Tianjin Medical Journal

Tianjin Med J ›› 2015, Vol. 43 ›› Issue (11): 1338-1341.doi: 10.11958/j.issn.0253-9896.2015.11.031

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Research progress of regulation mechanism of MDMX and CK1α in p53 tumor suppressor protein

WEI Xi1， ZHANG Sheng1， GAO Ming2△#br#   

  1. 1 Department of Diagnostic and Therapeutic Ultrasonography, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, China； 2 Thyroid Cancer Department
  • Received:2015-06-09 Revised:2015-07-02 Published:2015-11-15 Online:2015-11-15
  • Contact: GAO Ming E-mail： gaoming68@aliyun.com E-mail:weixi198204@126.com

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Abstract: As a tumor suppressor, p53 is activated by numerous cellular and environmental signals, and plays a critical role in the cell cycle regulation, cell apoptosis and senenscence. The murine double minute (MDM)2 and double minute murine 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 MDMX in the cooperation to regulate p53 activity. The process of MDMX and CK1α in the regulation of p53 is multi-step and complicated. In this paper the mechanism of MDMX and CK1α in the regulation of p53 protein was reviewed.

Key words: tumor suppressor protein p53, casein kinase 1 alpha, p53, murine double minute 4