c-Abl tyrosine kinase activates p21 transcription via interaction with p53

J Biochem. 2007 May;141(5):621-6. doi: 10.1093/jb/mvm068. Epub 2007 Mar 4.

Abstract

c-Abl non-receptor tyrosine kinase has been implicated in many cellular processes including cell differentiation, stress response and regulating gene transcription. The mechanism by which c-Abl is involved in the regulation of gene transcription remains to be elucidated. In this study, we investigated the functions of c-Abl in the activation of p21 promoter. Our results showed that overexpression of c-Abl tyrosine kinase activated p21 promoter and endogenous p21 transcription in U2OS cells. We found that p53 is involved in the activation of p21 promoter by c-Abl, and integrative structure of p53 is required for regulating p21 transcription. In addition, the chromatin immunoprecipitation study demonstrated that c-Abl and p53 can be recruited to the region containing p53 binding site of p21 promoter, and c-Abl increases the DNA binding activity of p53 to the p21 promoter. Furthermore, not only the activation of p21 promoter but also the recruitment to p21 promoter by c-Abl is dependent on the interaction between c-Abl and p53 protein.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Line, Tumor
  • Chromatin Immunoprecipitation
  • Cyclin-Dependent Kinase Inhibitor p21 / genetics
  • Cyclin-Dependent Kinase Inhibitor p21 / metabolism*
  • Humans
  • Promoter Regions, Genetic / physiology
  • Proto-Oncogene Proteins c-abl / physiology*
  • Transcription, Genetic / physiology*
  • Tumor Suppressor Protein p53 / physiology*

Substances

  • CDKN1A protein, human
  • Cyclin-Dependent Kinase Inhibitor p21
  • Tumor Suppressor Protein p53
  • Proto-Oncogene Proteins c-abl