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Eukaryotic translation initiation factor 2, subunit 2 beta, 38kDa

eIF2B, eukaryotic initiation factor 2B, eIF2beta
Eukaryotic translation initiation factor 2 (EIF-2) functions in the early steps of protein synthesis by forming a ternary complex with GTP and initiator tRNA and binding to a 40S ribosomal subunit. EIF-2 is composed of three subunits, alpha, beta, and gamma, with the protein encoded by this gene representing the beta subunit. The beta subunit catalyzes the exchange of GDP for GTP, which recycles the EIF-2 complex for another round of initiation. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, ACID, eIF4E, eIF2alpha, CLE
Papers on eIF2B
Moco biosynthesis and the ATAC acetyltransferase engage translation initiation by inhibiting latent PKR activity.
Workman et al., Kansas City, United States. In J Mol Cell Biol, Feb 2016
The suppression of eIF2α phosphorylation via MPT synthase and ATAC prevented sequestration of the guanine nucleotide exchange factor eIF2B, which recycles eIF2-GDP to eIF2-GTP, resulting in the promotion of translation initiation.
Structure-Activity Studies of Bis-O-Arylglycolamides: Inhibitors of the Integrated Stress Response.
Renslo et al., San Francisco, United States. In Chemmedchem, Feb 2016
Phosphorylation of eIF2α (eIF2α-P) results in attenuation of global protein synthesis via the inhibitory effects of eIF2α-P on eIF2B, the guanine exchange factor (GEF) for eIF2.
No evidence for a role of Ile587Val polymorphism of EIF2B5 gene in multiple sclerosis in Kashmir Valley of India.
Haq et al., Srīnagar, India. In J Neurol Sci, Jan 2016
It is already known that alterations in Eukaryotic Translation Initiation Factor 2B (EIF2B) gene encoding the five subunits of eIF2B complex cause Vanishing White Matter (VWM) disease of the brain and emerging evidences have advocated certain resemblances between MS and VWM in terms of clinical and epidemiological characteristics, thus validating the association study between EIF2B and MS.
eIF2B: recent structural and functional insights into a key regulator of translation.
Proud et al., Adelaide, Australia. In Biochem Soc Trans, Jan 2016
The eukaryotic translation initiation factor (eIF) eIF2B is a key regulator of mRNA translation, being the guanine nt exchange factor (GEF) responsible for the recycling of the heterotrimeric G-protein, eIF2, which is required to allow translation initiation to occur.
Stoichiometry of the eIF2B complex is maintained by mutual stabilisation of subunits.
Proud et al., Southampton, United Kingdom. In Biochem J, Dec 2015
UNASSIGNED: The eukaryotic translation initiation factor eIF2B is a multi-subunit complex with a crucial role in the regulation of global protein synthesis in the cell.
Endoplasmic reticulum stress intolerance in EIF2B3 mutant oligodendrocytes is modulated by depressed autophagy.
Wu et al., Beijing, China. In Brain Dev, Dec 2015
OBJECTIVE: Eukaryotic translation initiation factor 2B (eIF2B) is an essential factor for the initiation of protein synthesis.
Stress responses. Mutations in a translation initiation factor identify the target of a memory-enhancing compound.
Ron et al., Nottingham, United Kingdom. In Science, Jun 2015
When reintroduced by CRISPR-Cas9 gene editing of wild-type cells, these mutations reversed both ISRIB-mediated inhibition of the ISR and its stimulatory effect on eIF2B GEF activity toward its substrate, the translation initiation factor eIF2, in vitro.
Vanishing white matter disease presenting as opsoclonus myoclonus syndrome in childhood--a case report and review of the literature.
Ray Chaudhuri et al., London, United Kingdom. In Pediatr Neurol, 2014
BACKGROUND: Vanishing white matter disease is caused by mutations of the eukaryotic translation initiation factor 2B (EIF2B) and is a prevalent cause of inherited childhood leukoencephalopathy.
A new function and complexity for protein translation initiation factor eIF2B.
Pavitt et al., Manchester, United Kingdom. In Cell Cycle, 2013
eIF2B is critical for regulation of protein synthesis via a conserved mechanism of phosphorylation of eIF2, which converts eIF2 from a substrate to an inhibitor of eIF2B GEF.
Vanishing white matter disease in a spanish population.
Armstrong-Moron et al., Barcelona, Spain. In J Cent Nerv Syst Dis, 2013
It has been associated with mutations in genes encoding eukaryotic translation initiation factor (eIF2B).
Leukodystrophies with astrocytic dysfunction.
Rodriguez, Paris, France. In Handb Clin Neurol, 2012
CACH/VWM is due to mutations in one of the five subunits of EIF2B which compromise the astrocytic lineage.
Vanishing white matter disease caused by EIF2B2 mutation with the presentation of an adrenoleukodystrophy phenotype.
Alkuraya et al., Riyadh, Saudi Arabia. In Gene, 2012
analysis of vanishing white matter disease caused by EIF2B2 mutation with the presentation of an adrenoleukodystrophy phenotype [case report]
Toll-like receptor activation suppresses ER stress factor CHOP and translation inhibition through activation of eIF2B.
Tabas et al., New York City, United States. In Nat Cell Biol, 2012
As p-eIF2α decreases the functional interaction of eIF2 with eIF2B, a guanine nucleotide exchange factor (GEF), we explored the hypothesis that TLR-TRIF signalling activates eIF2B GEF activity to counteract the effects of p-eIF2α.
Functional elements in initiation factors 1, 1A, and 2β discriminate against poor AUG context and non-AUG start codons.
Hinnebusch et al., Bethesda, United States. In Mol Cell Biol, 2011
eIF1 autoregulates translation in yeast and discrimination against poor sequence context in vivo depends on specific domains and residues in eIF1, eIF1A, and eIF2beta
[Vanishing white matter disease: a stress-related leukodystrophy].
Weber et al., In Nervenarzt, 2011
A mutation .626G>A [p.Arg209Gln] in exon 7 and c.1399C>T [p.Arg467Trp] in exon 13 of the EIF2B4-Gens.
The alpha subunit of eukaryotic initiation factor 2B (eIF2B) is required for eIF2-mediated translational suppression of vesicular stomatitis virus.
Barber et al., Miami, United States. In J Virol, 2011
These data emphasize the importance of eIF2Balpha in mediating the eIF2 kinase translation-inhibitory activity and may provide insight into the complex nature of vesiculovirus oncolysis.
A point mutation in translation initiation factor eIF2B leads to function--and time-specific changes in brain gene expression.
Elroy-Stein et al., Tel Aviv-Yafo, Israel. In Plos One, 2010
A point mutation in translation initiation factor eIF2B leads to Vanishing White Matter disease.
eIF5 has GDI activity necessary for translational control by eIF2 phosphorylation.
Pavitt et al., Manchester, United Kingdom. In Nature, 2010
Second we show that eIF5 is a critical component of the eIF2(alphaP) regulatory complex that inhibits the activity of the guanine-nucleotide exchange factor (GEF) eIF2B.
Vanishing white matter disease.
Scheper et al., Amsterdam, Netherlands. In Lancet Neurol, 2006
The basic defect of this striking disease resides in either one of the five subunits of eukaryotic translation initiation factor eIF2B. eIF2B is essential in all cells of the body for protein synthesis and its regulation under different stress conditions.
EIF2B5 mutations compromise GFAP+ astrocyte generation in vanishing white matter leukodystrophy.
Pröschel et al., Rochester, United States. In Nat Med, 2005
Vanishing white matter disease (VWM) is a heritable leukodystrophy linked to mutations in translation initiation factor 2B (eIF2B).
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