Journal
CELL DEATH AND DIFFERENTIATION
Volume 18, Issue 11, Pages 1692-1701Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/cdd.2011.35
Keywords
mRNA translation; microRNA; mRNA binding protein; Rho GTPase; apoptosis
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Funding
- French National Institute of Health and Medical research (INSERM)
- Claudius Regaud Institute
- 'Fondation pour la Recherche Medicale' (FRM) ('Equipe labellisee FRM')
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Of critical importance in the stress response is the post-transcriptional control of the expression of important genes involved in the control of cell survival and apoptosis. Here we report that miR-19, an oncogenic component of the miR-17-92/Oncomir-1 microRNA polycistron, regulates the expression of Ras homolog B (RhoB) in keratinocytes upon exposure to ultraviolet (UV) radiation. Strikingly, we could not find any evidence for deregulated expression of miR-19 during UV treatment. However, we show that miR-19-mediated regulation of antiapoptotic RhoB expression requires the binding of human antigen R (HuR), an AU-rich element binding protein, to the 30-untranslated region of the rhoB mRNA. We propose that the loss of the interdependent binding between HuR and miR-19 to the rhoB mRNA upon UV exposure relieves this mRNA from miR-19-dependent inhibition of translation and contributes to the apoptotic response. Cell Death and Differentiation (2011) 18, 1692-1701; doi: 10.1038/cdd.2011.35; published online 29 April 2011
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