Activation of initiation factor 2 by ligands and mutations for rapid docking of ribosomal subunits.

Abstract

We previously identified mutations in the GTPase initiation factor 2 (IF2), located outside its tRNA-binding domain, compensating strongly (A-type) or weakly (B-type) for initiator tRNA formylation deficiency. We show here that rapid docking of 30S with 50S subunits in initiation of translation depends on switching 30S subunit-bound IF2 from its inactive to… (More)
DOI: 10.1038/emboj.2010.328

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