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[泛素蛋白连接酶MDM2活性与稳定性调控研究进展]

[Progress in regulation of activity and stability of ubiquitin protein ligase MDM2].

作者信息

Nie Jing, Tian Chun-Yan

机构信息

Department of Biological Sciences and Technology, Tsinghua University, Beijing 100084, China.

出版信息

Yi Chuan. 2009 Oct;31(10):993-8. doi: 10.3724/sp.j.1005.2009.00993.

Abstract

The ubiquitin protein ligase (E3) MDM2 (Murine double minute 2) possesses oncogenic activities. Overexpression of this protein enhances degradation and inactivation of the tumor suppressor p53. At least 7% of all human tumors exhibit inappropriate amplification of mdm2, whereas p53 gene remains in its wild-type configuration. This indicates that MDM2 may function in the p53-independent manner to promote tumorigenesis. Considering the critical role of MDM2, this review summarizes the current mechanisms and progress on MDM2 regulation in levels of gene control, mRNA transcription, post-translational modification, and interaction proteins.

摘要

泛素蛋白连接酶(E3)MDM2(小鼠双微体2)具有致癌活性。该蛋白的过表达会增强肿瘤抑制因子p53的降解和失活。在所有人类肿瘤中,至少7%表现出mdm2的不适当扩增,而p53基因仍处于野生型状态。这表明MDM2可能以不依赖p53的方式发挥作用来促进肿瘤发生。鉴于MDM2的关键作用,本综述总结了目前在基因控制、mRNA转录、翻译后修饰和相互作用蛋白水平上MDM2调控的机制和进展。

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