Recruitment of p300/CBP in p53-dependent signal pathways

Cell. 1997 Jun 27;89(7):1175-84. doi: 10.1016/s0092-8674(00)80304-9.


The products of the p53 and CBP/p300 genes have been individually implicated in control of cell growth and regulation of transcription. p53 is known to act as a positive and negative regulator of gene expression. Here we show that p53, in both wild-type and mutant conformation, forms a specific protein complex with p300. However, in its wild-type but not mutant conformation, p53 inhibits a promoter containing the DNA-binding sequences for the transcription factor AP1, in a p300-dependent manner. p300 stimulates the transcriptional activity of p53 on p53-regulated promoters, and it enhances the responsiveness to a physiological upstream modulator of p53 function, ionizing radiation. A dominant negative form of p300 prevents transcriptional activation by p53, and it counteracts p53-mediated G1 arrest and apoptosis. The data implicate p300 as an important component of p53-signaling, thus providing new insight into the mechanisms of cellular proliferation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / physiology
  • Breast Neoplasms
  • CREB-Binding Protein
  • Cell Division / physiology
  • Cell Line
  • Chlorocebus aethiops
  • G1 Phase / physiology
  • Humans
  • Kidney / cytology
  • Mutagenesis / physiology
  • Nuclear Proteins / genetics
  • Nuclear Proteins / metabolism*
  • Signal Transduction / physiology*
  • Trans-Activators*
  • Transcription Factor AP-1 / metabolism
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*
  • Transcription, Genetic / physiology
  • Transfection
  • Tumor Cells, Cultured
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*


  • Nuclear Proteins
  • Trans-Activators
  • Transcription Factor AP-1
  • Transcription Factors
  • Tumor Suppressor Protein p53
  • CREB-Binding Protein
  • CREBBP protein, human