Research progress of regulation mechanism of MDMX and CK1αin p53 tumor suppressor protein
10.11958/j.issn.0253-9896.2015.11.031
- VernacularTitle:MDMX与CK1α对p53抑癌蛋白调节机制的研究进展
- Author:
Xi WEI
;
Sheng ZHANG
;
Ming GAO
- Publication Type:Journal Article
- Keywords:
tumor suppressor protein p53;
casein kinase 1 alpha;
p53;
murine double minute 4
- From:
Tianjin Medical Journal
2015;(11):1338-1341
- CountryChina
- Language:Chinese
-
Abstract:
As a tumor suppressor, p53 is activated by numerous cellular and environmental signals, and plays a criticalrole in the cell cycle regulation, cell apoptosis and senenscence. The murine double minute (MDM)2 and double minute mu?rine 4 (MDMX) are two important regulators. MDMX is a p53 binding protein with strong sequence homology to MDM2, but lacks ubiquitin ligase activity, and which is unable to target p53 for proteasomal degradation. MDMX regulates p53 activity through its binding with p53 and its postranscriptional modification. MDMX in the closed and open structure binds to p53 to regulate its activity. As the main partner of MDMX, casein kinase 1 alpha (CK1α) disrupts the intramolecular binding in MD?MX in the cooperation to regulate p53 activity. The process of MDMX and CK1αin the regulation of p53 is multi-step and complicated. In this paper the mechanism of MDMX and CK1αin the regulation of p53 protein was reviewed.
