泛素蛋白连接酶MDM2(Murine double minute 2)具有癌基因活性, MDM2高表达会导致抑癌基因p53失活而诱发肿瘤, 但在至少7%的肿瘤中p53基因正常而mdm2异常扩增, 表明MDM2还具有其他底物分子, 以p53不依赖的方式促进肿瘤的发生。鉴于MDM2的重要作用, 文章在基因水平、转录水平、翻译后修饰水平、相互作用分子的调节等方面系统总结了目前对MDM2调控的主要研究机制及其进展。

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.