Regulation of p53 stability and function by the deubiquitinating enzyme USP42

EMBO J. 2011 Nov 15;30(24):4921-30. doi: 10.1038/emboj.2011.419.

Abstract

The p53 tumour suppressor protein is a transcription factor that prevents oncogenic progression by activating the expression of apoptosis and cell-cycle arrest genes in stressed cells. The stability of p53 is tightly regulated by ubiquitin-dependent degradation, driven mainly by the ubiquitin ligase MDM2. In this study, we have identified USP42 as a DUB that interacts with and deubiquitinates p53. USP42 forms a direct complex with p53 and controls level of ubiquitination during the early phase of the response to a range of stress signals. Although we do not find a clear role for USP42 in controlling either the basal or fully activated levels of p53, the function of USP42 is required to allow the rapid activation of p53-dependent transcription and a p53-dependent cell-cycle arrest in response to stress. These functions of USP42 are likely to contribute to the repair and recovery of cells from mild or transient damage.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Cycle Checkpoints
  • Cell Line, Tumor
  • Humans
  • Protein Stability
  • Proto-Oncogene Proteins c-mdm2 / metabolism
  • RNA, Small Interfering / genetics
  • Stress, Physiological
  • Thiolester Hydrolases / genetics
  • Thiolester Hydrolases / metabolism*
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*

Substances

  • RNA, Small Interfering
  • Tumor Suppressor Protein p53
  • USP42 protein, human
  • MDM2 protein, human
  • Proto-Oncogene Proteins c-mdm2
  • Thiolester Hydrolases