期刊
JOURNAL OF RECEPTORS AND SIGNAL TRANSDUCTION
卷 31, 期 2, 页码 139-146出版社
TAYLOR & FRANCIS LTD
DOI: 10.3109/10799893.2011.552914
关键词
Methylation; signal transduction; apoptosis
资金
- National Science Foundation of China [30870792, 81030025]
- Ministry of Science and Technology of China [973-2009CB918704]
- Special Funds of State Key Laboratories [2060204]
E2F1 promotes DNA damage-induced apoptosis and the post-translational modifications of E2F1 play an important role in the regulation of E2F1-mediated cell death. Here, we found that Set9 and LSD1 regulate E2F1-mediated apoptosis upon DNA damage. Set9 methylates E2F1 at lysine 185, a conserved residue in the DNA-binding domain of E2F family proteins. The methylation of E2F1 by Set9 leads to the stabilization of E2F1 and up-regulation of its proapoptotic target genes p73 and Bim, and thereby induces E2F1-mediated apoptosis in response to genotoxic agents. We also found that LSD1 demethylates E2F1 at lysine 185 and reduces E2F1-mediated cell death. The identification of the methylation/demethylation of E2F1 by Set9/LSD1 suggests that E2F1 is dynamically regulated by epigenetic enzymes in response to DNA damage.
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