p53泛素化：Mdm2及其他相关蛋白
p53 ubiquitination: Mdm2 and beyond.
作者信息
Brooks Christopher L, Gu Wei
机构信息
Institute for Cancer Genetics and Department of Pathology, College of Physicians and Surgeons, Columbia University, 1150 St. Nicholas Avenue, New York, New York 10032, USA.
出版信息
Mol Cell. 2006 Feb 3;21(3):307-15. doi: 10.1016/j.molcel.2006.01.020.
Abstract
Although early studies have suggested that the oncoprotein Mdm2 is the primary E3 ubiquitin ligase for the p53 tumor suppressor, an increasing amount of data suggests that p53 ubiquitination and degradation are more complex than once thought. The discoveries of MdmX, HAUSP, ARF, COP1, Pirh2, and ARF-BP1 continue to uncover the multiple facets of this pathway. There is no question that Mdm2 plays a pivotal role in downregulating p53 activities in numerous cellular settings. Nevertheless, growing evidence challenges the conventional view that Mdm2 is essential for p53 turnover.
摘要
尽管早期研究表明癌蛋白Mdm2是p53肿瘤抑制因子的主要E3泛素连接酶，但越来越多的数据表明，p53的泛素化和降解比之前认为的更为复杂。MdmX、HAUSP、ARF、COP1、Pirh2和ARF - BP1的发现不断揭示该途径的多个方面。毫无疑问，Mdm2在众多细胞环境中下调p53活性方面起着关键作用。然而，越来越多的证据对Mdm2是p53周转所必需的传统观点提出了挑战。
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