泛素连接酶
泛素
光形态发生
平方毫米
生物
细胞生物学
蛋白酶体
转录因子
调节器
小干扰RNA
无名指
突变体
细胞凋亡
基因
拟南芥
遗传学
转染
作者
David Dornan,Ingrid E. Wertz,Harumi Shimizu,David Arnott,Gretchen Frantz,Patrick J. Dowd,Karen O’Rourke,Hartmut Koeppen,Vishva M. Dixit
出处
期刊:Nature
[Springer Nature]
日期:2004-04-21
卷期号:429 (6987): 86-92
被引量:676
摘要
COP1 (constitutively photomorphogenic 1) is a RING-finger-containing protein that functions to repress plant photomorphogenesis, the light-mediated programme of plant development. Mutants of COP1 are constitutively photomorphogenic, and this has been attributed to their inability to negatively regulate the proteins LAF1 (ref. 1) and HY5 (ref. 2). The role of COP1 in mammalian cells is less well characterized. Here we identify the tumour-suppressor protein p53 as a COP1-interacting protein. COP1 increases p53 turnover by targeting it for degradation by the proteasome in a ubiquitin-dependent fashion, independently of MDM2 or Pirh2, which are known to interact with and negatively regulate p53. Moreover, COP1 serves as an E3 ubiquitin ligase for p53 in vitro and in vivo, and inhibits p53-dependent transcription and apoptosis. Depletion of COP1 by short interfering RNA (siRNA) stabilizes p53 and arrests cells in the G1 phase of the cell cycle. Furthermore, we identify COP1 as a p53-inducible gene, and show that the depletion of COP1 and MDM2 by siRNA cooperatively sensitizes U2-OS cells to ionizing-radiation-induced cell death. Overall, these results indicate that COP1 is a critical negative regulator of p53 and represents a new pathway for maintaining p53 at low levels in unstressed cells.
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