Micromanagement of the mitochondrial apoptotic pathway by p53

Front Biosci (Landmark Ed). 2011 Jan 1;16:749-58. doi: 10.2741/3717.

Abstract

It is now well established that p53 is the primary arbiter of stress-response and the principal barrier to neoplastic processes at the cellular level. Perhaps the most potent weapon in p53's tumor suppressive arsenal is apoptosis, enacted as a last resort when all other remedies are exhausted. Initially, the mechanism was thought to be simply activation or repression of Bcl-2 family members by p53. More recently, evidence of a more rapid pathway emerged whereby p53 physically interacts with Bcl-2 family members to tip the balance toward apoptosis. This review details the multiple levels of regulation of mitochondrially-directed apoptosis by p53, including recent findings of how p53 translocation is regulated.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis / genetics*
  • Chloride Channels / metabolism
  • Genes, p53*
  • Humans
  • Mitochondria / drug effects
  • Mitochondria / physiology*
  • Mitochondrial Membrane Transport Proteins / metabolism
  • Protein Transport / drug effects
  • Proto-Oncogene Proteins c-bcl-2 / metabolism*
  • Tumor Suppressor Protein p53 / physiology*
  • bcl-2-Associated X Protein / physiology

Substances

  • CLIC4 protein, human
  • Chloride Channels
  • Mitochondrial Membrane Transport Proteins
  • Proto-Oncogene Proteins c-bcl-2
  • Tumor Suppressor Protein p53
  • bcl-2-Associated X Protein
  • mitochondrial permeability transition pore