional differences between two group of PAKs. The human PAK4 is about 57-kb in length with 13 exons. The PAK4 generates 12 transcripts of which 10 coding transcripts are predicted to code proteins of about 438 to 591 amino acids long, while remaining two transcripts are non-coding in nature. In contrast to human PAK4, murine PAK4 contains four transcripts - two coding for 593 amino acids long polypeptides and two are non-coding RNA transcripts.

The possibility of altering the course of retinal degeneration through subretinal injection of recombinant replication defective adenovirus that contained the murine cDNA for wildtype PDE6β was tested in rd1 mice. Subretinal injection of rd1 mice was carried out 4 days after birth, before the onset of rod photoreceptor degeneration. Following therapy, Pde6β transcripts and enzyme activity were detected, and histologic studies revealed that photoreceptor cell death was significantly retarded. The albino FVB mouse laboratory strain become blind by weaning age due to a mutant allele of the PDE6b gene.

Studies suggest that maresins are involved in resolving inflammatory and allergic reactions, in wound healing, and in abating neuropathic pain. Mar1 enhances the uptake (i.e. stimulates the efferocytosis) of apoptotic human neutrophils by human macrophages, stimulates macrophage phagocytosis, and limits the infiltration of neutrophils into the inflamed peritoneum of mice. In a murine model of acute respiratory distress syndrome, MaR1 generation was detected in a temporally regulated manner with early MaR1 production was dependent on platelet-neutrophil interactions; intravascular MaR1 was organ-protective, leading to decreased lung neutrophils, edema, tissue hypoxia, and prophlogistic mediators.

Alternatively, single-domain antibodies can be made from common murine, rabbit or human IgG with four chains. The process is similar, comprising gene libraries from immunized or naïve donors and display techniques for identification of the most specific antigens. A problem with this approach is that the binding region of common IgG consists of two domains (VH and VL), which tend to dimerize or aggregate because of their lipophilicity. Monomerization is usually accomplished by replacing lipophilic by hydrophilic amino acids, but often results in a loss of affinity to the antigen.

A number of biologics, therapeutic vaccines and immunobiologics are also being investigated for treatment of infection caused by viruses. Therapeutic biologics are designed to activate the immune response to virus or antigens. Typically, biologics do not target metabolic pathways like anti-viral drugs, but stimulate immune cells such as lymphocytes, macrophages, and/or antigen-presenting cells, in an effort to drive an immune response towards a cytotoxic effect against the virus. Influenza models, such as murine influenza, are convenient models to test the effects of prophylactic and therapeutic biologics.

The global role of miRNA function in the heart has been addressed by conditionally inhibiting miRNA maturation in the murine heart. This revealed that miRNAs play an essential role during its development. miRNA expression profiling studies demonstrate that expression levels of specific miRNAs change in diseased human hearts, pointing to their involvement in cardiomyopathies. Furthermore, animal studies on specific miRNAs identified distinct roles for miRNAs both during heart development and under pathological conditions, including the regulation of key factors important for cardiogenesis, the hypertrophic growth response and cardiac conductance.

The human PAK3 gene, the longest group I family member, is 283-kb long. The PAK3 gene is composed of 22 exons of which 6 exons are for 5’-UTR and generates 13 alternative spliced transcripts. Among PAK3 transcripts, 11 transcripts are for coding proteins ranging from 181- to 580-amino acids long, while remaining two transcripts are non-coding RNAs. The murine PAK3 gene contains 10 transcripts, coding six proteins from 544 amino acids and 559 amino acids long, and four smaller polypeptides from 23 to 366 amino acids.

The Friend virus (FV) is a strain of murine leukemia virus. The Friend virus has been used for both immunotherapy and vaccines. Experiments have shown that it is possible to protect against Friend virus infection with several types of vaccines, including attenuated viruses, viral proteins, peptides, and recombinant vaccinia vectors expressing the Friend virus gene. In a study of vaccinated mice, it was possible to identify the immunological epitopes required for protection against the virus, thus determining the types of immunological responses necessary or required for protection against it.

The protein encoded by this gene shares significant sequence identity with the murine TSC-22 and Drosophila shs, both of which are leucine zipper proteins, that function as transcriptional regulators. GILZ shows ubiquitous expression across tissues, including thymus, spleen, lung, fat, liver, kidney, heart, and skeletal muscle. The expression of this gene is stimulated by glucocorticoids and interleukin 10, and it appears to play a key role in the anti-inflammatory and immunosuppressive effects of this steroid and chemokine. Transcript variants encoding different isoforms have been identified for this gene.

The PAK5 gene, the longest among the PAK family, contains a total of 12 exons of which four exons are for 5’-UTR and remaining 8 exons for protein coding(Gene from review). Alternative exon splicing of the PAK5 gene generates three transcripts, and one of the transcript encodes a 719 amino acids long protein(Gene from review). The exon splicing of the murine PAK5 gene generates three transcripts, two of which code an identical 719 amino acids long polypeptide while the 2.0-kb transcript is a non-coding RNA with retained intron.

Frank's laboratory projects include an evaluation of MALDI-TOF identification of microorganisms and molecular methods for microbial identification. Frank's research collaboration with Juliane Bubeck Wardenburg in the departments of pediatrics and microbiology at the University of Chicago focused on the pathogenesis of Staphylococcus aureus pneumonia. Using microarray analysis of murine lung RNA, we examined the response of the host to a virulent Staphylococcal strain compared to a strain deficient in the alpha-toxin. We determined that the cellular immune response to infection was characterized by a prominent TH17 response to the wild-type pathogen.

The activation of protein C is strongly promoted by thrombomodulin and endothelial protein C receptor (EPCR), the latter of which is found primarily on endothelial cells (cells on the inside of blood vessels). The presence of thrombomodulin accelerates activation by several orders of magnitude, and EPCR speeds up activation by a factor of 20. If either of these two proteins is absent in murine specimens, the mouse dies from excessive blood-clotting while still in an embryonic state. On the endothelium, APC performs a major role in regulating blood clotting, inflammation, and cell death (apoptosis).

In murine trials, TLR9-deficient mice had less myofibroblast proliferation, meaning cardiac muscle recovery is connected to TLR9 expression. Furthermore, class B CpG sequences induce proliferation and differentiation of fibroblasts via the NF-κB pathway, the same pathway that initiates pro-inflammatory reactions in the immune responses. TLR9 shows specific activity in post-heart attack fibroblasts, inducing them to differentiate into myofibroblasts and speed repair of left ventricle tissue. In contrast to pre-myocardial infarction, cardiomyocytes in recovering hearts do not induce an inflammation response via TLR9/NF-κB pathway.

Senescent cells undergo widespread fluctuations in epigenetic modifications in specific chromatin regions compared to mitotic cells. Human and murine cells undergoing replicative senescence experience a general global decrease in methylation; however, specific loci can differ from the general trend. Specific chromatin regions, especially those around the promoters or enhancers of proliferative loci, may exhibit elevated methylation states with an overall imbalance of repressive and activating histone modifications. Proliferative genes may show increases in the repressive mark H3K27me3 while genes involved in silencing or aberrant histone products may be enriched with the activating modification H3K4me3.

Owen was the first person to acutely delete the APC gene in the murine intestine, a model that he then used to elucidate the key pathways that APC controls in vivo. Using this model system, Owen's group identified critical functional roles for genes such as MYC, RAC and MTOR. Additionally, the use of this and other models has allowed Owen's group to identify potential chemoprevention strategies. For example, the group's work on aspirin showed that embryonic and perinatal exposure to aspirin suppresses neoplasia associated with the loss of Apc function.

Also when spontaneous murine model of systemic lupus erythematosus (SLE) was treated with recombinant IL-38, mice had less symptoms like proteinuria and skin lesions. Also serum levels of IL-17 and interleukin-22 were lower in these mice what approves in vitro observation that IL-38 could inhibit Th17 responses. Patients with SLE had higher concentrations of IL-38 in the serum than healthy patients and also patients with active disease had higher concentrations of IL-38 in the serum than patients with inactive form. Sjogren's disease is disease related to SLE.

In chemistry, 3,3,4,4-tetramethyltetrahydrofuran-2,5-dione is a heterocyclic compound with the formula , or (CH3)2(COC2COO)(CH3)2. It is a white crystalline solid with a pungent camphoraceous odor. The compound is also called 3,3,4,4-tetramethyloxolane-2,5-dione (its IUPAC name) or 3,3,4,4-tetramethylsuccinic anhydride, namely the anhydride of 2,2,3,3-tetramethylsuccinic acid, and sometimes abbreviated as TMSA.Subat Turdi, Peisheng Xu, Qun Li, Youqing Shen, Parhat Kerram, and Jun Ren (2008), Amidization of Doxorubicin Alleviates Doxorubicin-Induced Contractile Dysfunction and Reduced Survival in Murine Cardiomyocytes. Toxicology Letters volume 178, issue 3, pages 197–201.

Ch14.18 is a chimeric monoclonal antibody in which the variable heavy and light chain regions come from a mouse, with a human constant region for the heavy chain IgG1 and light chain kappa. The version of dinutuximab made by United Therapeutics, and marketed under the brand name Unituxin, is manufactured via industrial fermentation using a murine myeloma cell line, SP2/0. The version marketed by EUSA for Apeiron is called generically dinutuximab beta and is marketed under the brand name Isquette, and is manufactured in Chinese hamster ovary cells.

Subcellular findings in murine studies with induced T. cruzi infection revealed that the chronic state is associated with the persistent elevation of phosphorylated (activated) extracellular-signal-regulated kinase (ERK), AP-1, and NF-κB. Also, the mitotic regulator for G1 progression, cyclin D1 was found to be activated. Although there was no increase in any isoform of ERK, there was an increased concentration of phosphorylated ERK in mice infected with T. cruzi. It was found that within seven days the concentration of AP-1 was significantly higher in T. cruzi–infected mice when compared to the control.

The first evidence that antibodies binding the central amyloid beta domain are effective in the treatment of Alzheimer's disease was found in transgenic mice, which express the human amyloid beta precursor protein. Treatment with a murine analog of solanezumab (m266) lead to an increase in plasma amyloid beta, which was all bound to m266. Additionally, the amount of both free amyloid beta in the brain and amyloid beta in plaques was significantly decreased. Due to those results, it is postulated that m266 binds free amyloid beta in the plasma and, therefore, changes the amyloid beta equilibrium between plasma and brain.

In adult desmin-null mice, hearts from 10 week-old animals showed drastic alterations in muscle architecture, including a misalignment of myofibrils and disorganization and swelling of mitochondria; findings that were more severe in cardiac relative to skeletal muscle. Cardiac tissue also exhibited progressive necrosis and calcification of the myocardium. A separate study examined this in more detail in cardiac tissue and found that murine hearts lacking desmin developed hypertrophic cardiomyopathy and chamber dilation combined with systolic dysfunction. In adult muscle, desmin forms a scaffold around the Z-disk of the sarcomere and connects the Z-disk to the subsarcolemmal cytoskeleton.

AEE788 is a multitargeted human epidermal receptor (HER) 1/2 and vascular endothelial growth factor receptor (VEGFR) 1/2 receptor family tyrosine kinases inhibitor with IC50 of 2, 6, 77, 59 nM for EGFR, ErbB2, KDR, and Flt-1. In cells, growth factor-induced EGFR and ErbB2 phosphorylation was also efficiently inhibited with IC50s of 11 and 220 nM, respectively. It efficiently inhibited growth factor-induced EGFR and ErbB2 phosphorylation in tumors for >72 h, a phenomenon correlating with the antitumor efficacy of intermittent treatment schedules. It also inhibits VEGF-induced angiogenesis in a murine implant model.

One example is the neuronal transcription factor NPAS3, disruption of which is linked to schizophrenia and learning disability. Knockout mice lacking NPAS3 or the similar protein NPAS1 have significantly lower levels of reelin; the precise mechanism behind this is unknown. Another example is the schizophrenia-linked gene MTHFR, with murine knockouts showing decreased levels of reelin in the cerebellum. Along the same line, it is worth noting that the gene coding for the subunit NR2B that is presumably affected by reelin in the process of NR2B->NR2A developmental change of NMDA receptor composition, stands as one of the strongest risk gene candidates.

The co-engraftment allows for reconstitution of the murine immune system, giving insight into the interactions between xenogenic human stroma and tumor environments in cancer progression and metastasis. However, these strategies have yet to be validated for most tumor types and there remain questions over whether the reconstituted immune system will behave in the same way as it does in the patient. For example, the immune system could be 'hyper- activated' due to exposure to mouse tissues in a similar fashion to graft versus host disease. Humanized-xenograft models for acute lymphoblastic leukemia and acute myeloid leukemia have been created.

The murine double minute (mdm2) oncogene, which codes for the Mdm2 protein, was originally cloned, along with two other genes (mdm1 and mdm3) from the transformed mouse cell line 3T3-DM. Mdm2 overexpression, in cooperation with oncogenic Ras, promotes transformation of primary rodent fibroblasts, and mdm2 expression led to tumor formation in nude mice. The human homologue of this protein was later identified and is sometimes called Hdm2. Further supporting the role of mdm2 as an oncogene, several human tumor types have been shown to have increased levels of Mdm2, including soft tissue sarcomas and osteosarcomas as well as breast tumors.

A coastal taipan Species of this genus possess highly neurotoxic venom with some other toxic constituents that have multiple effects on victims. The venom is known to paralyse the victim's nervous system and clot the blood, which then blocks blood vessels and uses up clotting factors. Members of this genus are considered to be among the most venomous land snakes based on their murine , an indicator of the toxicity on mice. The inland taipan is considered to be the most venomous land snake and the coastal taipan, which is arguably the largest Australian venomous snake, is the third-most venomous land snake.

The overall structure of QSulf is followed closely by its orthologues and paralogues, including human and mouse. The human and murine orthologues of QSulf1, HSulf1 and MSulf1, respectively, were cloned and characterized after the discovery of QSulf1. In addition, a paralogue, Sulf2, sharing 63-65% identity (both mouse and human) with Sulf1 also was discovered through BLAST sequence analysis. The HSulf1 gene (GenBank accession number AY101175) has an open reading frame of 2616 bp, encoding a protein of 871 amino acid (aa), and HSulf2 (GenBank accession number AY101176) has an open reading frame of 2613 bp, encoding a protein of 870 aa.

Based on a sequence homology search for genes relate to the folate receptor, the gene for folate receptor 4 was first identified in mice and humans in 2000 at the University of Nebraska. In 2014, the function of folate receptor 4 was discovered by the researchers of the Wellcome Trust Sanger Institute who also proposed that the protein be renamed as Juno. Juno was initially found in murine oocytes, but its interaction with Izumo was subsequently found in other mammalian species, including humans. Being previously elusive, Juno was discovered nine years after its male counterpart, Izumo1.

Cycloastragenol was studied by Geron Corporation and sold to T.A. Sciences in early 2013 who are developing it as a product named TA-65. Bill Andrews of Sierra Sciences has done testing on the anti-aging aspect of TA-65;Dr. Bill Andrews anti-aging test of TA-65, as well as Maria Blasco in the journal Aging Cell, finding no increase in murine median or mean lifespan but some physiological anti-aging effects without augmenting cancer incidence. In late 2013, dietary supplement company RevGenetics released their conclusions on TA-65 that showed it is the single molecule cycloastragenol used in TA-65.

The HILIC mode of separation is used extensively for separation of some biomolecules, organic and some inorganic molecules by differences in polarity. Its utility has increased due to the simplified sample preparation for biological samples, when analyzing for metabolites, since the metabolic process generally results in the addition of polar groups to enhance elimination from the cellular tissue. This separation technique is also particularly suitable for glycosylation analysis and quality assurance of glycoproteins and glycoforms in biologic medical products.Glycosylation analysis by hydrophilic interaction chromatography (HILIC) – N-Glyco mapping of the ZP-domain of murine TGFR-3 (Application Note TOSOH Biosciences).

Murine MDSCs show two distinct phenotypes which discriminate them into either monocytic MDSCs or granulocytic MDSCs. The relationship between these two subtypes remains controversial, as they closely resemble monocytes and neutrophils respectively. While monocyte and neutrophil differentiation pathways within the bone marrow are antagonistic and dependent on the relative expression of IRF8 and c/EBP transcription factors (and hence there is not a direct precursor-progeny link between these two myeloid cell types), this seems not to be the case for MDSCs. Monocytic MDSCs seem to be precursors of granulocytic subsets demonstrated both in vitro and in vivo.

Both encode large multifunctional reverse transcriptase (RT) proteins containing RNase H domains. Retroviral RT proteins from HIV-1 and murine leukemia virus are the best-studied members of the family. Retroviral RT is responsible for converting the virus' single-stranded RNA genome into double-stranded DNA. This process requires three steps: first, RNA-dependent DNA polymerase activity produces minus-strand DNA from the plus-strand RNA template, generating an RNA:DNA hybrid intermediate; second, the RNA strand is destroyed; and third, DNA-dependent DNA polymerase activity synthesizes plus- strand DNA, generating double-stranded DNA as the final product.

Parvez et al., using in vitro transient coexpression of human STIM2 and different SOC channels in HEK293 cells, reported that STIM2 mediates SOCE via two store-dependent and store independent modes. Taking together, these results indicate a complex interaction finely regulated by the STIM1: STIM2: Orai cellular ratio and their endogenous levels. Studies performed in 2009-2010 using human in vitro or murine in vivo models confirmed Brandman et al. results and suggested that STIM2 participates in processes of the development and functioning of many cell types, including smooth muscle myoblasts, cells of the immune system and neurons.

There was limited research on it in the following years, including a report from a laboratory in showing it had activity against Friend virus, a murine virus that causes leukemia in mice, but retroviruses weren't thought to affect humans, and the paper drew little attention. Rideout was interested in AZT's other potential applications; she studied AZT as an antibacterial agent at the Burroughs Wellcome Company for several years. The compound was particularly effective against gram-negative bacteria. In addition to chemical characterization and optimization of its synthesis, their research included pharmacokinetic and safety testing in rats.

Acyl-coenzyme A thioesterase 11 also known as StAR-related lipid transfer protein 14 (STARD14) is an enzyme that in humans is encoded by the ACOT11 gene. This gene encodes a protein with acyl-CoA thioesterase activity towards medium (C12) and long-chain (C18) fatty acyl-CoA substrates which relies on its StAR-related lipid transfer domain. Expression of a similar murine protein in brown adipose tissue is induced by cold exposure and repressed by warmth. Expression of the mouse protein has been associated with obesity, with higher expression found in obesity-resistant mice compared with obesity-prone mice.

Activated microglia secrete cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF-α), which can cause toxic effects in the brain. Additionally, other soluble factors such as neurotoxins, excitatory neurotransmitters, prostaglandin, reactive oxygen, and nitrogen species are secreted by activated microglia. In a murine model of JE, it was found that in the hippocampus and the striatum, the number of activated microglia was more than anywhere else in the brain closely followed by that in the thalamus. In the cortex, the number of activated microglia was significantly less when compared with other regions of the mouse brain.

Whittemore and his wife Annette, together with chronic fatigue syndrome specialist Daniel Peterson, established a CFS research organization known as the Whittemore Peterson Institute for Neuro-Immune Disease (WPI). A study conducted by the WPI reported in October 2009 that the so-called xenotropic murine leukemia virus-related virus was found in most CFS patients they tested, sending many patients to doctors for tests and drugs. Repeated independent attempts to replicate this result were unsuccessful. Additional studies found that the WPI results were the result of contamination with a laboratory recombinant virus and that there was no evidence that humans have been infected.

Retrieved from The New York Times on November 27, 2006. Dick has transformed the study of human hematopoiesis and leukemogenesis, with his development of methodologies for transplanting human bone marrow into immune-deficient mice, with resultant multilineage repopulation of murine bone marrow and other hematopoietic tissues. Using this approach, he has identified long-term repopulating human hematopoietic stem cells and generated mouse models of leukaemia. His studies showing that a specific subset of leukemic cells are actually capable of recapitulating tumour growth are recognised as the foundation for all current work on the cancer stem cell model and its application to cancer therapy.

On February 20, 2019, CytoDyn announced that Leronlimab was able to reduce by more than 98% the incidence of human breast cancer metastasis in a mouse xenograft model for cancer through six weeks with Leronlimab (PRO 140). The temporal equivalency of the murine 6 weeks study may be up to 6 years in humans. In May 2019, the U.S. Food and Drug Administration (FDA) granted Fast Track Designation for Leronlimab (PRO 140) for use in combination with carboplatin for the treatment of patients with CCR5-positive mTNBC. In July 2019, CytoDyn announced the dosing of first mTNBC patient under compassionate use.

The protein encoded by RB1 regulates a signal transduction pathway while controlling the cell cycle progression as normally. Retinoblastoma seems to originate in cone precursor cells present in the retina that consist of natural signalling networks which restrict cell death and promote cell survival after losing the RB1, or having both the RB1 copies mutated. It has been found that TRβ2 which is a transcription factor specifically affiliated with cones is essential for rapid reproduction and existence of the retinoblastoma cell. A drug that can be useful in the treatment of this disease is MDM2 (murine double minute 2) gene.

Akt also positively regulates some transcription factors to allow expression of pro- survival genes. Akt can phosphorylate and activate the IκB kinase IKKα, causing degradation of IκB and nuclear translocation of NF-κB where it promotes expression of caspase inhibitors, c-Myb and Bcl-xL. Also promoting cell survival, cAMP response element binding protein (CREB) is phosphorylated by Akt at Ser133, stimulating recruitment of CREB-binding protein (CBP) to the promoter of target genes, such as Bcl-2. Akt has also been shown to phosphorylate murine double minute 2 (Mdm2), a key regulator of DNA damage responses, at Ser166 and Ser186.

Several XMRV genomic sequences have been published to date. These sequences are almost identical, an unusual finding as retroviruses replicate their genomes with relatively low fidelity, leading to divergent viral sequences in a single host organism. In 2010 the results of phylogenetic analyses of XMRV and related murine retroviruses led a group of researchers to conclude that XMRV "might not be a genuine human pathogen". Xenotropic viruses (xenos Gr. foreign; tropos Gr. turning) were initially discovered in the New Zealand Black (NZB) mouse and later found to be present in many other mouse strains including wild mice.

There is not a significant amount of information about regarding the natural pathogenesis of OROV infections because there have been no recorded fatalities to date. It is known that within 2–4 days from the initial onset of systematic symptoms in humans, the presence of this virus is detected in the blood. In some cases this virus has also been recovered from the cerebrospinal fluid, but the route of invasion to the central nervous system remains unclear. To further understand the pathogenesis of how this virus manifests in the body experimental studies using murine models have been performed.

Early work with Dr Bruce Yacyshyn showed differential expression in inflammatory bowel disease. Dr. Lazarovits isolated the antibody to produce the murine homologue MLN002 which he licensed with the Massachusetts General Hospital to Millennium Pharmaceuticals of Boston for further development. Scientists at LeukoSite realized the potential of this antibody to treat inflammatory bowel disease, and this company was eventually acquired by Millennium which took an exclusive license to the cell line from Massachusetts General Hospital. In vivo proof of concept ultimately led to the decision to humanize the antibody and move it into clinical trials as "Vedolizumab".

House mice are not usually a vector of human plague (bubonic plague) because they have fewer infestations with fleas than do rats, and because the fleas which house mice normally carry exhibit little tendency to bite humans rather than their natural host. Rickettsialpox, caused by the bacterium Rickettsia akari and similar to chickenpox, is spread by mice in general, but is very rare and generally mild and resolves within two or three weeks if untreated. No known deaths have resulted from the disease. Murine typhus (also called endemic typhus), caused by the bacterium Rickettsia typhi, is transmitted by the fleas that infest rats.

The majority of engineered zinc finger arrays are based on the zinc finger domain of the murine transcription factor Zif268, although some groups have used zinc finger arrays based on the human transcription factor SP1. Zif268 has three individual zinc finger motifs that collectively bind a 9 bp sequence with high affinity. The structure of this protein bound to DNA was solved in 1991 and stimulated a great deal of research into engineered zinc finger arrays. In 1994 and 1995, a number of groups used phage display to alter the specificity of a single zinc finger of Zif268.

The first pilot-scale clinical trial of ADEPT was carried out at Charing Cross Hospital, London, using an anti-CEA F(ab′)2 antibody conjugated to the bacterial enzyme carboxypeptidase G2 (CPG2). The antibody used in the first ADEPT clinical trial was of murine origin and the enzyme was bacterial. Host antibodies to both components of the AEC were present in the blood of all non-immunosuppressed patients by day 10 after AEC infusion. Several patients received ciclosporin since it had been shown in rabbits that this could delay the appearance of host antibodies to soluble proteins.

TRPV6 plays an indispensable role in placental Ca2+ transport. Fetal bone mineralization peaks during late pregnancy. At this stage, fetal blood has a higher concentration of Ca2+ in comparison to maternal blood thereby creating conditions that require active transcellular transport of Ca2+ from mother to the fetus. This process is very important since defects in placental transport of calcium can be precursors for Ca2+ deficiency syndromes and intrauterine growth restrictions. The expression of TRPV6 increases 14-fold during the last 4 days of the murine gestational period and coincides with the peak phase of fetal bone mineralization.

Loss of TRPV6 in murine placenta severely impairs Ca2+ transport across trophoblast and reduces embryo growth, induces bone calcification, and impairs bone development. In humans, the insufficient maternal-fetal transport caused by pathogenic genomic variants of TRPV6 is thought to be a cause for skeletal defects observed in selected case reports of transient neonatal hyperparathyroidism (TNHP) cases. These variants are believed to compromise the plasma membrane localization of the protein. Exome sequencing of an infant with severe antenatal onset thoracic insufficiency with accompanying fetal skeletal abnormalities indicates the critical role of TRPV6 in maternal-fetal transport.

Lactoferrin in sufficient strength acts on a wide range of human and animal viruses based on DNA and RNA genomes, including the herpes simplex virus 1 and 2, cytomegalovirus, HIV, hepatitis C virus, hantaviruses, rotaviruses, poliovirus type 1, human respiratory syncytial virus, murine leukemia viruses and Mayaro virus. The most studied mechanism of antiviral activity of lactoferrin is its diversion of virus particles from the target cells. Many viruses tend to bind to the lipoproteins of the cell membranes and then penetrate into the cell. Lactoferrin binds to the same lipoproteins thereby repelling the virus particles.

In the most common form liver cancer, the hepatocellular carcinoma (HCC), FHL2 is always downregulated in the clinical samples. Therefore, fhl2 is exhibiting a tumor- suppressive effect on HCC. Similar to p53, overexpression of FHL2 inhibit the proliferative activity of the HCC Hep3B cell line by decreasing its cyclin D1 expression and increasing P21 and P27 expression supporting the time-dependent cellular repair process. Of note, a database of FHL2-regulated genes in murine liver has recently been established by using microarray and bioinformatics analysis, which provide useful information concerning most of the pathways and new genes related to FHL2.

For instance, siRNA was used to reduce the amount of pro-inflammatory cytokines expressed in the cells of mice treated with lipopolysaccharide (LPS). The reduced expression of the inflammatory cytokine, tumor necrosis factor α (TNFα), in turn, caused a reduction in the septic shock felt by the LPS- treated mice. In addition, siRNA was used to prevent the bacteria, Psueomonas aeruginosa, from invading murine lung epithelial cells by knocking down the caveolin-2 (CAV2) gene. Thus, though bacteria cannot be directly targeted by siRNA mechanisms, they can still be affected by siRNA when the components involved in the bacterial infection are targeted.

In 2009 the Laboratory of Hans Clevers at Hubrecht Institute and University Medical Center Utrecht, Netherlands, showed that single LGR5-expressing intestinal stem cells self-organize to crypt-villus structures in vitro without necessity of a mesenchymal niche. In 2010, Mathieu Unbekandt & Jamie A. Davies demonstrated the production of renal organoids from murine fetus-derived renogenic stem cells. Subsequent reports showed significant physiological function of these organoids in vitro and in vivo. In 2013, Madeline Lancaster at the Austrian Academy of Sciences established a protocol for culturing cerebral organoids derived from stem cells that mimic the developing human brain's cellular organization.

The antigenic molecules that activate γδ T cells are still mostly unknown. However, γδ T cells are not MHC-restricted and seem to be able to recognize whole proteins rather than requiring peptides to be presented by MHC molecules on APCs. Some murine γδ T cells recognize MHC class IB molecules. Human γδ T cells which use the Vγ9 and Vδ2 gene fragments constitute the major γδ T cell population in peripheral blood, and are unique in that they specifically and rapidly respond to a set of nonpeptidic phosphorylated isoprenoid precursors, collectively named phosphoantigens, which are produced by virtually all living cells.

Syncytin-1 shares many structural elements with class I retroviral glycoproteins (such as, Murine Leukemia Virus gp, Ebolavirus gp, and HIV gp120, gp41). It is composed of a surface subunit (SU) and transmembrane subunit (TM), separated by a furin cleavage site. The two subunits form a heterodimer and are likely linked by a disulfide bond between two conserved cysteine rich motifs: CXXC in SU and CX6CC in TM. This heterodimer likely forms a homotrimer at the cell surface. Syncytin-1 TM contains the fusion peptide, and two heptad repeats separated by a chain reversal region common to class I retroviral glycoproteins.

Furthermore, abundant expression of Csx, the presumptive mouse homolog of tinman, is observed only in the heart from the time of cardiac differentiation. CSX, the human homolog of murine Csx, has a homeodomain sequence identical to that of Csx and is expressed only in the heart, again suggesting that CSX plays an important role in human heart formation. In humans, proper NKX2-5 expression is essential for the development of atrial, ventricular, and conotruncal septation, atrioventricular (AV) valve formation, and maintenance of AV conduction. Mutations in expression are associated with congenital heart disease (CHD) and related ailments.

Linifanib (ABT-869) is a structurally novel, potent inhibitor of receptor tyrosine kinases (RTK), vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) with IC50 of 0.2, 2, 4, and 7 nM for human endothelial cells, PDGF receptor beta (PDGFR-β), KDR, and colony stimulating factor 1 receptor (CSF-1R), respectively. It has much less activity (IC50s > 1 μM) against unrelated RTKs, soluble tyrosine kinases, or serine/threonine kinases. In vivo linifanib is effective orally in mechanism- based murine models of VEGF-induced uterine edema (ED50 = 0.5 mg/kg) and corneal angiogenesis (>50%inhibition, 15 mg/kg).

MDS1 and EVI1 complex locus protein EVI1 (MECOM) also known as ecotropic virus integration site 1 protein homolog (EVI-1) or positive regulatory domain zinc finger protein 3 (PRDM3) is a protein that in humans is encoded by the MECOM gene. EVI1 was first identified as a common retroviral integration site in AKXD murine myeloid tumors. It has since been identified in a plethora of other organisms, and seems to play a relatively conserved developmental role in embryogenesis. EVI1 is a nuclear transcription factor involved in many signaling pathways for both coexpression and coactivation of cell cycle genes.

OLIG2 is also associated with Down syndrome, as it locates at chromosome 21 within or near the Down syndrome critical region on the long arm. This region is believed to contribute to the cognitive defects of Down syndrome. The substantial increase in the number of forebrain inhibitory neurons often observed in Ts65dn mouse (a murine model of trisomy 21) could lead to imbalance between excitation and inhibition and behavioral abnormalities. However, genetic reduction of OLIG2 and OLIG1 from three copies to two rescued the overproduction of interneurons, indicating the pivotal role of OLIG2 expression level in Down syndrome.

The maresins have been detected primarily as products made by monocyte-macrophage cells types. MaR1 has been identified in the synovial fluid taken from the joins of patients with rheumatoid arthritis. In a murine model of acute respiratory distress syndrome, MaR1 production was detected; its generation appeared to reflect an interaction between blood platelets and neutrophils wherein 12-lipoxygenase-rich platelets generated 13(S),14(S)-epoxy-maresin which was then passed to neutrophils which hydrolyzed the epoxy maresin to MaR1. Planaria worms metabolize DHA to Mar1 during the healing phase of experimentally induced tissue injury.

MTA2 is localized on chromosome 11q12-q13.1 in human and on 19B in mice. The 8.6-kb long human MTA2 gene contains 20 exons and seven transcripts inclusive of three protein-coding transcripts but predicted to code for two polypeptides of 688 amino acids and 495 amino acids. The remaining four MTA2 transcripts are non-coding RNA transcripts ranging from 532-bp to 627-bp. The murine Mta2 consists of a 3.1-kb protein-coding transcript to code a protein of 668 amino acids, and five non-coding RNAs transcripts, ranging from 620-bp to 839-bp.

The composition of the murine commensal microbiota influences susceptibility to gastrointestinal infections and induced colitis and specific components of this microbiota promote the production of AHR ligands resulting in protection against intestinal damage induced by dextran sulfate sodium (DSS). Lamas and co- workers have shown that mice with dysbiotic microbiota due to their lack of the caspase recruitment domain 9 (CARD9) produced lower levels of endogenous AHR agonists and recovered more poorly from DSS-induced colitis. When 1 µg FICZ was injected i.p. one day after DSS administration, the severity of colitis in these animals was reduced significantly.

Over time a more nuanced picture of IL-10's function has emerged as treatment of tumor bearing mice has been shown to inhibit tumor metastasis. Additional investigation by multiple laboratories has generated data that further supports IL-10's immunostimulatory capacity in an immunoncology context. Expression of IL-10 from transfected tumor cell lines in IL-10 transgenic mice or dosing with IL-10 leads to control of primary tumor growth and decreased metastatic burden. More recently, PEGylated recombinant murine IL-10 (PEG- rMuIL-10) has been shown to induce IFNγ and CD8+ T cell dependent anti-tumor immunity.

The murine GSC niche in males, also called spermatogonial stem cell (SSC) niche, is located in the basal region of seminiferous tubules in the testes. The seminiferous epithelium is composed of sertoli cells that are in contact with the basement membrane of the tubules, which separates the sertoli cells from the interstitial tissue below. This interstitial tissue comprises Leydig cells, macrophages, mesenchymal cells, capillary networks, and nerves. During development, primordial germ cells migrate into the seminiferous tubules and downward towards the basement membrane whilst remaining attached to the sertoli cells where they will subsequently differentiate into SSCs, also referred to as Asingle spermatogonia.

In 2001 the Triebel group identified a LAG3-associated protein, called LAP, that seemed to participate in immune system down-regulation. Also in 2001 the Triebel group reported finding LAG3 expression on CD8+ tumor-infiltrating lymphocytes, with this LAG3 contributing to APC activation. In August 2002 the first phenotypic analysis of the murine LAG-3 was reported by a team at St. Jude Children's Research Hospital in Memphis. Molecular analysis reported by the St. Jude Children's Research Hospital team in November 2002 demonstrated that the inhibitory function of LAG-3 is performed via the protein's cytoplasmic domain.

Weiss has considered the mechanisms by which the phosphodiesterase antagonises Ribonuclease L. She has studied the role of inflammasome-related cytokines in mouse hepatitis virus-induced disease. Despite murine coronavirus being a useful model of coronaviruses, it is still unclear how mouse hepatitis virus is spread. There is only one receptor for the mouse hepatitis virus – the carcinoembryonic antigen – but highly virulent strains of the virus can spread even when this receptor is not present. In 2020, Weiss was made co-Director of the University of Pennsylvania Center of Research for Coronaviruses and Other Emerging Pathogens.

FGF18 signals through fibroblast growth factor receptor FGFR3 to promote chondrogenesis and has been shown to cause thickening of cartilage in a murine model of osteoarthritis, and the recombinant version of it (sprifermin) is in clinical trial as a potential treatment for osteoarthritis. Studies of the similar proteins in mouse and chick suggested that this protein is a pleiotropic growth factor that stimulates proliferation in a number of tissues, most notably the liver and small intestine. Knockout studies of the similar gene in mice implied the role of this protein in regulating proliferation and differentiation of midline cerebellar structures.

A murine species that was first described by George H. H. Tate in 1951, using specimens obtained in 1930. The holotype is a skin and skull of a young adult collected at Tambellup by J. Baldwin, with Tate referring to a second specimen with a damaged skull as slightly larger. Assigned to a diverse and poorly resolved genus, Pseudomys, the describing author allied the species to a subgeneric classification as Gyomys. The term walyadji is used to refer to the species, but this word does not appear in a literature review of Noongar language names for mammals of the region.

Lidicker (1968), who studies the morphology of the phallus of New Guinea rodents, speculated that Crossomys might not be as closely related to Hydromys as was then generally thought. Later on, this was supported by the immunological study of Watts & Baverstock (1994). This study placed Crossomys closer to Leptomys, Pseudohydromys and Xeromys than to Hydromys. The American mammalogists Guy Musser and Michael Carleton, in their contribution to the authoritative Mammal Species of the World (3rd ed.), divided the group of murine rodents that had before been called "Hydromyinae" or "Hydromyini" in two "divisions":Musser, G.G. & Carleton, M.D. (2005).

Linopirdine is a putative cognition-enhancing drug with a novel mechanism of action. Linopirdine blocks the KCNQ2\3 heteromer M current with an IC50 of 2.4 micromolar disinhibiting acetylcholine release, and increasing hippocampal CA3-schaffer collateral mediated glutamate release onto CA1 pyramidal neurons. In a murine model linopirdine is able to nearly completely reverse the senescence-related decline in cortical c-FOS, an effect which is blocked by atropine and MK-801, suggesting Linopirdine can compensate for the age related decline in acetylcholine release. Linopirdine also blocks homomeric KCNQ1 and KCNQ4 voltage gated potassium channels which contribute to vascular tone with substantially less selectivity than KCNQ2/3.

Figure B illustrates normal human epithelial tissue after incubation with TCT. Notice the damaged and extruded ciliated epithelial cells in Figure B. While previous studies using murine models reported evidence of TCT causing ciliostasis, in vitro studies using human tracheal cells have shown that TCT does not affect ciliary beat frequency of living cells, but instead causes damage and eventual extrusion of ciliated cells. In gonorrhea infections, vaginal ciliated epithelial cells have also displayed the same cytopathogenic effects due to TCT recognition. The extensive damage to ciliated epithilial tissue caused by TCT results in major disruption to the ciliary escalator; an important asset of the host's non- specific defenses.

Unlike creating xenograft mouse models using existing cancer cell lines, there are no intermediate in vitro processing steps before implanting tumor fragments into a murine host to create a PDX. The tumor fragments are either implanted heterotopically or orthotopically into an immunodeficient mouse. With heterotopical implantantion, the tissue or cells are implanted into an area of the mouse unrelated to the original tumor site, generally subcutaneously or in subrenal capsular sites. The advantages of this method are the direct access for implantation, and ease of monitoring the tumor growth. With orthotopic implantation, scientists transplant the patient’s tumor tissue or cells into the corresponding anatomical position in the mouse.

Neurochondrin (also known as its murine homologue, Norbin) is a protein that in humans is encoded by the NCDN gene. This gene encodes a leucine-rich cytoplasmic protein, which is highly similar to a mouse protein norbin that negatively regulates Ca/calmodulin-dependent protein kinase II phosphorylation and may be essential for spatial learning processes. Several alternatively spliced transcript variants of this gene have been described. Norbin can modulate signaling activity and expression of metabotropic glutamate receptor 5; modulating mice with targeted deletion of NCDN in the brain have phenotypic traits usually found in the rodent models of schizophrenia, including disruptions in prepulse inhibition.

Testosterone and DHT treatment of murine 3T3-L1 or human SGBS adipocytes for 24 h significantly decreased the mRNA expression of LKB1 via the androgen receptor and consequently reduced the activation of AMPK by phosphorylation. In contrast, 17β-estradiol treatment increased LKB1 mRNA, an effect mediated by oestrogen receptor alpha. However, in ER-positive breast cancer cell line MCF-7, estradiol caused a dose- dependent decrease in LKB1 transcript and protein expression leading to a significant decrease in the phosphorylation of the LKB1 target AMPK. ERα binds to the STK11 promoter in a ligand-independent manner and this interaction is decreased in the presence of estradiol.

Philippine cobra (naja philippinensis) The Philippine cobra (Naja philippinensis) is one of the most venomous cobra species in the world based on murine studies. The average subcutaneous for this species is 0.20 mg/kg. The lowest reported value for this snake is 0.14 mg/kg SC, while the highest is 0.48 mg/kg SC. and the average venom yield per bite is 90–100 mg. The venom of the Philippine cobra is a potent postsynaptic neurotoxin which affects respiratory function and can cause neurotoxicity and respiratory paralysis, as the neurotoxins interrupt the transmission of nerve signals by binding to the neuromuscular junctions near the muscles.

In mice, the majority of research was carried out with murine cytomegalovirus (MCMV) and in models of hapten- hypersensitivity reactions. Especially, in the MCMV model, protective memory functions of MCMV-induced NK cells were discovered and direct recognition of the MCMV-ligand m157 by the receptor Ly49 was demonstrated to be crucial for the generation of adaptive NK cell responses. In humans, most studies have focused on the expansion of an NK cell subset carrying the activating receptor NKG2C (KLRC2). Such expansions were observed primarily in response to human cytomegalovirus (HCMV), but also in other infections including Hantavirus, Chikungunya virus, HIV, or viral hepatitis.

This forms the basis of the investigation of ZFPs binding by phage display. Work is typically performed using the murine ZFP-TF Zif268 or one of its derivatives, as the basis of the zinc finger sequence modifications since it is the most well characterised of all zinc finger proteins. Its derivatives C7 or C7.GAT, are often used for their superior binding affinity and specificity. C7.GAT has been used to investigate the 5'-ANN-3' and 5'-CNN-3' families of sequences since the third finger of C7 defines a guanine or thymine in the 5' position of the finger two sequence (target site overlap).

Importantly, the histopathology of these tumors was indistinguishable from that of the parental tumors that develop in the MMTV-Neu mice. Application of the CRC system to mouse mammary epithelial cells provides an attractive model system to study the genetics and phenotype of normal and transformed mouse epithelium in a defined culture environment and in vivo transplant studies. A different approach to CRC is to inhibit CD47 – a membrane protein that is the thrombospondin-1 receptor. Loss of CD47 permits sustained proliferation of primary murine endothelial cells, increases asymmetric division and enables these cells to spontaneously reprogram to form multipotent embryoid body-like clusters.

The antigen Thy-1 was the first T cell marker to be identified. Thy-1 was discovered by Reif and Allen in 1964 during a search for heterologous antisera against mouse leukemia cells, and was demonstrated by them to be present on murine thymocytes, on T lymphocytes, and on neuronal cells. It was originally named theta (θ) antigen, then Thy-1 (THYmocyte differentiation antigen 1) due to its prior identification in thymocytes (precursors of T cells in the thymus). The human homolog was isolated in 1980 as a 25kDa protein (p25) of T-lymphoblastoid cell line MOLT-3 binding with anti-monkey-thymocyte antisera.

Prime-boost strategies have been successful in inducing protection against malarial challenge in a number of studies. Primed mice with plasmid DNA encoding Plasmodium yoelii circumsporozoite surface protein (PyCSP), then boosted with a recombinant vaccinia virus expressing the same protein had significantly higher levels of antibody, CTL activity and IFN-γ, and hence higher levels of protection, than mice immunized and boosted with plasmid DNA alone. This can be further enhanced by priming with a mixture of plasmids encoding PyCSP and murine GM-CSF, before boosting with recombinant vaccinia virus. An effective prime-boost strategy for the simian malarial model P. knowlesi has also been demonstrated.

In rural Thailand and Laos, murine and scrub typhus account for around a quarter of all adults presenting to hospital with fever and negative blood cultures. The incidence in Japan has fallen over the past few decades, probably due to land development driving decreasing exposure, and many prefectures report fewer than 50 cases per year. It affects females more than males in Korea, but not in Japan, which may be because sex-differentiated cultural roles have women tending garden plots more often, thus being exposed to vegetation inhabited by chiggers. The incidence is increasing in the southern part of the Indian subcontinent and in northern areas around Darjeeling.

One method of gene therapy involves modifying a virus to act as a vector to insert beneficial genes into cells. Unlike other retroviruses, which cannot penetrate the nuclear envelope and can therefore only act on cells while they are undergoing mitosis, lentiviruses can infect cells whether or not they are dividing. Many cell types, like neurons, do not divide in adult organisms, so lentiviral gene therapy is a good candidate for treating conditions that affect those cell types. Some experimental applications of lentiviral vectors have been done in gene therapy in order to cure diseases like Diabetes mellitus, Murine haemophilia A, prostate cancer, chronic granulomatous disease, and vascular diseases.

Entry mechanisms for noroviruses are still largely unknown, but the first proteinaceous receptor mediating norovirus entry was found with experiments on MNV. This receptor, CD300lf, is a membrane glycoprotein, that functions in regulation of multiple immune responses. CD300lf is found on mast cells of both murine species and humans, but definite proof of its function in human norovirus infections remains unknown. In mice however, CD300lf functions in virus binding thus having a role to play in the first steps of viral entry. Binding is essentially mediated by phospholipids of the virus' VP1 protein that bind to a cleft between CDR3 and CC’loop -domains of CD300lf -receptor.

Enhancers as sites of extragenic transcription were initially discovered in genome-wide studies that identified enhancers as common regions of RNA polymerase II (RNA pol II) binding and non-coding RNA transcription. The level of RNA pol II–enhancer interaction and RNA transcript formation were found to be highly variable among these initial studies. Using explicit chromatin signature peaks, a significant proportion (~70%) of extragenic RNA Pol II transcription start sites were found to overlap enhancer sites in murine macrophages. Out of 12,000 neuronal enhancers in the mouse genome, almost 25% of the sites were found to bind RNA Pol II and generate transcripts.

When megakaryocytes and endothelial cells are activated by agonists such as thrombin, P-selectin is rapidly translocated to the plasma membrane from granules. Secondly, increased levels of P-selectin mRNA and protein are induced by inflammatory mediators such as tumor necrosis factor-a (TNF-a), LPS, and interleukin-4 (IL-4). Although TNF-a and LPS increase levels of both mRNA and protein in murine models, they do not appear to affect mRNA in human endothelial cells, while IL-4 increases P-selectin transcription in both species. The elevated synthesis of P-selectin may play an important role in the delivery of protein to the cell surface.

STIM2 detects small decreases in Ca2+ content stored in the S/ER, switches to the activated state and interacts with so called store-operated Ca2+ (SOC) channels located in the plasma membrane, such as Orai or TRPC channels, allowing SOCE. Although the functional role of STIM2 has been elusive for many years, studies performed in 2009-2010 on murine models suggested that STIM2 participates in processes of the development and functioning of many cell types, including smooth muscle myoblasts, cells of the immune system and neurons, and is involved in tumorigenesis, the development of autoimmune diseases and mechanisms of neuronal damage after transient ischemic conditions.

Although AAV2 is the most popular serotype in various AAV-based research, it has been shown that other serotypes can be more effective as gene delivery vectors. For instance AAV6 appears much better in infecting airway epithelial cells, AAV7 presents very high transduction rate of murine skeletal muscle cells (similar to AAV1 and AAV5), AAV8 is superb in transducing hepatocytes and AAV1 and 5 were shown to be very efficient in gene delivery to vascular endothelial cells. In the brain, most AAV serotypes show neuronal tropism, while AAV5 also transduces astrocytes. AAV6, a hybrid of AAV1 and AAV2, also shows lower immunogenicity than AAV2.

After tens of millions of years of relative isolation, Africa-Arabia collided with Eurasia, and the formation of the Isthmus of Panama linked South America and North America, facilitating the distribution of mammals seen today. With the exception of bats and murine rodents, no placental land mammals reached Australasia until the first human settlers arrived approximately 50,000 years ago. It should however be noted that these molecular results are still controversial mainly because they are not reflected by morphological data and thus not accepted by many systematists. It is also important to note that fossil taxa are not and, in most cases cannot, be included.

A steady stream of consistently negative results followed the PLoS ONE report.Hohn, O; Strohschein, K; Brandt, AU; Seeher, S; Klein, S; Kurth, R; Paul, F; Meise, C; Scheibenbogen, C; Bannert, N. One study, later retracted, found no XMRV but did report evidence of murine retroviral sequences in the blood of some CFS patients. Mikovits and Ruscetti attributed the failure to replicate their results to the use of different PCR reactions and to the examination of patients who did not satisfy the same CFS diagnostic criteria. A study using the original reaction conditions did not detect XMRV in UK patients who "not only had CFS, but had considerable disability".

Several mouse strains carry the virus endogenously, but it is also transmitted vertically via milk from mother to pup. It is contained as a DNA provirus integrated in the DNA of milk lymphocytes. The viruses become transported through the gastrointestinal tract to the Peyer's patches where they infect the new host's macrophages, and then lymphocytes. The mouse mammary tumor virus (MMTV) has formerly been classified as a simple retrovirus; however, it has recently been established, that MMTV encodes an extra self-regulatory mRNA export protein, Rem, with resemblance to the Human Immunodeficiency Virus HIV Rev protein, and is therefore the first complex murine retrovirus to be documented.

The ABL1 gene encodes a non-receptor tyrosine kinase termed Abelson murine leukemia viral oncogene homolog 1. Among its numerous effects on cellular function, the ABL1 kinase- regulates cell proliferation and survival pathways during development. It mediates at least in part the cell proliferating signaling stimulated by PDGF receptors as well as by antigen receptors on T cell and B cell lymphocytes. The ABL1 gene is located on human chromosome 9q34.12; translocations between it and the BCR gene on human chromosome 22q11.23 create the well-known t(9;22)(q34;q11) BCR-ABL1 fusion gene responsible for Philadelphia chromosome positive chronic myelogenous leukemia and chronic lymphocytic leukemia.

The bacterial natural product rapamycin or sirolimus, a cytostatic agent, has been used in combination therapy with corticosteroids and cyclosporine in patients who received kidney transplantation to prevent organ rejection both in the US and Europe, due to its unsatisfying pharmacokinetic properties. In 2003, the U.S. Food and Drug Administration approved sirolimus-eluting coronary stents, which are used in patients with narrowing of coronary arteries, or so-called atherosclerosis. Recently rapamycin has shown effective in the inhibition of growth of several human cancers and murine cell lines. Rapamycin is the main mTOR inhibitor, but deforolimus (AP23573), everolimus (RAD001), and temsirolimus (CCI-779), are the newly developed rapamycin analogs.

The upregulation of Th 2 T cell proteins, like IL-4 and TGF-Beta, are the main focus of some research which aims to minimize the effects seen in the model organism disease EAE (experimental autoimmune encephalomyelitis), studied for its similarities to Multiple Sclerosis.Though this study of gene regulation is observed within murine models, it focuses on MS orthologs to humans and research has shown that it may also help to manage: Rheumatoid Arthritis, Diabetes mellitus type 1, Systemic lupus erythematosus (SLE), cardiovascular disease (CVD), and other chronic inflammatory diseasesDeluca H and Cantorna M. 2001. Vitamin D: Its role and uses in immunology. FASEB Journal 15(14):2579-85.

T. lewisi can be cultured in various media including in vivo in rat serum and in vitro in mammalian cell culture media. The parasite can also be grown in mice if the host is supplemented with a controlled diet and intraperitoneal injection of rat serum. Ablastin, an antibody that arises during an infection in the host’s body, prevents the parasite from reproducing although they remain in adult form. A research paper suggests that the data on the aftermath of introduction of a Trypanosoma lewisi to immunologically naïve murine hosts on Christmas Island around 1900 matches reports of complete extinction within the range of 1–9 years.

This compound was first synthesized by Bayer chemists Josef Klarer and Fritz Mietzsch as part of a research program designed to find dyes that might act as antibacterial drugs in the body. The molecule was tested and in the late autumn of 1932 was found effective against some important bacterial infections in mice by Gerhard Domagk, who subsequently received the 1939 Nobel Prize in Medicine. Prontosil was the result of five years of testing involving thousands of compounds related to azo dyes. The crucial test result (in a murine model of Streptococcus pyogenes systemic infection) that preliminarily established the antibacterial efficacy of Prontosil in mice dates from late December 1931.

2010 Jan;20(1):25-35. Epub 2009 Oct 19. . The nuclear PtdIns5P pool is controlled by the nuclear type I PtdIns(4,5)P2 4-phosphatase that, in conjunction with the PIPKIIbeta kinase, plays a role in UV stress, apoptosis and cell cycle progression.Clarke JH, Letcher AJ, D'santos CS, Halstead JR, Irvine RF, Divecha N. Inositol lipids are regulated during cell cycle progression in the nuclei of murine erythroleukaemia cells. Biochem J. 2001 Aug 1;357(Pt 3):905-10. Jones DR, Bultsma Y, Keune WJ, Halstead JR, Elouarrat D, Mohammed S, Heck AJ, D'Santos CS, Divecha N. Nuclear PtdIns5P as a transducer of stress signaling: an in vivo role for PIP4Kbeta.

The human PAK1 gene is 153-kb long and consists of 23 exons, six exons for 5’-UTR and 17 exons for protein coding (Gene from review). Alternative splicing of six exons generates 20 transcripts from 308-bp to 3.7-kb long; however, only 12 spliced transcripts have open reading frames and are predicted to code ten proteins and two polypeptides. The remaining 8 transcripts range are for non-coding long RNAs from 308-bp to 863-bp long. Unlike the human PAK1, murine PAK1 gene generates five transcripts: three protein-coding from 508-bp to 3.0-kb long, and two transcripts of about 900-bp for non-coding RNAs.

However, recent data shows that leptomycin causes G1 cell cycle arrest in mammalian cells and is a potent anti-tumor agent against murine experimental tumors in combination therapy. Leptomycin B has been shown to be a potent and specific nuclear export inhibitor in human and the fission yeast S. pombe. Leptomycin B alkylates and inhibits CRM1 (chromosomal region maintenance)/exportin 1 (), a protein required for nuclear export of proteins containing a nuclear export sequence (NES), by glycosylating a cysteine residue (cysteine 529 in S. pombe). In addition to antifungal and antibacterial activities, leptomycin B blocks the cell cycle and is a potent anti-tumor agent.

The venom of the Egyptian cobra consists mainly in neurotoxins and cytotoxins. The average venom yield is 175 to 300 mg in a single bite, and the murine subcutaneous value is 1.15 mg/kg. The venom affects the nervous system, stopping the nerve signals from being transmitted to the muscles and at later stages stopping those transmitted to the heart and lungs as well, causing death due to complete respiratory failure. Envenomation causes local pain, severe swelling, bruising, blistering, necrosis and variable non-specific effects which may include headache, nausea, vomiting, abdominal pain, diarrhea, dizziness, collapse or convulsions along with possible moderate to severe flaccid paralysis.

This technique has also been used to grow panda fetuses in a cat, but the cat mother died of pneumonia before completed term. Also, murine embryos of Ryukyu mouse (Mus caroli) will survive to term inside the uterus of a house mouse (Mus musculus) only if enveloped in Mus musculus trophoblast cells. Goat fetuses have likewise been successfully grown in sheep wombs by enveloping the goat inner cell mass in sheep trophoblast. Such envelopment can be created by first isolating the inner cell mass of blastocysts of the species to be reproduced by immunosurgery, wherein the blastocyst is exposed to antibodies toward that species.

Chronic use of amphetamine at excessive doses causes alterations in gene expression in the mesocorticolimbic projection, which arise through transcriptional and epigenetic mechanisms. The most important transcription factors that produce these alterations are Delta FBJ murine osteosarcoma viral oncogene homolog B (ΔFosB), cAMP response element binding protein (CREB), and nuclear factor-kappa B (NF-κB). ΔFosB is the most significant biomolecular mechanism in addiction because ΔFosB overexpression (i.e., an abnormally high level of gene expression which produces a pronounced gene-related phenotype) in the D1-type medium spiny neurons in the nucleus accumbens is necessary and sufficient for many of the neural adaptations and regulates multiple behavioral effects (e.g.

Haruko Obokata claimed that STAP cells were produced by exposing CD45+ murine spleen cells to certain stresses including an acidic medium with a pH of 5.7 for half an hour. Following this treatment, the cells were verified to be pluripotent by observing increasing levels of Oct-4 (a transcription factor expressed in embryonic stem cells) over the following week using an Oct4-GFP transgene. On average only 25% of cells survived the acid treatment, but over 50% of those that survived converted to Oct4-GFP+CD45− pluripotent cells. The researchers also claimed that treatment with bacterial toxins or physical stress were conducive to the acquisition of pluripotent markers.

Fli-1 is a member of the ETS transcription factor family that was first identified in erythroleukemias induced by Friend Murine Leukemia Virus (F-MuLV). Fli-1 is activated through retroviral insertional mutagenesis in 90% of F-MuLV-induced erythroleukemias. The constitutive activation of fli-1 in erythroblasts leads to a dramatic shift in the Epo/Epo-R signal transduction pathway, blocking erythroid differentiation, activating the Ras pathway, and resulting in massive Epo- independent proliferation of erythroblasts. These results suggest that Fli-1 overexpression in erythroblasts alters their responsiveness to Epo and triggers abnormal proliferation by switching the signaling event(s) associated with terminal differentiation to proliferation.

In 1958, Miller travelled to the United Kingdom on a Gaggin Research Fellowship from the University of Queensland. He was accepted to the Chester Beatty Research Institute of Cancer Research (part of the Institute of Cancer Research, London) and as a PhD student at the University of London. Miller chose to study the pathogenesis of lymphocytic leukemia in mice, expanding on the research of Ludwik Gross into murine leukemia virus. Miller showed that experimental animals without a thymus at birth were incapable of rejecting foreign tissues and resisting many infections, thus demonstrating that the thymus is vital for development and function of the adaptive immune system.

PD-1 has two ligands, PD-L1 and PD-L2, which are members of the B7 family. PD-L1 protein is upregulated on macrophages and dendritic cells (DC) in response to LPS and GM-CSF treatment, and on T cells and B cells upon TCR and B cell receptor signaling, whereas in resting mice, PD-L1 mRNA can be detected in the heart, lung, thymus, spleen, and kidney. PD-L1 is expressed on almost all murine tumor cell lines, including PA1 myeloma, P815 mastocytoma, and B16 melanoma upon treatment with IFN-γ. PD-L2 expression is more restricted and is expressed mainly by DCs and a few tumor lines.

EVI1 and the fusion transcript MDS1-EVI1 are both expressed in the adult human kidney, lung, pancreas, brain, and ovaries. ;Cell cycle and differentiation: In vitro experiments using both human and mouse cell lines have shown that EVI1 prevents the terminal differentiation of bone marrow progenitor cells to granulocytes and erythroid cells, however it favors the differentiation of hematopoietic cell to megakaryocytes. The chimeric gene of AML1-MDS1-EVI1 (AME) formed by the chromosomal translocation (3;21)(q26;q22) has also been shown in vitro to upregulate the cell cycle and block granulocytic differentiation of murine hematopoietic cells, as well as to delay the myeloid differentiation of bone marrow progenitors.

The cancer stem cell hypothesis states that a dedicated small population of cancerous stem cells that manages to evade anti-cancer therapy maintains benign and malignant tumours. This explains recurring malignancies even after surgical removal of the tumours. LGR5+ve stem cells were identified to fuel stem cell activity in murine intestinal adenomas via erroneous activation of the pro-cell cycle Wnt signalling pathway as a result of successive mutations, such as formation of adenoma via Adenomatous polyposis coli (APC) mutation. Studies on LGR5 in colorectal cancer revealed a rather perplexing mechanism: loss of LGR5 actually increased tumourigenicity and invasion whereas overexpression results a reduction in tumourigenicity and clonogenicity.

The genomes of exogenous and endogenous murine leukemia viruses have been fully sequenced. The viral genome is a single stranded, positive-sense RNA highly folded, molecule of around 8000 nucleotides. From 5' to 3' (typically displayed as "left" to "right"), the genome contains gag, pol, and env regions, coding for structural proteins, enzymes including the RNA-dependent DNA polymerase (reverse transcriptase), and coat proteins, respectively. In addition to these three polyproteins: Gag, Pol and Env, common to all retroviruses, MLV also produces the p50/p60 proteins issued from an alternative splicing of its genomic RNA.. The genomic molecule contains a 5' methylated cap structure and a 3' poly-adenosine tail.

He went on to attend the University of Texas, MD Anderson Hospital, Houston, Texas and received his Ph.D. in 1980. His dissertation described the biosynthesis of Rauscher murine leukemia virus reverse transcriptase. From 1980 to 1982, he continued his research training as a postdoctoral fellow at the Roche Institute of Molecular Biology in Nutley, New Jersey. He then accepted a position at the prestigious Merck Institute of Therapeutic Research where he conducted and facilitated research from 1982 to 1986, first as a senior research biochemist and later as a research fellow, and finally as a group leader of Molecular Biology at the Department of Animal Drug Discovery.

Because FOXO1 provides a link between transcription and metabolic control by insulin, it is also a potential target for genetic control of type 2 diabetes. In the insulin-resistant murine model, there is increased hepatic glucose production due to a loss in insulin sensitivity; the rates of hepatic gluconeogenesis and glycogenolysis are increased when compared to normal mice; this is presumably due to un-regulated FOXO1. When the same experiment was repeated with haploinsufficient FOXO1, insulin sensitivity was partially restored, and hepatic glucose production subsequently decreased. Similarly, in mice fed with a high fat diet (HFD), there is increased insulin resistance in skeletal and liver cells.

Working alone and anonymously late at night, he leaves notes to guide the cheesemakers in their work. His taste for good cheese leads to the factory's commercial success and to his murine fame to such an extent that Anatole is regularly hailed as a "mouse magnifique" by rodent contemporaries. The factory's human owners and workers also hold his work in high esteem, although they have no idea that the mysterious Anatole is a mouse, believing him simply an eccentric cheese connoisseur who prefers to work alone. In these works the author, through the character of Anatole, consistently places emphasis on the dignity of work.

These are short genomic regions with a high density of CpG dinucleotides, and are commonly found in an unmethylated state within or nearby to an active gene's promoter. Bird's group discovered that the MeCP2 protein binds specifically to methylated CpG sites, and further that disruption of this interaction causes the autism spectrum disorder Rett syndrome. The Bird lab also implicated nuclear receptor co-repressor 1 as an important binding partner in the MeCP2/methyl-CpG interaction. In 2007 the Bird laboratory published a paper in the journal Science describing a proof- of-principle that the murine equivalent of Rett syndrome could be successfully reversed in laboratory mice.

McLaren was the daughter of Sir Henry McLaren, 2nd Baron Aberconway and a Liberal MP, and Christabel Mary Melville MacNaghten. She was born in London and lived there until the war, when her family moved to their estate at Bodnant, North Wales. As a child she appeared in the film version of H.G. Wells' novel Things to Come, released in 1936.. She read zoology at Lady Margaret Hall, Oxford, later gaining an MA. Researching mite infestation of Drosophila under J.B.S. Haldane, she continued her post-graduate studies at University College London from 1949, first under Peter Medawar on the genetics of rabbits and then on neurotropic murine viruses under Kingsley Sanders. She obtained her D.Phil.

Two therapeutics have been approved by FDA so far inhibiting the phosphorylation on RIP2, which is necessary for proper NOD2 functioning, gefitinib and erlotinib. Additionally, research has been conducted on GSK583, a highly specific RIP2 inhibitor, which seems highly promising in inhibiting NOD1 and NOD2 signaling and therefore, limiting inflammation caused by NOD1, NOD2 signaling pathways. Another possibility is to remove the sensor for NOD2, which has been proved efficient in murine models in the effort to suppress the symptoms of Crohn's disease. Type II kinase inhibitors, which are highly specific, have shown promising results in blocking the TNF arising from NOD-dependent pathways, which shows a high potential in treatment of inflammation associated tumors.

In the 1990s it was widely used as a recipient cell line for the transduction of cytokine genes and other genes of immunological interest, to produce recombinant experimental vaccines that induced anti-tumor immunological responses.Allione A, M Consalvo, P Nanni, P-L Lollini, F Cavallo, M Giovarelli, M Forni, A Gulino, MP Colombo, P Dellabona, H Hock, T Blankenstein, FM Rosenthal, B Gansbacher, MC Bosco, T Musso, L Gusella, and Guido Forni. 1994. "Immunizing and curative potential of replicating and nonreplicating murine mammary adenocarcinoma cells engineered with interleukin (IL)-2, IL-4, IL-6, IL-7, IL-10, tumor necrosis factor alpha, granulocyte-macrophage colony-stimulating factor, and gamma-interferon gene or admixed with conventional adjuvants". Cancer Research.

Another shared aspect between NR2B and RELN is that they both can be regulated by the TBR1 transcription factor. The heterozygous reeler mouse, which is haploinsufficient for the RELN gene, shares several neurochemical and behavioral abnormalities with schizophrenia and bipolar disorder, but the exact relevance of these murine behavioral changes to the pathophysiology of schizophrenia remains debatable. As previously described, reelin plays a crucial role in modulating early neuroblast migration during brain development. Evidences of altered neural cell positioning in post-mortem schizophrenia patient brains and changes to gene regulatory networks that control cell migration suggests a potential link between altered reelin expression in patient brain tissue to disrupted cell migration during brain development.

The Nck (non-catalytic region of tyrosine kinase adaptor protein 1) belongs to the adaptor family of proteins. The nck gene was initially isolated from a human melanoma cDNA library using a monoclonal antibody produced against the human melanoma-associated antigen. The Nck family has two known members in human cells (Nck-1/Nckalpha and NcK2/NcKbeta), two in mouse cells (mNckalpha and mNckbeta/Grb4) and one in drosophila (Dock means dreadlocks-ortholog). The two murine gene products exhibit 68% amino acid identity to one another, with most of the sequence variation being located to the linker regions between the SH3 and SH2 domains, and are 96% identical to their human counterparts.

The Ras/MAPK/ERK pathway relays signals to nuclear transcription factors and plays a role in governing cell cycle control and differentiation. In Ph chromosome-containing cells, the BCR-ABL tyrosine kinase activates the RAS/RAF/MEK/ERK pathway, which results in unregulated cell proliferation via gene transcription in the nucleus. The BCR-ABL tyrosine kinase activates Ras via phosphorylation of the GAB2 protein, which is dependent on BCR-located phosphorylation of Y177. Ras in particular is shown to be an important downstream target of BCR-ABL1 in CML, as Ras mutants in murine models disrupt the development of CML associated with the BCR-ABL1 gene (Effect of Ras inhibition in hematopoiesis and BCR/ABL leukemogenesis).

In addition to its constitutive secretion by CD4+ and CD8+ T cells, the secreted form of FGL2 (sFGL2) can be inducibly secreted by Foxp3+ CD4+ CD25+ T regulatory cells (Tregs). Such Treg cells play a vital role in dampening the immune response after the clearance of an infection to prevent sterile inflammation. These cells also play a fundamental role in maintaining self tolerance by suppressing the activation and expansion of self-reactive lymphocytes that may instigate autoimmunity.9 Through their roles in immune homeostasis, it has been shown that depletion of the Treg cell population in murine models for disease lead to enhanced immune responses to a variety of infectious agents including hepatitis C virus (HCV).

PTPkappa mRNA is also observed in the adult mouse cerebellum. Using a β-galactosidase (β-gal) reporter gene inserted into the phosphatase domain of the murine PTPkappa (PTPRK) gene, Shen and colleagues determined the detailed expression pattern of endogenous PTPRK. β-gal activity was observed in many areas of the adult forebrain, including layers II and IV, and to a lesser extent in layer VI of the cortex. β-gal activity was also observed in apical dendrites of cortical pyramidal cells, the granule layer of the olfactory and accessory olfactory bulbs, the anterior hypothalamus, paraventricular nucleus, and in granule and pyramidal layers of the dentate gyrus and CA 1-3 regions of the hippocampus.

In addition to the transport of iron from the intestine and into the circulation, ferroxidases also seem to play an important role in facilitating iron export from retinal cells. While deficiency in hephaestin or ceruloplasmin alone do not seem to cause iron buildup in the retina, studies done on murine models suggest that the combined deficiency is sufficient to cause age-dependent retinal pigment epithelium and retinal iron accumulation, with features consistent with macular degeneration. Hephaestin has been detected in mouse and human RPE (retinal pigment epithelial) cells as well as in rMC-1 cells (a rat Müller glial cell line), with greatest expression in the Müller endnote next to the internal limiting membrane.

The CDC lists the following areas as active foci of human epidemic typhus: Andean regions of South America, some parts of Africa; on the other hand, the CDC only recognizes an active enzootic cycle in the United States involving flying squirrels (CDC). Though epidemic typhus is commonly thought to be restricted to areas of the developing world, serological examination of homeless persons in Houston found evidence for exposure to the bacterial pathogens that cause epidemic typhus and murine typhus. A study involving 930 homeless people in Marseilles, France found high rates of seroprevalence to R. prowazekii and a high prevalence of louse-borne infections in the homeless. Typhus has been increasingly discovered in homeless populations in developed nations.

Moreover, to increase their pathogen-killing ability, they produce increased amounts of chemicals called reactive oxygen species (ROS) and nitrogen radicals (caused by upregulation of inducible NO synthase iNOS). Thanks to their ability to fight pathogens, M1 macrophages are present during acute infectious diseases. A number of studies have shown that bacterial infection induces polarization of macrophages toward the M1 phenotype, resulting in phagocytosis and intracellular killing of bacteria in vitro and in vivo. For instance, Listeria monocytogenes, a Gram positive bacteria causing listeriosis is shown to induce an M1 polarization, as well as Salmonella typhi (the agent of typhoid fever) and Salmonella typhimurium (causing gastroenteritis), which are shown to induce the M1 polarization of human and murine macrophages.

In addition to researching post- translation modifications of clock proteins, Kramer has also studied the function of the circadian clock in the immune system. He has shown how TNF-α and IL-6 secretion by lipopolysaccharide (LPS)-stimulated murine splenic macrophages display circadian rhythms that are not dependent on either variations in glucocorticoid concentrations or the circadian changes that occur in the cellular constitution of the spleen. This exhibits how the molecular clock in immune cells can remain functional regardless of systemic cues. Kramer was also able to show that approximately 8% of the macrophage transcriptome in mice exhibits circadian oscillation, including genes (such as JUN and FOS) that are involved in LPS-induced responses.

Murine polyomavirus was the first polyomavirus discovered, having been reported by Ludwik Gross in 1953 as an extract of mouse leukemias capable of inducing parotid gland tumors. The causative agent was identified as a virus by Sarah Stewart and Bernice Eddy, after whom it was once called "SE polyoma". The term "polyoma" refers to the viruses' ability to produce multiple (poly-) tumors (-oma) under certain conditions. The name has been criticized as a "meatless linguistic sandwich" ("meatless" because both morphemes in "polyoma" are affixes) giving little insight into the viruses' biology; in fact, subsequent research has found that most polyomaviruses rarely cause clinically significant disease in their host organisms under natural conditions.

Another lab-on-a-chip similarly combined a microfluidic network in PDMS with planar microelectrodes, this time to measure extracellular potentials from single adult murine cardiomyocytes. A reported design of a heart-on-a-chip claims to have built "an efficient means of measuring structure-function relationships in constructs that replicate the hierarchical tissue architectures of laminar cardiac muscle." This chip determines that the alignment of the myocytes in the contractile apparatus made of cardiac tissue and the gene expression profile (affected by shape and cell structure deformation) contributes to the force produced in cardiac contractility. This heart-on-a-chip is a biohybrid construct: an engineered anisotropic ventricular myocardium is an elastomeric thin film.

Kode Technology has been used for the in vitro modification of murine embryos, spermatozoa, zebra fish, epithelial/endometrial cells and red blood cells to create cellular quality controls systems, serologic kits (teaching), rare antigen expression, add infectious markers onto cells, modified cell adhesion/interaction/separation/immobilisation, and labelling. It has also been intravascularly infused for in vivo modification of blood cells and neutralisation of circulating antibodies and in in vivo imaging of circulating bone marrow kodecytes in zebrafish. Kode FSL constructs have also been applied to non-biological surfaces such as modified cellulose, paper, silica, polymers, natural fibers, glass and metals and has been shown to be ultra-fast in labelling these surfaces.

The enzymes produced by X-linked genes AWAT1 and AWAT2 have been shown to esterify long chain alcohols to produce wax esters and is most predominantly expressed in skin. Both enzymes have dissimilar substrate specificities: AWAT1 prefers decyl alcohol (C10) and AWAT2 prefers C16 and C18 alcohols while using oleoyl-CoA as the acyl donor. However, when using acetyl alcohol as the acyl acceptor, AWAT1 prefers saturated acyl groups, while AWAT2 shows activity with all four acyl-CoAs and performs two times better with unsaturated acyl-CoAs than with saturated ones. Along with the murine wax ester synthase, AWAT1 and AWAT2 are likely the most significant contributors in wax ester production in mammals.

The neural cell adhesion molecule N-CAM simultaneously combines with another N-CAM and a fibroblast growth factor receptor to stimulate the tyrosine kinase activity of that receptor to induce the growth of neurites. There are several software kits available to facilitate neurite tracing in images (see external links). Weak endogenous electric fields may be used to both facilitate and direct the growth of projections from cell soma neurites, EFs of moderate strength have been used to direct and enhance neurite outgrowth in both murine, or mouse, and xenopus models. Co-culture of neurons with electrically aligned glial tissue also directs neurite outgrowth, as it is rich in neurotrophins that promote nerve growth .

The CD4 receptor in particular interacts with murine MHC-II following the "ball-on-stick" model, where the Phe-43 ball fits into the conserved hydrophobic α2 and β2 domain residues. During binding with MHC- II, CD4 maintains independent structure and does not form any bonds with the TCR receptor. The members of the CD family of co-receptors have a wide range of function. As well as being involved in forming a complex with MHC-II with TCR to control T-cell fate, the CD4 receptor is infamously the primary receptor that HIV envelope glycoprotein GP120 binds to. In comparison, CD28 acts as a ‘co-coreceptor’ (costimulatory receptor) for the MHC-II binding with TCR and CD4.

The beta subunit is a non-DNA binding regulatory subunit; it allosterically enhances DNA binding by the alpha subunit as the complex binds to the core site of various enhancers and promoters, including murine leukemia virus, polyomavirus enhancer, T-cell receptor enhancers and GM-CSF promoters. Alternative splicing generates two mRNA variants, each encoding a distinct carboxyl terminus. In some cases, a pericentric inversion of chromosome 16 [inv(16)(p13q22)] produces a chimeric transcript consisting of the N terminus of core-binding factor beta in a fusion with the C-terminal portion of the smooth muscle myosin heavy chain 11. This chromosomal rearrangement is associated with acute myeloid leukemia of the M4Eo subtype.

Isoflavones genistein and daidzein bind to and transactivate all three PPAR isoforms, α, δ, and γ. For example, membrane-bound PPARγ-binding assay showed that genistein can directly interact with the PPARγ ligand binding domain and has a measurable Ki of 5.7 mM. Gene reporter assays showed that genistein at concentrations between 1 and 100 uM activated PPARs in a dose dependent way in KS483 mesenchymal progenitor cells, breast cancer MCF-7 cells, T47D cells and MDA-MD-231 cells, murine macrophage-like RAW 264.7 cells, endothelial cells and in Hela cells. Several studies have shown that both ERs and PPARs influenced each other and therefore induce differential effects in a dose-dependent way.

Interferon-γ signaling mediates transcriptional repression of the perlecan gene. This was first shown in colon cancer cell lines, and subsequently in cell lines of other tissue origins, but in each case intact STAT1 transcription factor was required for the signal to take effect. This led the investigators to believe that the transcription factor STAT1 was interacting with the Pln promoter in the distal region, localized to 660 base pairs upstream of the transcription start site. Interferon- γ treatment of blastocyst-stage murine embryos leads to a loss of perlecan expression on the trophectoderm, and thus an embryonic morphology and phenotype in cell culture, which is suggestive that these interferon-γ treated blastocysts would be defective in implantation.

Increased levels of intracerebral IFNα are also thought to play a detrimental role in Aicardi–Goutières syndrome (AGS), HIV-associated dementia and CNS lupus. While type I IFNs are one of the classical cytokines required for an effect antiviral response, higher type I IFN levels are associated with worsening disease in bacterial infections, such as tuberculosis and lepromatous leprosy. Type I IFN is also being investigated for a potential role in neurodegeneration; loss of IFNAR expression prolonged survival in murine models of amyotrophic lateral sclerosis (ALS). IFNα has also been used in the clinic for the treatment of type I IFN responsive hematological malignancies, such as chronic myelogenous leukemia (CML), multiple myeloma, and hairy cell leukemia.

Intratumoral and intra-organ spread of recombinant SeV virions in vivo in a hepatoma xenograft murine model. alt= Non invasive SeV imaging of variable constructs Trafficking of Sendai Virus Nucleocapsids Is Mediated-by-Intracellular Vesicles SeV has been known to the research community more since late 1950s and it has been widely used to create multiple variants of genetic engineering constructs, including vectors for trans-genes delivery. Creation of SeV genetic constructs is easier compared to other viruses, many SeV genes have a transcriptional initiation and termination signals. Therefore, constructing a recombinant virus is straightforward; the foreign gene can be introduced into the viral genome by replacing or adding viral protein expressing gene(s).

Annotation of the human and mouse genomes has led to the identification of >20 000 protein-coding genes and >3 000 noncoding RNA genes, which guide the development of the organism from fertilization through embryogenesis to adult life. Although dramatic progress is noted, the relevance of rare gene variants has remained a central topic of research. As one of the most important platforms for dealing with vertebrate gene functions on a large scale, genome- wide genetic resources of mutant murine ES cells have been established. To this end four international programs aimed at saturation mutagenesis of the mouse genome have been founded in Europe and North America (EUCOMM, KOMP, NorCOMM, and TIGM).

Mutations in the murine Mafb gene are responsible for the mutant mouse Kreisler (kr) that presents an abnormal segmentation of the hindbrain and exhibit hyperactive behavior, including head tossing and running in circles. This mice dies at birth due to renal failure whereas the Mafb -/- mice dies of central apnea. Recently, single-nucleotide polymorphisms (SNPs) near MAFB have been found associated with nonsyndromic cleft lip and palate. The GENEVA Cleft Consortium study, a genomewide association study involving 1,908 case-parent trios from Europe, the United States, China, Taiwan, Singapore, Korea, and the Philippines, first identified MAFB as being associated with cleft lip and/or palate with stronger genome-wide significance in Asian than European populations.

FSL have been used to create human red cell kodecytes that have been used to detect and identify blood group allo-antibodies as ABO sub-group mimics, ABO quality control systems, serologic teaching kits and a syphilis diagnostic. Kodecytes have also demonstrated that FSL-FLRO4 is a suitable reagent for labelling packed red blood cells (PRBC) at any point during routine storage and look to facilitate the development of immunoassays and transfusion models focused on addressing the mechanisms involved in tansfusion-related immunomodulation (TRIM). Murine kodecytes have been experimentally used to determine in vivo cell survival, and create model transfusion reactions. Zebrafish kodecytes have been used to determine real time in vivo cell migration.

Mice that had a latent infection of the virus had an increased resistance to the bacteria, but those with a non-latent strain of virus had no change in susceptibility to the bacteria. The study went on to test mice with murine cytomegalovirus, a member of the betaherpesvirinae subfamily, which provided similar results. However, infection with human herpes simplex virus type-1 (HSV-1), a member of the alphaherpesvirinae subfamily, did not provide increased resistance to bacterial infection. They also used Yersinia pestis (the causative agent of the Black Death) to challenge mice with a latent infection of gammaherpesvirus 68, and they found the mice did have an increased resistance to the bacteria.

Proteins of the matrix metalloproteinase (MMP) family are involved in the breakdown of extracellular matrix in normal physiological processes, such as embryonic development, reproduction, angiogenesis, bone development, wound healing, cell migration, learning and memory, as well as in pathological processes, such as arthritis, intracerebral hemorrhage, and metastasis. Most MMPs are secreted as inactive proproteins which are activated when cleaved by extracellular proteinases. The enzyme encoded by this gene degrades type IV and V collagens and other extracellular matrix proteins. Studies in rhesus monkeys suggest that the enzyme is involved in IL-8-induced mobilization of hematopoietic progenitor cells from bone marrow, and murine studies suggest a role in tumor-associated tissue remodeling.

Arachidonic acid can bind to E-cat and E-allo, but the affinity of AA for E-allo is 25 times that for Ecat. Palmitic acid, an efficacious stimulator of huPGHS-2, binds only E-allo in palmitic acid/murine PGHS-2 co-crystals. Non-substrate FAs can potentiate or attenuate PTGS (COX) inhibitors depending on the fatty acid and whether the inhibitor binds E-cat or E-allo. Studies suggest that the concentration and composition of the free fatty acid pool in the environment in which PGHS-2 functions in cells, also referred to as the FA tone, is a key factor regulating the activity of PGHS-2 and its response to PTGS (COX) inhibitors.

Bogen graduated with a medical degree from the University of Oslo in 1977. In the following two years, he completed his internship at Sandnessjøen hospital and in the municipalities of Lurøy and Træna at the coastline of northern Norway.University of Oslo: Bjarne Bogen In 1984, at the University of Tromsø he defended his PhD thesis entitled "Murine Th and B Lymphocyte Recognition of Isologous Immunoglobulin". Since 1986, Bogen has been working at the Institute for Clinical Medicine at the University of Oslo, first as an associate professor before becoming full professor in 1993. In 1991, he was authorized as a specialist in clinical immunology, and has since 1995 had a part-time position as a senior consultant at the Oslo University Hospital.

In the 1950s, an Italian research company, Farmitalia Research Laboratories, began an organized effort to isolate anticancer compounds from soil-based microbes. A soil sample was isolated from the area surrounding the Castel del Monte, a 13th-century castle in Apulia. A new strain of Streptomyces peucetius which produced a red pigment was isolated, and an antibiotic was produced from this bacterium that was found to have good activity against murine tumors. Since a group of French researchers discovered the same compound at about the same time, the two teams named the compound daunorubicin, combining the name Dauni, a pre-Roman tribe that occupied the area of Italy where the compound was isolated, with the French word for ruby, rubis, describing the color.

Generating arrays of engineered Cys2His2 zinc fingers is the most developed method for creating proteins capable of targeting desired genomic DNA sequences. The majority of engineered zinc finger arrays are based on the zinc finger domain of the murine transcription factor Zif268, although some groups have used zinc finger arrays based on the human transcription factor SP1. Zif268 has three individual zinc finger motifs that collectively bind a 9 bp sequence with high affinity. The structure of this protein bound to DNA was solved in 1991 and stimulated a great deal of research into engineered zinc finger arrays. In 1994 and 1995, a number of groups used phage display to alter the specificity of a single zinc finger of Zif268.

KCTD7 expression hyperpolarizes the cell membrane and reduces the excitability of transfected neurons in patch clamp experiments. KCTD7 mRNA and protein are expressed in hippocampal neurons, deep layers of the cerebral cortex and Purkinje cells of the murine brain as shown by in situ hybridization and immunohistochemistry experiments. Immunoprecipitation assays demonstrates that KCTD7 is able to prudhommerie and directly interacts with cullin-3 (CUL3), a component of the ubiquitin ligase complex. These interactions are thought to be mediated via the BTB/POZ domain of KCTD7. However, KCTD7 does not show any interaction cullin-1 (CUL1). Immunoprecipitation assays also shows that KCTD7 does not interact with Ubiquitin-flag, suggesting a potential role of KCTD7 in the ubiquitin ligase complex without being itself subject to uiquitination.

Anticancer activities of cecropin B, cecropin P1, and Shiva-1 were first demonstrated with in vitro studies of mammalian leukemia and lymphoma cell lines, where cells were sensitive to peptide concentrations on the order of 10−6 M. Two multidrug- resistant breast and ovarian cancer cell lines also showed sensitivity to the peptides. Further, peptide anticancer activity is reported as being complete within one hour of treatment. In vivo studies of murine ascitic colon adenocarcinoma cells showed a similar trend, where mice treated with cecropin B exhibited increased survival time compared to untreated mice. Structural studies of cecropin B and its derivative cecropin B3 showed that anticancer activity arises from the ability of the antimicrobial peptides to form pores in stomach carcinoma cell membranes.

June 2016 In 2019, CytoDyn initiated a Phase 1b/2 trial with its humanized monoclonal antibody, leronlimab (PRO 140), in combination with chemotherapy following strong results in animal murine models. Among other mechanisms of action, leronlimab is believed to inhibit metastasis by inhibiting the CCR5 receptor on cell surfaces, which is commonly expressed in triple-negative breast cancer. On November 11, 2019, CytoDyn reported that the first TNBC patient injected under its naïve protocol (not previously treated for triple-negative breast cancer) demonstrated significantly reduced levels of circulating tumor cells (CTCs) and decreased tumor size at two-week and five-week observation intervals compared to baseline observations. CTCs are a potential surrogate endpoint in oncology trials, with reduced levels suggesting long-term clinical benefit.

Template-switching polymerase chain reaction (TS-PCR) is a method of reverse transcription and polymerase chain reaction (PCR) amplification that relies on a natural PCR primer sequence at the polyadenylation site, also known as the poly(A) tail, and adds a second primer through the activity of murine leukemia virus reverse transcriptase. This permits reading full cDNA sequences and can deliver high yield from single sources, even single cells that contain 10 to 30 picograms of mRNA, with relatively low levels (3-5%) of contaminating rRNA sequence. This technique is often employed in whole transcriptome shotgun sequencing. It is marketed by Clontech as Switching Mechanism At the 5' end of RNA Template (SMART) as well as by Diagenode as Capture and Amplification by Tailing and Switching (CATS).

Proteins of the matrix metalloproteinase (MMP) family are involved in the breakdown of extracellular matrix in normal physiological processes, such as embryonic development, reproduction, and tissue remodeling, as well as in disease processes, such as arthritis and metastasis. The primary function of MMP-8 is the degradation of type I, II and III collagens. In cancer, loss of MMP-8 in the murine MMTV-PyMT breast cancer model has been associated with increased tumor growth and metastatic burden, as well as enhanced tumor vascularity and altered immune cell infiltration. Furthermore, analysis of MMP-8 in breast cancer cell lines revealed a causal connection between MMP-8 activity and IL6 and IL8 production, suggesting a role for MMP-8 in the regulation of the innate immune system.

To perform this work, she created the single-letter amino acid code to minimize the data file size for each sequence. This work, co-authored with Richard Eck, was the first application of computers to infer phylogenies from molecular sequences. It was the first reconstruction of a phylogeny (evolutionary tree) by computers from molecular sequences using a maximum parsimony method. In later years, she applied these methods to study a number of molecular relationships, such as the catalytic chain and bovine cyclic AMP-dependent protein kinase and the src gene product of Rous avian and Moloney murine sarcoma viruses; antithrombin-III, alpha-antitrypsin, and ovalbumin; epidermal growth factor and the light chain of coagulation factor X; and apolipoproteins A-I, A-II, C-I and C-III.

As a result, imidazole engineering has been suggested as a means to specifically inhibit NO dioxygenases. In addition, genetically modified plants with heterologous flavohemoglobin-NODs are being developed to limit NO toxicity created by metabolism of nitrogen fertilizers by soil microbes and as a means towards plant self-fertilization through absorption of environmental NO. Recently a lentiviral vector that allows for expression of E. coli flavoHb in mammalian cells has been described. This approach demonstrated that flavoHb is indeed enzymatically active within human and murine cells and potently blocks exogenous and endogenous sources of nitrosative stress. This technology was then extended to interrogate the role of NO synthesis in the highly tumorigenic cancer stem cells (CSCs) from human glioblastoma (brain tumor) samples.

The AHR seems to play important roles in normal embryonic development and a reversible repression of the receptor is essential for the maintenance of the pluripotency of embryonic stem cells (ESC). It has been shown that expansion of early progenitor murine hematopoietic stem cells is promoted by down-regulation of AHR signaling through the RNA-binding protein Musashi-2 and 250 nM FICZ reversed this effect.Furthermore, expansion of human induced pluripotent stem cells was enhanced by the AHR inhibitor CH223191 and blocked by FICZ.In contrast, by applying a novel, pluripotent stem-cell based in vitro culture system Smith et al. demonstrated that the potent AhR ligand FICZ resulted in an exponential expansion (600-fold increase) of induced pluripotent stem cells (iPSC)-derived hematopoietic progenitor cell (HP) populations.

In the late 1980s gene targeting in murine embryonic stem cells (ESCs) enabled the transmission of mutations into the mouse germ line, and emerged as a novel option to study the genetic basis of regulatory networks as they exist in the genome. Still, classical gene targeting proved to be limited in several ways as gene functions became irreversibly destroyed by the marker gene that had to be introduced for selecting recombinant ESCs. These early steps led to animals in which the mutation was present in all cells of the body from the beginning leading to complex phenotypes and/or early lethality. There was a clear need for methods to restrict these mutations to specific points in development and specific cell types.

Numerous putative chimeric transcripts have been identified among the expressed sequence tags using high throughput RNA sequencing technology. In humans, chimeric transcripts can be generated in several ways such as trans-splicing of pre- mRNAs, RNA transcription runoff, from other errors in RNA transcription or they can also be the result of gene fusion following inter-chromosomal translocations or rearrangements. Among the few corresponding protein products that have been characterized so far, most result from chromosomal translocations and are associated with cancer. For instance, gene fusion in chronic myelogenous leukemia (CML) leads to an mRNA transcript that encompasses the 5′ end of the breakpoint cluster region protein (BCR) gene and the 3′ end of the Abelson murine leukemia viral oncogene homolog 1 (ABL) gene.

Murine polyomavirus (also known as mouse polyomavirus, Polyomavirus muris, or Mus musculus polyomavirus 1, and in older literature as SE polyoma or parotid tumor virus; abbreviated MPyV) is an unenveloped double-stranded DNA virus of the polyomavirus family. The first member of the family discovered, it was originally identified by accident in the 1950s. A component of mouse leukemia extract capable of causing tumors, particularly in the parotid gland, in newborn mice was reported by Ludwik Gross in 1953 and identified as a virus by Sarah Stewart and Bernice Eddy at the National Cancer Institute, after whom it was once called "SE polyoma". Stewart and Eddy would go on to study related polyomaviruses such as SV40 that infect primates, including humans.

MPyV contains three proteins extensively studied for their ability to induce neoplastic transformation (that is, carcinogenesis); these proteins are expressed from the early region of the viral genome and are known as large, middle, and small tumor antigen. Murine polyomavirus and its close relative hamster polyomavirus are historically the only two known viruses whose genomes contain middle tumor antigen, by far the most efficient of the three early proteins at inducing carcinogenesis. In 2015 the genome sequence of a rat polyomavirus was reported to contain middle tumor antigen as well, consistent with expectations that it evolved uniquely in the rodent lineage of the polyomavirus family. Expression of MT from a transgene or introduction in cell culture can be sufficient to induce transformation.

In 1998, a murine model of pancreatic cancer was used to study the effect of implanting genetically modified cytochrome P450 expressing feline epithelial cells encapsulated in cellulose sulfate polymers for the treatment of solid tumors. The approach demonstrated for the first time the application of enzyme expressing cells to activate chemotherapeutic agents. On the basis of these results, an encapsulated cell therapy product, NovaCaps, was tested in a phaseI/II clinical trial for the treatment of pancreatic cancer in patients and has recently been designated by the European medicines agency (EMEA) as an orphan drug in Europe. A further phase I/II clinical trial using the same product confirmed the results of the first trial, demonstrating an approximate doubling of survival time in patients with stage IV pancreatic cancer.

The various transcription variants are based on a different usage of the exons that are encoding for CSNK1D. The whole gene consists of eleven different exons and is located in humans on chromosome 17 at position 17q25.3. CSNK1D has a length of 35kb and is overlapping with the gene Slc16a3. The intersecting part is exon 11, which is located downstream of exon 10. However, it does not interfere with Slc16a3 since it is located in a non-coding area. TV1 and TV2 were postulated during an early analysis of human and murine genes in 2002. Both transcription variants share the first 399 amino acids, but differ at the following 16 amino acids for TV1 and ten amino acids for TV2, respectively. This is linked to the exon usage.

Bilastine binds to guinea-pig cerebellar histamine H1-receptors (Ki=44 nM) and to human recombinant histamine H1-receptors (Ki=64 nM) with an affinity comparable to that of astemizole and diphenhydramine, and superior than that of cetirizine by three- fold and fexofenadine by five-fold (Corcóstegui). In different murine models, bilastine by oral route, antagonizes the effects of histamine in a dose- dependent manner, with potency similar to that of cetirizine and between 5.5 and 10 times greater than that of fexofenadine. Preclinical investigations demonstrate the affinity and specificity of bilastine for histamine H1-receptors compared with other histamine receptors subtypes and other 30 receptors from different amines. In vivo experimentation confirmed the antihistaminic and antiallergic activity, which was at least comparable to that of other second-generation H1-antihistamines such as cetirizine.

A map of the murine polyomavirus genome, indicating the early genes (LTag, MTag, and STag) at right in blue and the late genes (the viral capsid proteins) at left in red. Each region is transcribed as a single messenger RNA and alternatively spliced to express multiple proteins; the exons are shown as thickened lines. The genes for the small tumor antigen (STag), middle tumor antigen (MTag), and large tumor antigen (LTag) are encoded in the "early region" of the polyomavirus genome, so named because this region of the genome is expressed early in the infectious process. (The "late region" contains genes encoding the viral capsid proteins.) In MTag- containing polyomaviruses, the early region contains at least three genes encoding STag, MTag, and LTag, and is transcribed as a single messenger RNA processed by alternative splicing.

Different cecropins act on different types of human cancer cells and show activity at concentrations that are not harmful to normal cells. For example, a recent study of Cecropins A and B demonstrated strongly cytotoxic activity against four bladder cancer cell lines, while benign murine and human fibroblasts were not susceptible to Cecropin A or B. Cecropins from many insect species have been shown to be active against a diverse range of human cancer cell lines. For example, Mdcec, a cecropin originating from the common housefly, has been shown to have an antiproliferative effect on human hepatocellular carcinoma cell line BEL-7402 without affecting normal liver cells. Flow cytometry and RT-PCR experiments revealed that treatment with Mdcec increased expression of pro-apoptotic genes such as caspase-3, leading to cancer cell death.

MyoD was cloned by a functional assay for muscle formation reported in Cell in 1987 by Davis, Weintraub, and Lassar. It was first described as a nuclear phosphoprotein in 1988 by Tapscott, Davis, Thayer, Cheng, Weintraub, and Lassar in Science. The researchers expressed the complementary DNA (cDNA) of the murine MyoD protein in a different cell lines (fibroblast and adipoblast) and found MyoD converted them to myogenic cells. The following year, the same research team performed several tests to determine both the structure and function of the protein, confirming their initial proposal that the active site of the protein consisted of the helix loop helix (now referred to as basic helix loop helix) for dimerization and a basic site upstream of this bHLH region facilitated DNA binding only once it became a protein dimer.

The untimely cancer death of a family friend led him to switch to medicine, completing his MD and internship in 1969. During his medical training he was greatly influenced by Dr. Ross Langley, a research-oriented hematologist who suggested that Eaves do a PhD at the Princess Margaret Hospital in Toronto where Dr. Robert Bruce was collaborating with Drs. James Till and Ernest McCulloch (Lasker Award) on how different types of cancer chemotherapeutic agents killed tumour stem cells while sparing normal stem cells. Working under the supervision of Bruce (AACR Award), and in association with Till and McCulloch and a vibrant group of graduate students and post-doctoral fellows, Eaves completed his PhD in Medical Biophysics at the University of Toronto with a thesis entitled Studies on the Control of Murine Bone Marrow Function (1974).

Human and murine PTX3, localized in the syntenic region of chromosome 3 (q24-28), are highly conserved, sharing 82% identical and 92% conserved amino acids. The human PTX3 gene is organized into three exons coding for the leader peptide (which is cleaved from the mature protein), the amino-terminal domain and the pentraxin domain of the protein. The transcribed PTX3 protein is 381 amino acids long, has a predicted molecular weight of 40,165 Da and consists of a carboxy-terminal 203 amino acid long pentraxin domain coupled with an amino-terminal 178 amino acid long domain unrelated to other known proteins. The PTX3 carboxy-terminal domain contains a canonical pentraxin signature (HxCxS/TWxS) and two conserved cysteines (Cys-210 and Cys-271), and shares 57% conserved and 17% identical amino acids with short pentraxins.

EVI1 is a proto-oncogene conserved across humans, mice, and rats, sharing 91% homology in nucleotide sequence and 94% homology in amino acid sequence between humans and mice. It is a transcription factor localized to the nucleus and binds DNA through specific conserved sequences of GACAAGATA with the potential to interact with both corepressors and coactivators. ;Embryogenesis: The role of EVI1 in embryogenesis and development is not completely understood, but it has been shown that EVI1 deficiency in mice is an embryonic lethal mutation, characterized primarily by widespread hypocellularity and poor/disrupted development of the cardiovascular and neural system. EVI1 is highly expressed in the murine embryo, found in the urinary system, lungs, and heart, but is only minutely detectable in most adult tissues, indicating a likely role in tissue development.

Drevs has conducted research on the topic of angiogenesis, and was present during the making of a new group of medications for the treatment of tumor patients called Molecular Targeted Therapy. He has also carried out research projects with James F. Holland, Gerd Nagel, and Hubert Blum.Effects of PTK787/ZK 222584, a Specific Inhibitor of Vascular Endothelial Growth Factor Receptor Tyrosine Kinases, on Primary Tumor, Metastasis, Vessel Density, and Blood Flow in a Murine Renal Cell Carcinoma Model. Joachim Drevs, Inga Hofmann, Harald Hugenschmidt, Christine Wittig, Helmut Madjar, Marianne Müller, Jeanette Wood, Georg Martiny-Baron, Clemens Unger and Dieter Marmé. Cancer Res September 1 2000 (60) (17) 4819-4824;Phase I Clinical Study of AZD2171, an Oral Vascular Endothelial Growth Factor Signaling Inhibitor, in Patients With Advanced Solid Tumors.

This variation is larger than would be expected on the basis of a Poisson distribution of numbers of metastases per mouse in each clone and when the variance of the number of metastases per mouse was plotted against the corresponding mean a power law was found. The variance-to-mean power law for metastases was found to also hold for spontaneous murine metastases and for cases series of human metastases. Since hematogenous metastasis occurs in direct relationship to regional blood flow and videomicroscopic studies indicate that the passage and entrapment of cancer cells within the circulation appears analogous to the microsphere experiments it seemed plausible to propose that the variation in numbers of hematogenous metastases could reflect heterogeneity in regional organ blood flow. The blood flow model was based on the Tweedie compound Poisson–gamma distribution, a distribution governing a continuous random variable.

Ongoing research projects currently funded by ME Research UK include a Swedish study to provide an independent investigation into the link between xenotropic murine leukemia virus-related virus (XMRV) and ME/CFS, an investigation into autonomic dysfunction (dysautonomia) in ME/CFS, research to identify key single-nucleotide polymorphisms associated with ME/CFS, and a study of the relationship between vitamin D status and cardiovascular function in ME/CFS. In addition to funding research into biomedical aspects of ME/CFS, the charity produces reviews and reports, organises and presents research at professional meetings and conferences, and was instrumental in forming a cross party group on the condition at the Scottish Parliament. Most of its funds come from private and corporate donations, and the Friends of ME Research UK Friends scheme has been set up to support the charity and help with fundraising.

While SSADH deficiency has been studied for nearly 30 years, knowledge of the disorder and its pathophysiology remains unclear. However, the progress that has been made with both murine and human models of the disorder have provided a lot of insights into how the disease manifests itself and what more can be done in terms of therapeutic interventions. Much of the current research into SSADH has been led by a dedicated team of physicians and scientists, including Phillip L. Pearl, MD of the Boston Children's Hospital at Harvard Medical School and K. Michael Gibson, PhD of Washington State University College of Pharmacy. Both have contributed significant efforts to finding appropriate therapies for SSADH deficiency and have specifically spent most of their recent efforts into understanding the efficacy of the ketogenic diet for patients with SSADH deficiency.

ALL and CML therapies have targeted JAK2 as well as BCR-ABL using nilotinib and ruxolitinib within murine models to downregulate downstream cytokine signaling by silencing STAT3 and STAT5 transcription activation (appelmann et al). The interaction between JAK2 and BCR-ABL within these hematopoietic malignancies implies an important role of JAK-STAT-mediated cytokine signaling in promoting the growth of leukemic cells exhibiting the Ph chromosome and BCR-ABL tyrosine kinase activity. Though the centrality of the JAK2 pathway to direct proliferation in CML has been debated, its role as a downstream effector of the BCR-ABL tyrosine kinase has been maintained. Impacts on the cell cycle via JAK-STAT are largely peripheral, but by directly impacting the maintenance of the hematopoietic niche and its surrounding microenvironment, the BCR-ABL upregulation of JAK-STAT signaling plays an important role in maintaining leukemic cell growth and division.

Daley's research seeks to translate insights in stem cell biology into improved therapies for genetic and malignant diseases. His laboratory has pioneered human cell culture-based and murine models of human blood disease and cancer.Biography, Stem Cell Program Leadership, Children's Hospital Boston Retrieved 2010-08-30. Important research contributions from his laboratory include the creation of customized stem cells to treat genetic immune deficiency in a mouse model (together with Rudolf Jaenisch),RIDEOUT ET AL, CELL 2002 the differentiation of germ cells from embryonic stem cells (cited as a "Top Ten Breakthrough" by Science in 2003),Biography, 2004 Recipients, NIH Director's Pioneer Award Retrieved 2010-08-30.GEIJSEN ET AL., NATURE 2003/4 the generation of disease-specific pluripotent stem cells by direct reprogramming of human fibroblasts (cited in the "Breakthrough of the Year" issue of Science magazine in 2008),Bios, Team, MPM Capital Retrieved 2010-08-30.

Dr. Andrew Lazarovits, a postdoctoral fellow in the laboratory, discovered the murine homologue of MLN0002, chiefly published the original key papers, and up until the late 1990s, coordinated and led the studies for its development and application for Crohn's disease and ulcerative colitis. Dr. Lynn Baird's group showed the antibody reacted with a single protein band of 63Kd, and Dr. Atul Bhan's group showed that it stained tissue lymphocytes but did not react with non-lymphoid tissues. Although Act-1 had limited efficacy in its ability to prevent kidney rejection in a sub-human primate transplantation model, Dr. Lazarovits continued to investigate the activities of Act-1 when he returned to Canada to become the Director of Transplantation at the University of Western Ontario. It was later determined that the Act-1 monoclonal antibody reacted with an α4β7 integrin that was subsequently shown to interact with a gut-associated addressin, MadCAM.

In 1989 a virally encoded portion of the chromosomal mouse Cbl gene was the first member of the Cbl family to be discovered and was named v-Cbl to distinguish it from normal mouse c-Cbl. The virus used in the experiment was a mouse-tropic strain of Murine leukemia virus isolated from the brain of a mouse captured at Lake Casitas, California known as Cas-Br-M, and was found to have excised approximately a third of the original c-Cbl gene from a mouse into which it was injected. Sequencing revealed that the portion carried by the retrovirus encoded a tyrosine kinase binding domain, and that this was the oncogenic form as retroviruses carrying full-length c-Cbl did not induce tumor formation. The resultant transformed retrovirus was found to consistently induce a type of pre-B lymphoma, known as Casitas B-lineage lymphoma, in infected mice.

Having already received approval for Zolgensma in May 2019, on June 28 AveXis (a Novartis company) voluntarily disclosed to the FDA that some data previously submitted to the agency as part of the Biologics License Application (BLA) package was inaccurate. Specifically, the data manipulation related to an in vivo murine potency assay used in the early development of the product but the issue the FDA and wider community has taken is that AveXis was aware of the data manipulation as early as 14 March 2019, almost two months before the BLA was approved. To compound the problem in early August it emerged a senior manager sold almost $1 million worth of stock immediately before the FDA probe became public on August 6, but after the company had informed the FDA of the problem. As of September 2019 the FDA was still preparing its response to the scandal.

S100A1 has shown efficacy in feasibility in treating heart failure symptoms in large, preclinical models and human cardiomyocytes, and thus shows great promise for clinical trials. Reduced expression of this protein has been implicated in cardiomyopathies, and left ventricular assist device-based therapy does not restore S100A1 levels in patients. S100A1 has shown promise as an early diagnostic biomarker for acute myocardial ischemia, presenting with a distinct timecourse in human plasma following an ischemic event relative to traditional markers creatine kinase, CKMB and troponin I. This injury-released, extracellular pool of S100A1 was investigated in neonatal murine cardiomyocytes and was shown to prevent apoptosis via an ERK1/2-dependent pathway, suggesting that the release of S100A1 from injured cells is an intrinsic survival mechanism for viable myocardium. S100 has also shown promise as a biomarker for uncontrolled hyperoxic reoxygenation during cardiopulmonary bypass in infants with cyanotic heart disease and in adults.

The two platforms currently available for this purpose come from corporate and academic sources. Affymetrix's Hu/Mu ProtIn Microarray uses 516 and 456 probe sets to evaluate human and murine proteases, inhibitors, and interactors respectively.Schwartz D.R., Moin K., Yao B., Matrisian L.M., Coussens L.M., Bugge T.H., Fingleton B., Acuff H.B., Sinnamon M., Nassar H., Platts A.E., Krawetz S.A., Linebaugh B.E., Sloane B.F. Hu/Mu ProtIn oligonucleotide microarray: dual-species array for profiling protease and protease inhibitor gene expression in tumors and their microenvironment. Mol. Cancer Res., 5 (5) 443–454 (2007).Acuff H.B., Sinnamon M., Fingleton B., Boone B., Levy S.E., Chen X., Pozzi A., Carbone D.P., Schwartz D.R., Moin K., Sloane B.F., Matrisian L.M. Analysis of host- and tumor-derived proteinases using a custom dual species microarray reveals a protective role for stromal matrix metalloproteinase-12 in non-small cell lung cancer Cancer Res.

ALC-2 expression has proven to be a useful marker of cardiac muscle chamber distinction, development and differentiation. ALC-2 shows a pattern distinct from atrial essential light chain (ALC-1) during cardiogenesis. ALC-2 expression in adult murine hearts is cardiac-specific throughout embryonic days 8-16, and from day 12 and on is restricted to atria, showing very low levels in aorta and undetectable in ventricles, skeletal muscle, uterus, and liver. This atrial patterning occurs prior to septation. Expression of ALC-2 has been shown to correlate with expression of alpha-myosin heavy chain in cardiac atria of non-human primates. ALC-2 and VLC-2 appear to function in the stabilization of thick filaments and regulation of contractility in the vertebrate heart. Functional insights into ALC-2 function have come from studies employing transgenesis. A study in which the ventricular isoform of regulatory light chain was overexpressed to replace the ALC-2 in cardiac atria was performed.

HS enzymatic specificity of QSulf1 was first analyzed. QSulf1 enzymatic specificity on 6-O sulfates was linked to the trisulfated disaccharides (HexA,2SGlcNS,6S) in S domains of HS (HS regions where most of the GlcNS residues are in contiguous sequences) and not NA/NS domains (regions of alternating N-acetylated and N-sulfated units; transition zones). Sulf1 and 2 null murine embryonic fibroblasts were generated to test the HS specificity of mammalian Sulf as opposed to avian Sulf (QSulf). Investigators found mSulf1−/−;mSulf2−/− HS showed overall large increases in all 6S disaccharides. Cooperativity between mSulf1/2 was found because a 2-fold increase in S-domain-associated disaccharides (UA–GlcNS(6S) and UA(2S)–GlcNS(6S)) was observed in double knock-out HS as compared with either single knock-out HS alone. However, one difference from mSulf1 is that mSulf2−/− HS shows an increase in 6S almost exclusively within the non- sulfated and transition zones.

Changing sea levels during the Plio- Pleistocene likely affected the migration of the Murinae throughout the Indo- Pacific archipelagos because areas which are now submerged would at certain times have been exposed. The current distribution pattern of the Murinae may reflect the Rattini's role as the most recently successful clade within the Southeast Asian region; they diversified greatly since the late Miocene, possibly displacing older murine lineages from the Indo-Pacific. The rat has a long face, spiky brownish grey fur on its back and a greyish white belly with scattered bristly and spiny hairs, and a tail shorter than the head-body length with a white tip. Other characteristics that when put together set H. bokimekot apart from other members of the family Muridae include: a medium sized body, moderately long muzzle with dark brown/greyish ears, white digits and dorsal surfaces of carpel and metacarpal regions, three pairs of teats (two inguinal and one post auxiliary), and at least three young per litter.

An additional advantage is the fact, that simple rules can be applied to generate heterospecific FRT sites which undergo crossovers with equal partners but nor with wild type FRTs. These facts have enabled, since 1994, the development and continuous refinements of recombinase-mediated cassette exchange (RMCE-)strategies permitting the clean exchange of a target cassette for an incoming donor cassette. Based on the RMCE technology, a particular resource of pre-characterized ES-strains that lends itself to further elaboration has evolved in the framework of the EUCOMM (European Conditional Mouse Mutagenesis) program, based on the now established Cre- and/or Flp-based "FlExing" (Flp-mediated excision/inversion) setups, involving the excision and inversion activities. Initiated in 2005, this project focused first on saturation mutagenesis to enable complete functional annotation of the mouse genome (coordinated by the International Knockout-Mouse Consortium, IKMC) with the ultimate goal to have all protein genes mutated via gene trapping and -targeting in murine ES cells.

Halichondrin B is a large naturally occurring polyether macrolide originally isolated from the marine sponge Halichondria okadai by Hirata and Uemura in 1986. In the same report, these authors also reported the exquisite anticancer activity of halichondrin B against murine cancer cells both in culture and in in vivo studies. Halichondrin B was highly prioritized for development as a novel anticancer therapeutic by the United States National Cancer Institute and, in 1991, was the original test case for identification of mechanism of action (in this case, tubulin-targeted mitotic inhibitor) by NCI's then-brand- new "60-cell line screen" The complete chemical synthesis of halichondrin B was achieved by Yoshito Kishi and colleagues at Harvard University in 1992, an achievement that ultimately enabled the discovery and development of the structurally simplified and pharmaceutically optimized analog eribulin (E7389, ER-086526, NSC-707389). Eribulin was approved by the U.S. Food and Drug Administration on November 15, 2010, to treat patients with metastatic breast cancer who have received at least two prior chemotherapy regimens for late- stage disease, including both anthracycline- and taxane-based chemotherapies.

Jade1 expression was detected in extraembryonic ectoderm and trophoblast, which are placental components important for vasculogenesis, as well as in sites enriched with multipotent or tissue-specific progenitors, including neural progenitors(2). The dynamics of Jade1 reporter expression in these areas indicates the involvement in the determination and elongation of anterior posterior axis, an important point of the study). The potential role for human JADE1 in the renewal of embryonic stem cell and embryonal carcinoma cell cultures was suggested in another screening study which showed that, in cultured stem cells activation of stem cell transcription factor OCT4 pathway upregulated JADE1 gene expression along with stem cell factors NANOG, PHC1, USP44 and SOX2. Role of JADE1 in epithelial cell proliferation was addressed in a murine model of acute kidney injury and regeneration. Expression patterns and dynamics of HBO1-JADE1S/L were examined in regenerating tubular epithelial cells. Ischemia and reperfusion injury resulted in an initial decrease in JADE1S, JADE1L, and HBO1 protein levels, which returned to the baseline during renal recovery.

The murine Fat1 knockout mouse is not embryonically lethal but pups die within 48-hours due to the abnormal fusion of foot processes of the podocytes within the kidney. These Fat1 knockout mice also showed partially penetrant but often severe midline defects including holoprosencephaly, microphthalmia-anophthalmia and in rare cases cyclopia. It has been shown that the EVH motifs in the cytoplasmic tail of mouse Fat1 interact with Ena/VASP and ablation of Fat1 by RNAi leads to decreased cell migration of rat epithelial cells The cytoplasmic tail of Fat1 has also been shown to bind the transcriptional repressor Atrophin in rat vascular smooth muscle cells At the carboxyl terminus of FAT1 lies a PDZ domain (PSD95/Dlg1/ZO-1) ligand motif (-HTEV). Zebrafish Fat1 was found to bind the protein scribble and regulate Hippo signalling Using the human SHSY5Y cell line as a model of neuronal differentiation, human FAT1 was shown to regulate Hippo kinase components with loss of FAT1 leading to nucleocytoplasmic relocation of TAZ and enhanced transcription of the Hippo target gene CTGF.

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a chronic condition characterized by extreme fatigue after exertion that is not relieved by rest and includes other symptoms, such as muscle and joint pain and cognitive dysfunction. In September 2017, the NIH awarded a $9.6 million grant to Columbia University for the "CfS for ME/CFS" intended for the pursuit of basic research and the development of tools to help both physicians and patients effectively monitor the course of the illness. This collaboration effort led by Lipkin includes other institutions, such as the Bateman Horne Center (Lucinda Bateman), Harvard University (Anthony L. Komaroff), Stanford University (Kegan Moneghetti), Sierra Internal Medicine (Daniel Peterson), University of California, Davis (Oliver Fiehn), and Albert Einstein College of Medicine (John Greally), along with private clinicians in New York City. The team of researchers and clinicians initially collaborated to de-link xenotropic murine leukemia virus-related virus (XMRV) to ME/CFS after the NIH requested research into the conflicting reports between XMRV and ME/CFS.

MTA1 modulates the expression of target genes due to its ability to act as a corepressor or coactivator. MTA1 targets and/or effector pathways regulate pathways with cellular functions in both normal and cancer cells. Physiological functions of MTA1 include: its role in the brain due to MTA1 interactions with DJ1 and endophilin-3; regulation of Rhodopsin expression in the murine eye; modifier of circadian rhythm due to MTA1 interactions with the CLOCK-BMAL1 complex and stimulation of Cry-transcription; in heart development due to MTA1-FOG2 interaction; in mammary gland development as MTA1 depletion leads to ductal hypobranching, in spermatogenesis; in immunomodulation due to differential effects on the expression of cytokines in the resting and activated macrophage; in liver regeneration following hepatic injury; differentiation of mesenchymal stem cells into osteogenic axis; and a component of DNA-damage response. In cancer cells, MTA1 and its downstream effectors regulate genes and/or pathways with roles in transformation, invasion, survival, angiogenesis, epithelial-to-mesenchymal transition, metastasis, DNA damage response, and hormone-independence of breast cancer.

Chronic low-grade inflammation (CLGI) plays a key role in metabolic deterioration in the obese population. Jak3 expression and activation provide protection against development of CLGI and associated health complications. Studies in rodent model show that loss of Jak3 results in increased body weight, basal systemic CLGI, compromised glycemic homeostasis, hyperinsulinemia, and early symptoms of liver steatosis. Lack of Jak3 also results in exaggerated symptoms of metabolic syndrome by western high-fat diet. Mechanistically, it is shown that Jak3 is essential for reduced expression and activation of toll like receptors (TLRs) in murine intestinal mucosa and human intestinal epithelial cells where Jak3 interacted with and activated p85, the regulatory sub-unit of the PI3K, through tyrosine phosphorylation of adapter protein insulin receptor substrate (IRS1). These interactions resulted in activation of PI3K-Akt axis, which was essential for reduced TLR expression and TLR associated NF-κB activation. Overall, Jak3 plays an essential role in promoting mucosal tolerance through suppressed expression and limiting activation of TLRs thereby preventing intestinal and systemic CLGI and associated obesity and MetS.

Researchers are beginning to attribute the reason that only 5% of anti-cancer agents are approved by the Food and Drug Administration after pre-clinical testing to the lack of tumor heterogeneity and the absence of the human stromal microenvironment. Specifically, cell line-xenografts often are not predictive of the drug response in the primary tumors because cell lines do not follow pathways of drug resistance or the effects of the microenvironment on drug response found in human primary tumors. Many PDX models have been successfully established for breast, prostate, colorectal, lung, and many other cancers because there are distinctive advantages when using PDX over cell lines for drug safety and efficacy studies as well as predicting patient tumor response to certain anti-cancer agents. Since PDX can be passaged without in vitro processing steps, PDX models allow the propagation and expansion of patient tumors without significant genetic transformation of tumor cells over multiple murine generations. Within PDX models, patient tumor samples grow in physiologically-relevant tumor microenvironments that mimic the oxygen, nutrient, and hormone levels that are found in the patient’s primary tumor site.

The cDNAs encoding rat, human, murine, bovine, dog and two Schistosome cathepsin Cs have been cloned and sequenced and show that the enzyme is highly conserved. The human and rat cathepsin C cDNAs encode precursors (prepro-cathepsin C) comprising signal peptides of 24 residues, pro-regions of 205 (rat cathepsin C) or 206 (human cathepsin C) residues and catalytic domains of 233 residues which contain the catalytic residues and are 30-40% identical to the mature amino acid sequences of papain and a number of other cathepsins including cathepsins, B, H, K, L, and S. The translated prepro-cathepsin C is processed into the mature form by at least four cleavages of the polypeptide chain. The signal peptide is removed during translocation or secretion of the pro-enzyme (pro-cathepsin C) and a large N-terminal proregion fragment (also known as the exclusion domain), which is retained in the mature enzyme, is separated from the catalytic domain by excision of a minor C-terminal part of the pro-region, called the activation peptide. A heavy chain of about 164 residues and a light chain of about 69 residues are generated by cleavage of the catalytic domain.

Here, however, the eventual result is organ damage and often profound or even fatal disease, not resolution of the infection. An emerging concept is that IL-13 may antagonize Th1 responses that are required to resolve intracellular infections. In this immune dysregulated context, marked by the recruitment of aberrantly large numbers of Th2 cells, IL-13 inhibits the ability of host immune cells to destroy intracellular pathogens. IL-13 expression has demonstrated to be increased in bronchoalveolar lavage (BAL) fluid and cells in patients with atopic mild asthma after allergen challenge. Genome-wide association studies have identified multiple polymorphisms of IL-13 and genes encoding the IL-13 receptors as associated with asthma susceptibility, bronchial hyperresponsiveness, and increased IgE levels. The overexpression of IL-13 induces many features of allergic lung disease, including airway hyperresponsiveness, goblet cell metaplasia, mucus hypersecretion and airway remodelling which all contribute to airway obstruction. murine studies demonstrated that IL-13 was both necessary and sufficient to generate asthma-like Th2 responses in the mouse lung. IL-13 is mainly overexpressed in sputum, bronchial submucosa, peripheral blood and mast cells in the airway smooth muscle bundle.

Targeted deletion of Dicer in the FoxD1-derived renal progenitor cells in a murine model resulted in a complex renal phenotype including expansion of nephron progenitors, fewer renin cells, smooth muscle arterioles, progressive mesangial loss and glomerular aneurysms. High throughput whole transcriptome profiling of the FoxD1-Dicer knockout mouse model revealed ectopic upregulation of pro-apoptotic gene, Bcl2L11 (Bim) and dysregulation of the p53 pathway with increase in p53 effector genes including Bax, Trp53inp1, Jun, Cdkn1a, Mmp2, and Arid3a. p53 protein levels remained unchanged, suggesting that FoxD1 stromal miRNAs directly repress p53-effector genes. Using a lineage tracing approach followed by Fluorescent-activated cell sorting, miRNA profiling of the FoxD1-derived cells not only comprehensively defined the transcriptional landscape of miRNAs that are critical for vascular development, but also identified key miRNAs that are likely to modulate the renal phenotype in its absence. These miRNAs include miRs‐10a, 18a, 19b, 24, 30c, 92a, 106a, 130a, 152, 181a, 214, 222, 302a, 370, and 381 that regulate Bcl2L11 (Bim) and miRs‐15b, 18a, 21, 30c, 92a, 106a, 125b‐5p, 145, 214, 222, 296‐5p and 302a that regulate p53-effector genes.

Coronavirus was accepted as a genus name by ICNV in its first report in 1971. IBV was then officially designated the type species as Avian infectious bronchitis virus (but renamed to Avian coronavirus in 2009). Mouse hepatitis virus approved in 1971 was merged with Rat coronavirus (discovered in 1970) as Murine coronavirus in 2009. 229E and OC43 were collectively named Human respiratory virus but merged as Human coronavirus 229E (HCoV-229E) in 2009. The first discovered human coronavirus B814 was antigenically different from 229E and OC43, but it could not be propagated in culture and was exhausted during experiments in 1968, thus, was excluded in taxonomy. Coroniviridae was adopted as the family name in the ICNV (soon after renamed International Committee on Taxonomy of Viruses, ICTV) second report in 1975. 229E and OC43 were together named Human respiratory virus in the ICNV first report. The species was split into Human coronavirus 229E (HCoV-OC229E) and Human coronavirus OC43 (HCoV-OC43) in 1995. While HCoV-OC229E is retained as a valid species, HCoV-OC43 was merged with Porcine hemagglutinating encephalomyelitis virus (discovered in 1962), Bovine coronavirus (discovered in 1973), Human enteric coronavirus (discovered in 1975), Equine coronavirus (discovered in 2000) and Canine respiratory coronavirus (discovered in 2003) into a single species Betacoronavirus 1 in 2009.