期刊
GENES & DEVELOPMENT
卷 25, 期 3, 页码 220-225出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.607011
关键词
DNA damage; pre-mRNA 3 '-end processing; polyadenylation; p53 tumor suppressor; hnRNP H; hnRNP F
资金
- INSERM
- Institut Claudius Regaud
- FRM (Equipe FRM, Soutenue par la Fondation Recherche Medicale)
- Fondation RITC (Recherche et Innovation Therapeutique en Cancerologie)
- ARC (Association pour la Recherche sur le Cancer)
- FRM
Following DNA damage, mRNA 39-end formation is inhibited, contributing to repression of mRNA synthesis. Here we investigated how DNA-damaged cells accomplish p53 mRNA 39-end formation when normal mechanisms of pre-mRNA 39-end processing regulation are inhibited. The underlying mechanism involves the interaction between a G-quadruplex structure located downstream from the p53 cleavage site and hnRNP H/F. Importantly, this interaction is critical for p53 expression and contributes to p53-mediated apoptosis. Our results uncover the existence of a specific rescue mechanism of 39-end processing regulation allowing stress-induced p53 accumulation and function in apoptosis.
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