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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, Insulin
Papers on eIF2B
The eIF2B-interacting domain of RGS2 protects against GPCR agonist-induced hypertrophy in neonatal rat cardiomyocytes.
New
Nguyen et al., London, Canada. In Cell Signal, 24 Mar 2014
However, RGS2 is known to have additional functions beyond its activity as a GTPase accelerating protein, such as the ability to bind to eukaryotic initiation factor, eIF2B, and inhibit protein synthesis.
Analysis of the subunit organization of the eIF2B complex reveals new insights into its structure and regulation.
New
Proud et al., Southampton, United Kingdom. In Faseb J, 14 Mar 2014
UNLABELLED: Eukaryotic initiation factor 2B (eIF2B) is the guanine nucleotide exchange factor for eIF2 and a critical regulator of protein synthesis, (e.g., as part of the integrated stress response).
eIF2B promotes eIF5 dissociation from eIF2*GDP to facilitate guanine nucleotide exchange for translation initiation.
New
Pavitt et al., Manchester, United Kingdom. In Genes Dev, Jan 2014
In this study, we used protein-protein interaction and nucleotide exchange assays to monitor the kinetics of eIF2 release from the eIF2•GDP/eIF5 GDI complex and determine the effect of eIF2B on this release.
DYRK2 negatively regulates cardiomyocyte growth by mediating repressor function of GSK-3β on eIF2Bε.
Hardt et al., Heidelberg, Germany. In Plos One, 2012
A central regulator of translation initiation is Eukaryotic initiation factor 2B (eIF2B).
Vanishing white matter disease caused by EIF2B2 mutation with the presentation of an adrenoleukodystrophy phenotype.
GeneRIF
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.
Impact
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.
GeneRIF
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.
Review
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].
GeneRIF
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.
GeneRIF
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.
Review
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.
GeneRIF
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.
Leukoencephalopathy with vanishing white matter: a review.
Review
van der Knaap et al., Amsterdam, Netherlands. In J Neuropathol Exp Neurol, 2010
Vanishing white matter is caused by mutations in any of the genes encoding the 5 subunits of the eukaryotic translation initiation factor 2B (eIF2B), EIF2B1 through EIF2B5.
Roles of GSK3 in metabolic shift toward abnormal anabolism in cell senescence.
Review
Yoon et al., Suwŏn, South Korea. In Ann N Y Acad Sci, 2010
Anabolism was accomplished through glycogen synthase, eIF2B, and SREBP1.
eIF5 has GDI activity necessary for translational control by eIF2 phosphorylation.
Impact
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.
Protein synthesis and its control in neuronal cells with a focus on vanishing white matter disease.
Review
Proud et al., Manchester, United Kingdom. In Biochem Soc Trans, 2009
VWM/CACH is caused by mutations in the translation initiation factor, eIF2B, a component of the basal translational machinery in all cells.
Vanishing white matter disease.
Review
Impact
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.
Impact
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).
Defective translational control facilitates vesicular stomatitis virus oncolysis.
Impact
Barber et al., Miami, United States. In Cancer Cell, 2004
Nevertheless, eIF2B-mediated guanine nucleotide exchange activity downstream of eIF2 was frequently aberrant in transformed cells, neutralizing eIF2alpha phosphorylation and permitting VSV mRNA translation.
Uncharged tRNA-phosphofructokinase interaction in amino acid deficiency.
Rabinovitz, Bethesda, United States. In Amino Acids, 1996
This diphosphate has been shown to be the proximate effector binding to eIF-2B, the guanine nucleotide exchange factor (Singh, L. P. Arror, A. R. and Wahba, A. J. (1994), FASEB J. 8: 279) which by releasing GDP bound to the inactive GDP: eIF-2 complex, permits the factor to initiate a new peptide chain.
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