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p300/CBP/p53 interaction and regulation of the p53 response

S R Grossman1

  • 1Department of Adult Oncology and Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02115, USA. sgrossman@partners.org

European Journal of Biochemistry
|May 19, 2001
PubMed

Insights

The p300/CREB binding protein (CBP) coactivators are crucial for p53

Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Biochemistry

Background:

  • The p53 protein is a critical tumor suppressor involved in DNA damage response.
  • Coactivators like p300/CREB binding protein (CBP) and P/CAF are known to interact with p53.
  • Previous models suggested a straightforward role for p300/CBP in p53-mediated transactivation.

Purpose of the Study:

  • To investigate the complex regulatory roles of p300/CBP coactivators in p53 responses to DNA damage.
  • To elucidate the intricate molecular mechanisms governing the p53/p300/CBP interaction.
  • To understand how p300/CBP influence p53 transactivation and protein stability.

Main Methods:

  • Biochemical assays to study protein-protein interactions.
  • Acetylation assays to assess p53 modification.
  • Cellular assays to evaluate p53-dependent gene expression and cellular outcomes (growth arrest, apoptosis).

Main Results:

  • p300/CBP and P/CAF bind to and acetylate p53 following DNA damage.
  • These coactivators are essential for full p53 transactivation, growth arrest, and apoptosis.
  • p300/CBP act as complex signal integrators, modulating p53 activity and protein turnover in a context-dependent manner.

Conclusions:

  • The interaction between p53 and p300/CBP is more complex than previously thought.
  • p300/CBP play a dual role, both positively and negatively regulating p53 activity and stability.
  • Cellular context and stimuli like DNA damage critically influence the outcome of p300/CBP-p53 interactions.

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