| Literature DB >> 20067791 |
Hyung Chul Lee1, Nara Oh, Hana Cho, Junho Choe, Yoon Ki Kim.
Abstract
Human transforming growth factor-beta receptor type 2 (TGFbetaR2) mRNA harboring a premature translation termination codon (PTC) generated by frameshift mutation is targeted for nonsense-mediated translational repression (NMTR), rather than nonsense-mediated mRNA decay (NMD). Here we show that exon junction complex (EJC) downstream of a PTC plays an inhibitory role in translation of TGFbetaR2 mRNA. Translational repression by core EJC components occurs after formation of 80S ribosome complex, which is demonstrated using different types of internal ribosome entry sites (IRESes). Our findings implicate EJCs or core EJC components as negative regulators of translation. Copyright 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.Entities:
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Year: 2010 PMID: 20067791 DOI: 10.1016/j.febslet.2010.01.003
Source DB: PubMed Journal: FEBS Lett ISSN: 0014-5793 Impact factor: 4.124