It's almost like Betty completely dissociates from herself in the heat of the moment, calling herself Polly and yelling at Chuck like he's Jason.
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If Trump scandals reach the benchmark of Watergate in the eyes of the public, a Republican who dissociates from Trump will be well positioned to articulate an alternate vision.
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The network brings down the curtain on "Bates Motel," its ambitious prequel to "Psycho," having taken Norman Bates from harmless-seeming youth to killer who dissociates from reality so often it's impossible to tell which personality is the true one.
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After formation of the autophagosome, the ATG12-ATG5:ATG16L complex dissociates from the autophagosome.
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When SAM concentration becomes low, the repressor dissociates from the operator site, allowing more methionine to be produced.
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In this monocation, the chloride spontaneously dissociates from this conjugate base of the starting complex. This pathway is called the Sn1CB mechanism.
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Eventually, CASQ2 completely dissociates from Triadin and the RYR2 channel becomes completely uninhibited, although Triadin remains bound to RYR2 at all luminal concentrations of Ca2+.
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It facilitates the phosphorylation of the R-SMAD, which subsequently dissociates from SARA and the receptor and binds a coSMAD where they enter the nucleus as transcription factors.
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During the period of The Emergency (India) Prabhakaran was part of the outfit Students for Human Rights. At present he is associated with All India Forum Right to Education. The writer dissociates from political affiliations of late.
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Centrosomal protein of 68 kDa is a protein that in humans is encoded by the CEP68 gene. CEP68 is required for centrosome cohesion. It decorates fibres emanating from the proximal ends of centrioles. During mitosis, CEP68 dissociates from centrosomes.
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In response to iron limitation in their environment, genes involved in microbe siderophore production and uptake are derepressed, leading to manufacture of siderophores and the appropriate uptake proteins. In bacteria, Fe2+-dependent repressors bind to DNA upstream to genes involved in siderophore production at high intracellular iron concentrations. At low concentrations, Fe2+ dissociates from the repressor, which in turn dissociates from the DNA, leading to transcription of the genes. In gram-negative and AT- rich gram-positive bacteria, this is usually regulated by the Fur (ferric uptake regulator) repressor, whilst in GC-rich gram-positive bacteria (e.g.
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Hydrogen dissociates on nickel surfaces. The dissociation energies on a Ni(111), Ni(100), and Ni(11O) are respectively 46, 52, and 36 kJ/mol. The H2 dissociates from each of these surfaces at distinct temperatures: 320–380, 220–360, and 230–430 K.
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In each of the other three types of mukti, liberation is gained during life, not after death. In all cases, after the soul dissociates from the body, it eternally experiences Infinite Power, Knowledge and Bliss. However, after the soul dissociates from the gross body and associates with the subtle body, the most important aspect of the experience is Infinite Bliss. Therefore, while there is a difference in the eternal experience of the souls who gain liberation during life and the experience of souls who gain liberation after death, the most important aspect of the experience is the same: the eternal experience of infinite bliss.
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In response to receptor activation, the α subunit releases bound guanosine diphosphate (GDP), which is displaced by guanosine triphosphate (GTP), thus activating the α subunit, which then dissociates from the β and γ subunits. The activated α subunit can further affect intracellular signaling proteins or target functional proteins directly.
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AD is also classified as an amyloidosis because of the presence of senile plaques. When tau becomes hyperphosphorylated, the protein dissociates from the microtubules in axons. Then, tau becomes misfolded and the protein begins to aggregate, which eventually forms the neurofibrillary tangles seen in Alzheimer’s patients. Microtubules also destabilize when tau is dissociated.
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"Deaf cinema" is a movement that dissociates from the "Cinema of the deaf". “The two are worlds apart" while the Cinema of the deaf is "a mainstream cinema in need of character types as grist for its mercantile mill", the Deaf Cinema is "an outsider cinema serving to nurture and develop a culture's self-image”.
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T7 polymerase by itself has a very low processivity. It dissociates from the primer-template after incorporating about 15 nucleotides. Upon infection of the host, T7 polymerase binds to host thioredoxin in 1:1 ratio. The hydrophobic interaction between thioredoxin and T7 polymerase helps to stabilize the binding of T7 polymerase to primer-template.
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The alpha Subunit of the Gs protein releases bound GDP and binds GTP. The alpha subunit-GTP complex dissociates from the beta and gamma dimer and interacts with adenylate cyclase. Binding of glucagon molecule activates many of the alpha subunit, which amplifies the hormonal signal. Then, the alpha subunit activates the adenylate cyclase, which converts ATP to cAMP.
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In the process of deprotonating the C3 hydroxyl group, Tyr200 dissociates from the catalytic complex. Oxygen is bonded to the substrate through a series of trans influences and stabilizing hydrogen bonding between the substrate and other active site amino acid residues. His226 accepts electron density from the substrate, consequently decreasing the bond between Fe3+ and the C4 hydroxyl.
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Telomere-binding proteins not present may cause the exposed telomeres to undergo a DNA repair response, having mistakenly identified the ends as a double-stranded break. This is due to the 3’ overhang, which gradually shortens over time. A process known as uncapping occurs, in which the shelterin complex dissociates from the telomere when shrunk to a critical length.
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TRNA (guanine26-N2)-dimethyltransferase (, Trm1p, TRM1, tRNA (m22G26)dimethyltransferase) is an enzyme with systematic name S-adenosyl-L- methionine:tRNA (guanine26-N2)-dimethyltransferase. This enzyme catalyses the following chemical reaction : 2 S-adenosyl-L-methionine + guanine26 in tRNA \rightleftharpoons 2 S-adenosyl-L-homocysteine + N2-dimethylguanine26 in tRNA The enzyme dissociates from its tRNA substrate between the two consecutive methylation reactions.
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Until today human development is far advanced in all of the world's CW areas, that is in Western Europe, in Japan, in distinctive areas of Northern America, Australia, and New Zealand. Welzel stresses that — in the era of globalization — human empowerment begins to diffuse elsewhere and slowly dissociates from the CW condition. This erodes the monopoly of the West over human empowerment.
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The new bases eventually dissociate from the DNA bases but stay linked to each other, forming a new mRNA strand. This mRNA strand is synthesized in the 5’ to 3’ direction. Once the RNA reaches a terminator sequence, it dissociates from the DNA template strand and terminates the mRNA sequence as well. Transcription is regulated in the cell via transcription factors.
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Is secreted from seminal vesicles to the seminal fluid. A number of alternatively spliced transcript variants have been observed at this locus, but the full- length nature of only two, each encoding the same protein, has been determined. During the passage of the sperm through the cervix, glycodelin S is de-glycosylated and dissociates from the sperm, allowing the sperm to mature.
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BiP is both a target of the ER stress response, or UPR, and an essential regulator of the UPR pathway. During ER stress, BiP dissociates from the three transducers (IRE1, PERK, and ATF6), effectively activating their respective UPR pathways. As a UPR target gene product, BiP is upregulated when UPR transcription factors associate with the UPR element in BiP’s DNA promoter region.
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From mid-zygotene to early pachytene, as part of the recombinational repair process, DMC1 dissociates from the ssDNA and counts decrease until all breaks (except those on the XY chromosomes) are repaired at late pachytene. Several other proteins are involved in this process, including ZCWPW1, the first protein directly positioned by PRDM9’s dual histone marks. ZCWPW1 is important for homologous DSB repair, not positioning.
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GDP dissociates from inactive GTPases very slowly. The binding of GEFs to their GTPase substrates catalyzes the dissociation of GDP, allowing a GTP molecule to bind in its place. GEFs function to promote the dissociation of GDP. After GDP has disassociated from the GTPase, GTP generally binds in its place, as the cytosolic ratio of GTP is much higher than GDP at 10:1.
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Replication slippage is an error in DNA replication that can produce duplications of short genetic sequences. During replication DNA polymerase begins to copy the DNA. At some point during the replication process, the polymerase dissociates from the DNA and replication stalls. When the polymerase reattaches to the DNA strand, it aligns the replicating strand to an incorrect position and incidentally copies the same section more than once.
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This binding to phosphorylase a prevents any phosphatase activity of PP1 and maintains the glycogen phosphorylase in its active phosphorylated configuration. Therefore, there phosphorylase a will accelerate glycogen breakdown until adequate levels of glucose are achieved. When glucose concentrations get too high, phosphorylase a is converted to its inactive, T state. By shifting phosphorylase a to its T state, PP1 dissociates from the complex.
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Phase 1 blocking has the principal paralytic effect. Binding of suxamethonium to the nicotinic acetylcholine receptor results in opening of the receptor's monovalent cation channel; a disorganized depolarization of the motor end-plate occurs and calcium is released from the sarcoplasmic reticulum. In normal skeletal muscle, acetylcholine dissociates from the receptor following depolarization and is rapidly hydrolyzed by the enzyme acetylcholinesterase. The muscle cell is then ready for the next signal.
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Centrosome-associated protein CEP250 is a protein that in humans is encoded by the CEP250 gene. This gene encodes a core centrosomal protein required for centriole-centriole cohesion during interphase of the cell cycle. The encoded protein dissociates from the centrosomes when parental centrioles separate at the beginning of mitosis. The protein associates with and is phosphorylated by NIMA-related kinase 2, which is also associated with the centrosome.
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In the GTP-bound form, ARF conformation changes such that the myristate and hydrophobic N-terminal become more exposed and associate with the membrane. The interconversion between GTP and GDP bound states is mediated by ARF GEFs and ARF GAPs. At the membrane, ARF-GTP is hydrolyzed to ARF-GDP by ARF GAPs. Once in the GDP-bound conformation, ARF converts to a less hydrophobic conformation and dissociates from the membrane.
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Endosomes provide an environment for material to be sorted before it reaches the degradative lysosome. For example, low-density lipoprotein (LDL) is taken into the cell by binding to the LDL receptor at the cell surface. Upon reaching early endosomes, the LDL dissociates from the receptor, and the receptor can be recycled to the cell surface. The LDL remains in the endosome and is delivered to lysosomes for processing.
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Only the unbound fraction of the drug undergoes metabolism in the liver and other tissues. As the drug dissociates from the protein, more and more drug undergoes metabolism. Changes in the levels of free drug change the volume of distribution because free drug may distribute into the tissues leading to a decrease in plasma concentration profile. For the drugs which rapidly undergo metabolism, clearance is dependent on the hepatic blood flow.
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Brassinosteroid signal cascade: in the absence of BR, BKI1 blocks BRI1 activity and BIN2 inhibits transcription factors. When BR is present, BKI1 dissociates from BRI1 and the BRI1:BAK1 complex is formed. This complex promotes the inactivation of BIN2 and transcription factors can then exert their effects. BRs are perceived at the cell membrane by a co-receptor complex, comprising brassinosteroid insensitive-1 (BRI1) and BRI1-associated receptor kinase 1 (BAK1).
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The role of vitamin A in the visual cycle is specifically related to the retinal form. Within the eye, 11-cis-retinal is bound to the protein "opsin" to form rhodopsin in rods and iodopsin (cones) at conserved lysine residues. As light enters the eye, the 11-cis-retinal is isomerized to the all-"trans" form. The all-"trans" retinal dissociates from the opsin in a series of steps called photo-bleaching.
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Is secreted by granulosa cells into the follicular fluid. Glycodelin-F reduces the blinding of spermatozoa to the zona pellucida which is mainly expressed in the ovary, and synthesised in the granulosa cells, has a function in principle similar to that of Glycodelin-A. It also binds the sperm head, thereby inhibiting acrosome reaction and sperm- egg binding. Upon de-glycosilation, glycodelin F dissociates from the sperm and sperm-egg binding is possible.
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In the blood, it mainly circulates in a stable noncovalent complex with von Willebrand factor. Upon activation by thrombin (factor IIa), it dissociates from the complex to interact with factor IXa in the coagulation cascade. It is a cofactor to factor IXa in the activation of factor X, which, in turn, with its cofactor factor Va, activates more thrombin. Thrombin cleaves fibrinogen into fibrin which polymerizes and crosslinks (using factor XIII) into a blood clot.
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After the formation of the spherical structure, the complex of ATG12-ATG5:ATG16L1 dissociates from the autophagosome. LC3 is cleaved by ATG4 protease to generate cytosolic LC3. LC3 cleavage is required for the terminal fusion of an autophagosome with its target membrane. LC3 is commonly used as a marker of autophagosomes in immunocytochemistry, because it is the essential part of the vesicle and stays associated until the last moment before its fusion.
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Yeast carry one or two copies of each histone gene, which are not clustered but rather scattered throughout chromosomes. Histone gene transcription is controlled by multiple gene regulatory proteins such as transcription factors which bind to histone promoter regions. In budding yeast, the candidate gene for activation of histone gene expression is SBF. SBF is a transcription factor that is activated in late G1 phase, when it dissociates from its repressor Whi5.
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When calcium dissociates from the binding site, calcium levels fall rapidly. Due to the differences in calcium concentration at the cytostolic binding site when calcium is bound to the MET channel versus when calcium dissociates, a calcium gradient is created, generating chemical energy. The oscillation of calcium concentration and force generation contributes to amplification. The timecourse of this mechanism is on the order of hundreds of microseconds, which reflects the speed that is necessary for amplification of high frequencies.
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Upon deflection of the basilar membrane upwards and subsequent deflection of the hair bundles toward the tallest steroecilia, channels within the stereocilia open allowing the inflow of ions and depolarizing the OHC results. Intracellular chloride dissociates from the allosteric binding sites in prestin, causing contraction of prestin. Upon BM deflection downwards hyperpolarization of the OHC results, and intracellular chloride ions bind allosterically causing prestin expansion. The binding or dissociation of chloride causes a shift in prestin's membrane capacitance.
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In this state, Rb binds to a protein transcription factor E2F and prevents E2F from activating transcription of proteins essential for S-phase. During a normal cell cycle, as G1 progresses, Rb will become phosphorylated in a specific set of sequential steps by proteins called cyclin dependent kinases (cdks) bound to cyclin proteins. The specific complexes that phosphorylate Rb are cyclin D-cdk4 and cyclin E-cdk2. When Rb has been phosphorylated many times, it dissociates from E2F.
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It mediates docking to the nuclear pore complex through binding to nucleoporin and is subsequently translocated through the pore by an energy requiring mechanism. Then, in the nucleus Ran binds to Transportin-1, it dissociates from cargo, and Transportin-1 is re-exported from the nucleus to the cytoplasm where GTP hydrolysis releases Ran. Then Transportin-1 is free to bind new cargo. In addition, Transportin-1 is implicated in helping protein transport into primary cilium.
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The dissociation rate in chemistry, biochemistry, and pharmacology is the rate or speed at which a ligand dissociates from a protein, for instance, a receptor. It is an important factor in the binding affinity and intrinsic activity (efficacy) of a ligand at a receptor. The dissociation rate for a particular substrate can be applied to enzyme kinetics, including the Michaelis-Menten model. Substrate dissociation rate contributes to how large or small the enzyme velocity will be.
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The APC/CCDH1 targets crosslinking microtubule-associated proteins (NuMA, Ase1, Cin1 and more). AuroraB (yeast IpI1) phosphorylates the spindle-associated stabilizing protein EB1 (yeast Bim1), which then dissociates from microtubules, and the destabilizer She1, which then associates with microtubules. Kinesin8 (yeast Kip3), an ATP-dependent depolymerase, accelerate microtubule depolymerization at the plus end. It was shown the concurrent disruption of these mechanisms, but not of any one, results in dramatic spindle hyperstability during telophase, suggesting functional overlap despite the diversity of the mechanisms.
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In turn HRAS can bind to proteins of the Guanine Nucleotide Exchange Factor (GEF) class, for example SOS1, which forces the release of bound nucleotide. Subsequently, GTP present in the cytosol binds and HRAS-GTP dissociates from the GEF, resulting in HRAS activation. HRAS is in the Ras family, which also includes two other proto- oncogenes: KRAS and NRAS. These proteins all are regulated in the same manner and appear to differ largely in their sites of action within the cell.
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In other words: Guanylate Cyclase Activating Protein (GCAP) is a calcium binding protein, and as the calcium levels in the cell have decreased, GCAP dissociates from its bound calcium ions, and interacts with Guanylate Cyclase, activating it. Guanylate Cyclase then proceeds to transform GTP to cGMP, replenishing the cell's cGMP levels and thus reopening the sodium channels that were closed during phototransduction. Finally, Metarhodopsin II is deactivated. Recoverin, another calcium binding protein, is normally bound to Rhodopsin Kinase when calcium is present.
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Modern application of denaturation mapping: DNA is stained with a dye(green) that dissociates from single stranded DNA, changes in the environment like temperature increases that are not enough to completely dissociate the molecule causes parts of it to dissociate in a predictable manner from AT rich regions (red). fluorescence emissions from this partially denatured molecule is measured with photospectroscopy. The graph shown is a simplified output of such an analysis. Denaturation Mapping is a form of optical mapping, first described in 1966.
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11β-Chloromethylestradiol (11β-CME2; developmental code name ORG-4333) is a synthetic steroidal estrogen which was never marketed. It has very high affinity from the estrogen receptors and dissociates from them very slowly. It was originally thought that 11β-CME2 might be a covalent ligand of the estrogen receptors, but its binding was subsequently shown to be fully reversible. The relative binding affinity of 11β-CME2 for the estrogen receptors ranges from 230 to 3,320% of that of estradiol depending on the study.
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A formin dimer remains constantly bound to the plus end of an actin filament despite ongoing polymerization. One formin of a dimer dissociates from the barbed end to take the next step while the second formin of the dimer remains bound. Thus the formin dimer processively adds actin monomers to the barbed end and are constantly present at the barbed end of an actin filament (processive capping). The FH1 domain recruits actin monomers through profilin binding, but it does not promote nucleation.
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Transducin is activated by metarhodopsin II, a conformational change in rhodopsin caused by the absorption of a photon by the rhodopsin moiety retinal. The light causes isomerization of retinal from 11-cis to all-trans. Isomerization causes a change in the opsin to become metarhodopsin II. When metarhodopsin activates transducin, the guanosine diphosphate (GDP) bound to the α subunit (Tα) is exchanged for guanosine triphosphate (GTP) from the cytoplasm. The α subunit dissociates from the βγ subunits (Tβγ.) Activated transducin α-subunit activates cGMP phosphodiesterase.
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Through a microflow system, a solution with the prey analyte is injected over the bait layer. As the prey analyte binds the bait ligand, an increase in SPR signal (expressed in response units, RU) is observed. After desired association time, a solution without the prey analyte (usually the buffer) is injected on the microfluidics that dissociates the bound complex between bait ligand and prey analyte. Now as the prey analyte dissociates from the bait ligand, a decrease in SPR signal (expressed in resonance units, RU) is observed.
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2-Hydroxyestradiol has approximately 7% and 11% of the affinity of estradiol at the estrogen receptors (ERs) ERα and ERβ, respectively. It dissociates from the estrogen receptors more rapidly than does estradiol. The steroid is only very weakly estrogenic, and is able to antagonize the estrogenic effects of estradiol, indicating that its intrinsic activity at the estrogen receptor is less than that of estradiol and hence that it possesses the profile of a selective estrogen receptor modulator. It shows estrogenic activity in human breast cancer cells.
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In the eukaryotic chromatin, DNA is rarely present in the free supercoiled form because nucleosomes restrain almost all negative supercoiling through tight binding of DNA to histones. Similarly, in E. coli, nucleoprotein complexes formed by NAPs restrain half of the supercoiling density of the nucleoid. In other words, if a NAP dissociates from a nucleoprotein complex, the DNA would adopt the free, plectonemic form. DNA binding of HU, Fis, and H-NS has been experimentally shown to restrain negative supercoiling in a relaxed but topologically constrained DNA.
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When the calcium levels fall during phototransduction, the calcium dissociates from recoverin, and rhodopsin kinase is released, when it (what?) proceeds to phosphorylate metarhodopsin II, which decreases its affinity for transducin. Finally, arrestin, another protein, binds the phosphorylated metarhodopsin II, completely deactivating it. Thus, finally, phototransduction is deactivated, and the dark current and glutamate release is restored. It is this pathway, where Metarhodopsin II is phosphorylated and bound to arrestin and thus deactivated, which is thought to be responsible for the S2 component of dark adaptation.
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DHT is synthesized in the prostate from circulating testosterone by the action of the enzyme 5α-reductase, type 2. DHT can act in an autocrine fashion on the stromal cells or in paracrine fashion by diffusing into nearby epithelial cells. In both of these cell types, DHT binds to nuclear androgen receptors and signals the transcription of growth factors that are mitogenic to the epithelial and stromal cells. DHT is ten times more potent than testosterone because it dissociates from the androgen receptor more slowly.
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Evidence also exists for a carbocation based mechanism of dealkylation similar to an SN1 reaction, where the R1 group initially dissociates from the phosphonium salt followed by attack of the anion. Phosphite esters with tertiary alkyl halide groups can undergo the reaction, which would be unexpected if only an SN2 mechanism was operating. Further support for this SN1 type mechanism comes from the use of the Arbuzov reaction in the synthesis of neopentyl halides, a class of compounds that are notoriously unreactive towards SN2 reactions.
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Importin beta is a specific type of karyopherin that facilitates the transport of cargo proteins into the nucleus. First, it is binding importin alpha – another type of karyopherin that binds the cargo protein in the cytoplasm - before the cargo protein is imported into the nucleus through the nuclear pore using energy derived from the Ran gradient. Once inside the nucleus, the cargo dissociates from the karyopherins. Importin beta can also carry proteins into the nucleus without the aid of the importin alpha adapter protein.
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However, upon ligand binding, the receptor switches to an active conformation, and this is driven by intermolecular rearrangement between the trans-membrane helices. The receptor activation releases an ‘ionic lock’ which holds together the cytoplasmic sides of transmembrane helices three and six, causing them to rotate. This conformational change exposes the intracellular receptor domains at the cytosolic side, which further leads to the activation of the G protein. When the GDP molecule dissociates from the Gα sub-unit, a GTP molecule binds to the free nucleotide-binding pocket, and the G protein becomes active.
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The most common metal halide compound used is sodium iodide. Once the arc tube reaches its running temperature, the sodium dissociates from the iodine, adding orange and reds to the lamp's spectrum from the sodium D line as the metal ionizes. As a result, metal-halide lamps have high luminous efficacy of around 75–100 lumens per watt, which is about twice that of mercury vapor lights and 3 to 5 times that of incandescent lights and produce an intense white light. Lamp life is 6,000 to 15,000 hours.
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These channels open temporarily to allow neurons to "reset" after they fire; lolitrem B blocks them, preventing the neuron from firing again after it depolarizes, which at low doses leads to tremors and at high doses to paralysis and death. The binding site of lolitrem B is likely to be located in this α subunit. When lolitrem B is added, the potassium current quickly gets abolished and this inhibition cannot be reversed by washout (this reversal is possible for paxilline). However, over time lolitrem B slowly dissociates from the binding site.
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When cholesterol levels fall, INSIG-1 dissociates from the SREBP-SCAP complex, which allows the complex to migrate to the Golgi apparatus. Here SREBP is cleaved by S1P and S2P (site-1 protease and site-2 protease), two enzymes that are activated by SCAP when cholesterol levels are low. The cleaved SREBP then migrates to the nucleus, and acts as a transcription factor to bind to the sterol regulatory element (SRE), which stimulates the transcription of many genes. Among these are the low-density lipoprotein (LDL) receptor and HMG-CoA reductase.
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As shown by Uhlmann et al., during the attachment of chromosomes to the mitotic spindle the chromatids remain paired because cohesion between the sisters prevents separation. Cohesion is established during DNA replication and depends on cohesin, which is a multisubunit complex composed of Scc1, Scc3, Smc2, and Smc3. In yeast at the metaphase-to-anaphase transition, Scc1 dissociates from the chromosomes and the sister chromatids separate. This action is controlled by the Esp1 protein, which is tightly bound by the anaphase inhibitor Pds1 that is destroyed by the anaphase- promoting complex.
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The molecular chaperone BiP/Grp78 has a range of functions within the ER. It maintains specific transmembrane receptor proteins involved in initiating of the downstream signalling of the UPR in an inactive state by binding to their luminal domains. An overwhelming load of misfolded proteins or simply the over- expression of proteins (e.g. IgG) requires more of the available BiP/Grp78 to bind to the exposed hydrophobic regions of these proteins, and consequently BiP/Grp78 dissociates from these receptor sites to meet this requirement. Dissociation from the intracellular receptor domains allows them to become active.
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Albert lives in his apartment with his fiancé, Vanessa, and works doing data input from home. His secret shame is an obsession with an Artificial Intelligence dating simulator on which he pretends to have a relationship with an anime-influenced avatar called Vanessa2. Albert's stable relationship with Vanessa is jeopardized as he increasingly dissociates from reality, experiencing nightmares in which he masturbates a metallic phallus. After a fight in which Vanessa tells Albert that he "loves his computer," she temporarily moves to her sister's, leaving Albert alone to his online vices.
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Membrane is Grey. The G beta-gamma complex (Gβγ) is a tightly bound dimeric protein complex, composed of one Gβ and one Gγ subunit, and is a component of heterotrimeric G proteins. Heterotrimeric G proteins, also called guanosine nucleotide-binding proteins, consist of three subunits, called alpha, beta, and gamma subunits, or Gα, Gβ, and Gγ. When a G protein-coupled receptor (GPCR) is activated, Gα dissociates from Gβγ, allowing both subunits to perform their respective downstream signaling effects. One of the major functions of Gβγ is the inhibition of the Gα subunit.
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A cancerous cell growth often accompanies with deregulation of Cyclin D-Cdk 4/6 activity. The hyperphosphorylated Rb dissociates from the E2F/DP1/Rb complex (which was bound to the E2F responsive genes, effectively "blocking" them from transcription), activating E2F. Activation of E2F results in transcription of various genes like cyclin E, cyclin A, DNA polymerase, thymidine kinase, etc. Cyclin E thus produced binds to CDK2, forming the cyclin E-CDK2 complex, which pushes the cell from G1 to S phase (G1/S, which initiates the G2/M transition).
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The GTP/G-alpha complex dissociates from the trimer and associates to an effector until the intrinsic GTPase activity of G-alpha returns the protein to GDP bound form. Reassociation of GDP-bound G-alpha with G-beta/G-gamma dimer terminates the signal. Several mechanisms regulate the signal output at different stage of the G-protein cascade. Two classes of intracellular proteins act as inhibitors of G protein activation: GTPase activating proteins (GAPs), which enhance GTP hydrolysis (see PDOC50132), and guanine dissociation inhibitors (GDIs), which inhibit GDP dissociation.
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In addition, although not antiestrogenic in the uterus, 2-hydroxyestrone shows antiestrogenic effects on luteinizing hormone and prolactin levels. The lack of estrogenic or antiestrogenic activity of 2-hydroxyestrone in the uterus may be attributable to an extremely high metabolic clearance rate. When incubated at very high concentrations or in combination with a catechol O-methyltransferase (COMT) inhibitor to prevent its metabolism, 2-hydroxyestrone shows antiestrogenic effects in estrogen receptor-positive human breast cancer cells. 2-Hydroxyestrone dissociates from the estrogen receptors much more rapidly than does estradiol.
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Transmission electron micrograph of Chikungunya virus particles The virus consists of four nonstructural proteins and three structural proteins. The structural proteins are the capsid and two envelope glycoproteins: E1 and E2, which form heterodimeric spikes on the viron surface. E2 binds to cellular receptors in order to enter the host cell through receptor-mediated endocytosis. E1 contains a fusion peptide which, when exposed to the acidity of the endosome in eukaryotic cells, dissociates from E2 and initiates membrane fusion that allows the release of nucleocapsids into the host cytoplasm, promoting infection.
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Toward alkyllithium reagents, TMEDA functions as a donor ligand, reduces the degree of aggregation, and increases the nucleophilicity of these species. However, TMEDA does not always function as a donor ligand to lithium cation, especially in the presence of anionic oxygen and nitrogen centers. For example, it only weakly interacts with LDA and LiHMDS even in hydrocarbon solvents with no competing donor ligands. In imine lithiation, while THF acts as a strong donating ligand to LiHMDS, the weakly coordinating TMEDA readily dissociates from LiHMDS, leading to the formation of LiHMDS dimers that is the more reactive species.
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In one such pathway, caspase-independent apoptosis, the E3 ligase C-terminal of Hsc-70 interacting protein (CHIP), a regulator of EndoG expression, functions as a protective mechanism against oxidative stress. Under normal conditions, EndoG remains bound to Hsp70 and CHIP; however, when undergoing oxidative stress, EndoG dissociates from Hsp70 and CHIP and translocates to the nucleus, where it degrades DNA to effect apoptosis. Therefore, maintaining low levels of EndoG could prevent cell death caused by stress conditions. In epithelial cells, the nuclear localization and proapoptotic function of EndoG leads it to play a role in cell senescence.
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In addition to RNA polymerase II, mediator must also associate with transcription factors and DNA. A model of such interactions is shown in the figure to the right. Note that the different morphologies of mediator do not necessarily mean that one of the models is correct; rather those differences may reflect the flexibility of mediator as it interacts with other molecules. For example, after binding the enhancer and core promoter, the mediator complex undergoes a compositional change in which the kinase module dissociates from the complex to allow association with RNA polymerase II and transcriptional activation.
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The glycogen itself however, after purified, is found with very little protein, less than three percent normally, showing that the glycosome is responsible and functions by having the proteins and enzymes needed for the glycogen in the glycosome. With the uranyl staining, as an acid, it would cause dissociation of the protein from the glycogen. The glycogen without the protein would form large aggregates and the stain would be the protein. This gives the illusion of glycogen disappearing as it is not stained, but it dissociates from the protein that it is normally associated with in the glycosome.
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The general mechanism for this cycle begins with the reaction of an electron-poor metal center with a diazocompound to form a metallo- carbene intermediate. In order for this reaction to occur, the diazocompound must be very electrophilic, since the C-H bond is such a poor nucleophile as well as being an unactivated alkane. The reaction then proceeds in a concerted manner, where the C-H bond of the incoming molecule coordinates with the carbene carbon of the metallocarbene complex. The hydrocarbon then dissociates from the metal center to regenerate the catalyst and free the newly formed carbon-carbon bond ().
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Their central pore is sufficiently large to admit the DNA strands and some surrounding water molecules, which allows the clamp to slide along the DNA without dissociating from it and without loosening the protein-protein interactions that maintain the toroid shape. When associated with a DNA clamp, DNA polymerase is dramatically more processive; without the clamp most polymerases have a processivity of only about 100 nucleotides. The interactions between the polymerase and the clamp are more persistent than those between the polymerase and the DNA. Thus, when the polymerase dissociates from the DNA, it is still bound to the clamp and can rapidly reassociate with the DNA.
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When active, mTORC1 inhibits autophagy by phosphorylating both ULK1 and ATG13, which reduces the kinase activity of ULK1. Under starvation conditions, mTORC1 is inhibited and dissociates from ULK1 allowing it to become active. AMPK is activated when intracellular AMP increases which occurs under starvation conditions, which inactivates mTORC1, and thus directly activates ULK1. AMPK also directly phosphorylates ULK1 at multiple sites in the linker region between the kinase and C-terminal domains. ULK1 can phosphorylate itself as well as ATG13 and RB1CC1, which are regulatory proteins; however, the direct substrate of ULK1 has not been identified although recent studies suggest it phosphorylates Beclin-1.
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The RecA protein is then actively loaded onto the 3' tail by RecBCD. At some undetermined point RecBCD dissociates from the DNA, although RecBCD can unwind at least 60 kb of DNA without falling off. RecA initiates exchange of the DNA strand to which it is bound with the identical, or nearly identical, strand in an intact DNA duplex; this strand exchange generates a joint DNA molecule, such as a D-loop (Figure 2). The joint DNA molecule is thought to be resolved either by replication primed by the invading 3’ ended strand containing Chi or by cleavage of the D-loop and formation of a Holliday junction.
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The protein encoded by this gene is a peripheral membrane protein which recycles between the cytosol and the Golgi apparatus during interphase. It is regulated by phosphorylation: dephosphorylated protein associates with the Golgi membrane and dissociates from the membrane upon phosphorylation. Ras-associated protein 1 recruits this protein to coat protein complex II (COPII) vesicles during budding from the endoplasmic reticulum (ER), where it interacts with a set of COPII vesicle- associated SNAREs to form a cis-SNARE complex that promotes targeting to the Golgi apparatus. Transport from the ER to the cis/medial Golgi compartments requires the action of this gene product, GOLGA2, and giantin in a sequential manner.
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The primary gp5 subunit of T7 DNA Polymerase by itself has low processivity and dissociates from DNA after the incorporation of just a few nucleotides. In order to become efficiently processive, T7 DNA polymerase recruits host thioredoxin to form a thioredoxin- gp5 complex. Thioredoxin binds the thioredoxin binding domain of gp5 thereby stabilizes a flexible DNA binding region of gp5. The stabilization of this region of gp5 alosterically increases the amount of protein surface interaction with the duplex portion of the primer-template. The resulting thioredoxin-gp5 complex increases the affinity of T7 polymerase for the primer terminus by ~80-fold and acts processively around 800 nucleotide incorporation steps.
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The proteolytic maturation of P62 into E2 and E3 causes a change in the viral surface. Together the E1, E2, and sometimes E3, glycoprotein "spikes" form an E1/E2 dimer or an E1/E2/E3 trimer, where E2 extends from the centre to the vertices, E1 fills the space between the vertices, and E3, if present, is at the distal end of the spike. Upon exposure of the virus to the acidity of the endosome, E1 dissociates from E2 to form an E1 homotrimer, which is necessary for the fusion step to drive the cellular and viral membranes together. The alphaviral glycoprotein E1 is a class II viral fusion protein, which is structurally different from the class I fusion proteins found in influenza virus and HIV.
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CcrM in complex with a dsDNA structure was resolved, showing that the enzyme presents a novel DNA interaction mechanism, opening a bubble in the DNA recognition site (The concerted mechanism of Methyltransferases relies in the flip of the target base), the enzyme interacts with DNA forming an homodimer with differential monomer interactions. CcrM is a highly efficient enzyme capable of methylating a high number of 5'-GANTC-3' sites in low time, however if the enzyme is processive (the enzyme binds to the DNA and methylate several methylation sites before dissociation) or distributive (the enzyme dissociates from DNA after each methylation) it is still in discussion. First reports indicated the second case, however more recent characterisation of CcrM indicate that it is a processive enzyme.
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The weak and atypical estrogenicity of estriol is thought to be related to its short duration in the body and hence the fact that it stays bound to the ER for a relatively short amount of time. Whereas estradiol remains bound to the ER for 6 to 24 hours with a single short-acting injection, estriol dissociates from the receptor much more rapidly and stays bound for only 1 to 6 hours. As a result, estriol can only induce estrogenic effects which require short-term interaction with the ERs. Induction of endometrial mitoses requires the ligand to remain bound for at least 9 to 12 hours, and this is thought to be responsible for the lack of endometrial proliferation with estriol in many studies.
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In eukaryotic transcription of mRNAs, terminator signals are recognized by protein factors that are associated with the RNA polymerase II and which trigger the termination process. Once the poly-A signals are transcribed into the mRNA, the proteins cleavage and polyadenylation specificity factor (CPSF) and cleavage stimulation factor (CstF) transfer from the carboxyl terminal domain of RNA polymerase II to the poly-A signal. These two factors then recruit other proteins to the site to cleave the transcript, freeing the mRNA from the transcription complex, and add a string of about 200 A-repeats to the 3' end of the mRNA in a process known as polyadenylation. During these processing steps, the RNA polymerase continues to transcribe for several hundred to a few thousand bases and eventually dissociates from the DNA and downstream transcript through an unclear mechanism; there are two basic models for this event known as the torpedo and allosteric models.
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This rotated ribosomal intermediate, in which the first tRNA occupies a hybrid A/P position and the second tRNA occupies a hybrid P/E position is a substrate for EF-G-GTP. As a GTPase, EF-G binds to the rotated ribosome near the A site in its GTP-bound state, and hydrolyzes GTP, releasing GDP and inorganic phosphate: : GTP + H2O -> GDP + P_{i} The hydrolysis of GTP allows for a large conformational change within EF-G, forcing the A/P tRNA to fully occupy the P site, the P/E tRNA to fully occupy the E site (and exit the ribosome complex), and the mRNA to shift three nucleotides down relative to the ribosome. The GDP-bound EF-G molecule then dissociates from the complex, leaving another free A-site where the elongation cycle can start again. Crystal structure of the ribosome with two tRNAs (orange and green) and EF-G (in cyan) after translocation.
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Preformed complexes of the adaptor molecule Tollip and IRAK-1 are also recruited to the receptor complex, allowing IRAK-1 to bind MyD88. IRAK-1 binding to MyD88 brings it into close proximity with IRAK-4 so that IRAK-4 can phosphorylate and activate IRAK-1. Once phosphorylated, IRAK-1 recruits the adaptor protein TNF receptor associated factor 6 (TRAF6) and the IRAK-1-TRAF6 complex dissociates from the IL-1R complex. The IRAK-1-TRAF6 complex interacts with a pre-existing complex at the plasma membrane consisting of TGF-β activated kinase 1 (TAK1), and two TAK binding proteins, TAB1 and TAB2. TAK1 is a mitogen-activated protein kinase kinase kinase (MAPKKK). This interaction leads to the phosphorylation of TAB2 and TAK1, which then translocate to the cytosol with TRAF6 and TAB1. IRAK-1 remains at the membrane and is targeted for degradation by ubiquitination. Once the TAK1-TRAF6-TAB1-TAB2 complex is in the cytosol, ubiquitination of TRAF6 in triggers the activation of TAK1 kinase activity.
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