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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
Proteomics-level analysis of myelin formation and regeneration in a mouse model for Vanishing White Matter disease.
Elroy-Stein et al., Tel Aviv-Yafo, Israel. In J Neurochem, 28 May 2015
UNASSIGNED: Vanishing White Matter (VWM) is a recessive neurodegenerative disease caused by mutations in translation initiation factor eIF2B and leading to progressive brain myelin deterioration, secondary axonal damage and death in early adolescence.
Mutations in a translation initiation factor identify the target of a memory-enhancing compound.
Ron et al., Nottingham, United Kingdom. In Science, 09 May 2015
When reintroduced by CRISPR-Cas9 gene editing of wildtype 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.
Mutations in the genes encoding eukaryotic translation initiation factor 2B in Japanese patients with vanishing white matter disease.
Yamamoto et al., Tokyo, Japan. In Brain Dev, 02 May 2015
METHOD: The genes encoding all five subunits of eukaryotic translation initiation factor 2B (EIF2B) were analyzed in patients, who were tentatively diagnosed with VWM, by Sanger sequencing.
Alcohols inhibit translation to regulate morphogenesis in C. albicans.
Ashe et al., Manchester, United Kingdom. In Fungal Genet Biol, 02 May 2015
Using molecular techniques, we have identified the likely translational target of these alcohols in C. albicans as the eukaryotic translation initiation factor 2B (eIF2B).
Infantile onset Vanishing White Matter disease associated with a novel EIF2B5 variant, remarkably long life span, severe epilepsy, and hypopituitarism.
Rohena et al., San Antonio, United States. In Am J Med Genet A, 30 Apr 2015
Vanishing White Matter disease (VWM) is an inherited progressive leukoencephalopathy caused by mutations in the genes EIF2B1-5, which encode for the 5 subunits of the eukaryotic initiation factor 2B (eIF2B), a regulator of protein synthesis.
Pharmacological dimerization and activation of the exchange factor eIF2B antagonizes the integrated stress response.
Walter et al., San Francisco, United States. In Elife, Dec 2014
The general translation initiation factor eIF2 is a major translational control point.
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, Jul 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.
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
Recent progress toward understanding the molecular mechanisms that regulate skeletal muscle mass.
Hornberger et al., Madison, United States. In Cell Signal, 2011
Not surprisingly, many of these molecules are intimately involved in the regulation of protein synthesis and protein degradation [e.g. the mammalian target of rapamycin (mTOR), eukaryotic initiation factor 2B (eIF2B), eukaryotic initiation factor 3f (eIF3f) and the forkhead box O (FoxO) transcription factors].
[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.
Eukaryotic type translation initiation factor 2: structure-functional aspects.
Garber et al., Moscow, Russia. In Biochemistry (mosc), 2011
There are also new data on initiation factors eIF5 and eIF2B that directly interact with eIF2 and control its participation in nucleotide exchange.
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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