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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 p53 family and programmed cell death

E C Pietsch1, S M Sykes, S B McMahon

  • 1Division of Medical Sciences, Fox Chase Cancer Center, Philadelphia, PA 19107, USA.

Oncogene
|October 29, 2008
PubMed

Insights

The p53 tumor suppressor, along with its homologs p63 and p73, induces apoptosis to eliminate damaged cells. This review details how these proteins decide between growth arrest and cell death, influenced by modifications and interactions.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Cellular Stress Response

Background:

  • p53 is a critical tumor suppressor frequently mutated in human cancers.
  • p53's tumor suppressor function is mediated by inducing apoptosis in stressed cells.
  • p53 has homologs, p63 and p73, that also contribute to apoptosis.

Purpose of the Study:

  • To review the mechanisms by which p53, p63, and p73 induce apoptosis.
  • To focus on factors governing the decision between growth arrest and apoptosis.
  • To examine post-translational modifications and protein-protein interactions influencing this decision.

Main Methods:

  • Literature review of apoptosis induction mechanisms.
  • Analysis of factors mediating cell fate decisions (growth arrest vs. apoptosis).
  • Examination of post-translational modifications and protein interactions.

Main Results:

  • p53, p63, and p73 are key mediators of apoptosis.
  • The decision between growth arrest and apoptosis is complex.
  • Post-translational modifications and protein interactions critically regulate p53 family function.

Conclusions:

  • p53, p63, and p73 play vital roles in tumor suppression via apoptosis.
  • Understanding the regulatory mechanisms is crucial for cancer therapy.
  • Further research into protein interactions and modifications can reveal therapeutic targets.

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