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SIRT1 interacts with p73 and suppresses p73-dependent transcriptional activity

Jin Ming Dai1, Zhi Yan Wang, Dao Chun Sun

  • 1Beijing Institute of Radiation Medicine, Beijing, China.

Journal of Cellular Physiology
|September 26, 2006
PubMed

Insights

The tumor suppressor p73, similar to p53, is regulated by SIRT1. SIRT1 binds to p73, reducing its transcriptional activity and apoptosis induction through deacetylation.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • The p53-related protein p73 shares sequence and functional similarities with p53.
  • Sirtuin 1 (SIRT1) is known to interact with p53 and repress its target gene expression.
  • The interaction and regulatory role of SIRT1 on p73 remain largely uncharacterized.

Purpose of the Study:

  • To investigate the interaction between SIRT1 and p73.
  • To determine if SIRT1 modulates p73-dependent transcriptional activity and apoptosis.
  • To elucidate the mechanism by which SIRT1 affects p73 function.

Main Methods:

  • Co-immunoprecipitation assays to detect SIRT1-p73 binding.
  • Reporter assays to measure p73 transcriptional activity.
  • Apoptosis assays to assess p73-induced cell death.
  • In vitro and in vivo deacetylation assays.

Main Results:

  • SIRT1 binds to p73 in human cells.
  • SIRT1 suppresses p73-dependent transcriptional activity.
  • SIRT1 partially inhibits p73-induced apoptosis.
  • SIRT1 deacetylates p73 protein both in vitro and in vivo.

Conclusions:

  • SIRT1 interacts with and negatively regulates the activity of p73.
  • SIRT1 modulates p73 function, including transcriptional activity and apoptosis induction, through deacetylation.
  • These findings reveal a novel regulatory mechanism for p73 by SIRT1, with implications for cancer biology.

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