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Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

The ARF/oncogene pathway activates p53 acetylation within the DNA binding domain

Hestia Mellert1, Stephen M Sykes, Maureen E Murphy

  • 1Biomedical Graduate Studies, University of Pennsylvania, Philadelphia, Pennsylvania, USA.

Cell Cycle (Georgetown, Tex.)
|May 31, 2007
PubMed

Insights

Cellular stress stabilizes the p53 tumor suppressor through distinct pathways. Both DNA damage and oncogene activation pathways induce acetylation of p53 at lysine 120, a critical modification for its tumor-suppressing function.

Area of Science:

  • Molecular Biology
  • Cellular Biology
  • Cancer Research

Background:

  • p53 tumor suppressor stabilization is crucial for cellular stress response.
  • Two pathways, DNA damage response and p19ARF/oncogene activation, mediate p53 stabilization.
  • The p19ARF pathway's impact on p53 post-translational modifications is less understood compared to the DNA damage pathway.

Purpose of the Study:

  • To investigate the post-translational modifications of p53 induced by different cellular stress pathways.
  • To determine if the p19ARF pathway, similar to the DNA damage pathway, affects p53 modification.
  • To confirm the role of p53 acetylation at lysine 120 in response to oncogene-induced stress.

Main Methods:

  • Analysis of p53 modifications in response to genotoxic stress.
  • Investigation of p53 stabilization and modification following oncogene activation and p19ARF induction.
  • Site-specific analysis of p53 acetylation at lysine 120.

Main Results:

  • Both DNA damage response and p19ARF/oncogene stress pathways lead to p53 stabilization.
  • Acetylation of p53 at lysine 120 is induced by both pathways.
  • This specific acetylation event is essential for p53's tumor-suppressive apoptotic function and is impaired in tumor-derived mutations.

Conclusions:

  • Acetylation of p53 at lysine 120 is a common modification event occurring via both DNA damage and oncogene stress response pathways.
  • This modification is a key mechanism linking cellular stress to p53's tumor suppressor activity.
  • Understanding this conserved modification provides insights into cancer development and potential therapeutic strategies.

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