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Mol Cell. 2012 Aug 24;47(4):648-55. doi: 10.1016/j.molcel.2012.06.027. Epub 2012 Jul 26.

LincRNA-p21 suppresses target mRNA translation.

Author information

1
Laboratory of Molecular Biology and Immunology, National Institute on Aging-Intramural Research Program, National Institutes of Health, Baltimore, MD 21224, USA.

Erratum in

  • Mol Cell. 2013 Apr 25;50(2):303.

Abstract

Mammalian long intergenic noncoding RNAs (lincRNAs) are best known for modulating transcription. Here we report a posttranscriptional function for lincRNA-p21 as a modulator of translation. Association of the RNA-binding protein HuR with lincRNA-p21 favored the recruitment of let-7/Ago2 to lincRNA-p21, leading to lower lincRNA-p21 stability. Under reduced HuR levels, lincRNA-p21 accumulated in human cervical carcinoma HeLa cells, increasing its association with JUNB and CTNNB1 mRNAs and selectively lowering their translation. With elevated HuR, lincRNA-p21 levels declined, which in turn derepressed JunB and β-catenin translation and increased the levels of these proteins. We propose that HuR controls translation of a subset of target mRNAs by influencing lincRNA-p21 levels. Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.

PMID:
22841487
PMCID:
PMC3509343
DOI:
10.1016/j.molcel.2012.06.027
[Indexed for MEDLINE]
Free PMC Article

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