Nonsense-mediated translational repression involves exon junction complex downstream of premature translation termination codon
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Updated: Jun 17, 2026

Identification of Footprints of RNA:Protein Complexes via RNA Immunoprecipitation in Tandem Followed by Sequencing (RIPiT-Seq)
Published on: July 10, 2019
Hyung Chul Lee1, Nara Oh, Hana Cho
1School of Life Sciences and Biotechnology, Korea University, Seoul, Republic of Korea.
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.
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