1999
DOI: 10.1128/mcb.19.4.3224
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The β Subunit of Eukaryotic Translation Initiation Factor 2 Binds mRNA through the Lysine Repeats and a Region Comprising the C2-C2 Motif

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Cited by 24 publications
(48 citation statements)
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“…Both motifs have been implicated in mRNA binding and could aid in codon-anticodon interactions. (17) The lysine repeats furthermore mediate the mutually exclusive interaction of eIF5 and the e-subunit of eIF2B with eIF2b. (18) The a-subunit of eIF2 functions predominantly as a regulator of translation initiation.…”
Section: Introductionmentioning
confidence: 99%
“…Both motifs have been implicated in mRNA binding and could aid in codon-anticodon interactions. (17) The lysine repeats furthermore mediate the mutually exclusive interaction of eIF5 and the e-subunit of eIF2B with eIF2b. (18) The a-subunit of eIF2 functions predominantly as a regulator of translation initiation.…”
Section: Introductionmentioning
confidence: 99%
“…In the archaeal aIF2 complex, the C-terminal zinc-binding domain of aIF2b packs against the central a-b domain (Sokabe et al 2006;Yatime et al 2007). While the function of the zinc-binding domain has not been resolved, removal of this domain impairs RNA binding to isolated yeast eIF2b (Laurino et al 1999) and confers a dominant Gcd 2 and recessive lethal phenotype (CastilhoValavicius et al 1992), while point mutations confer a dominant Sui 2 phenotype CastilhoValavicius et al 1992).…”
Section: Ternary Complex Formationmentioning
confidence: 99%
“…30) As mentioned above, SUI1 and SUI3 encode the translation initiation factors eIF1 and eIF2β, respectively, which are involved in the recognition of initiation codons on mRNAs. [24][25][26] Despite the current lack of direct evidence, we speculate that the mutation of these factors might cause the His + phenotype by promoting translation of the His3 protein from codons, other than the AUG located within the region near the promoter. Given that mutations in the specific genes mentioned above were repeatedly isolated (note that more sui1 and sui3 mutants were isolated, but excluded from further analyses by testing whether plasmids containing the SUI1 or SUI3 gene suppressed the ts and His + phenotypes of the mutant strains), the genetic screen appeared to be saturated.…”
Section: Resultsmentioning
confidence: 99%
“…Furthermore, the endogenous SUI1 gene of these three strains contained a mutation within the open reading frame (ORF) (A63T, A63V, or G66S; Table 1), indicating that their His + phenotype was caused by these mutations. Similarly, a mutation in the SUI3 gene (L254Q ; Table 1), which encodes the β-subunit of eIF2, 25,26) was found to underlie the ts and His + phenotypes of the remaining ts strain.…”
Section: Resultsmentioning
confidence: 99%