p53 moves to mitochondria: a turn on the path to apoptosis

Cell Cycle. 2004 Jul;3(7):836-9. Epub 2004 Jul 4.

Abstract

It has been said that no matter which direction cancer research turns, the p53 tumor suppressor protein comes into view. The widespread role of p53 as a suppressor of tumor development is believed to rely on its ability to induce programmed cell death in response to stress, either the replicative stress associated with uncontrolled cellular proliferation, or the environmental stresses that accompany tumor development, such as hypoxia. For some time it has been believed that the role of p53 in inducing apoptosis in response to such stress was as a master regulator coordinating the expression of other molecules whose ultimate role was the execution of the cell. New data, however, suggest that p53 itself also has a direct role in accomplishing cell death, at the mitochondria.

Publication types

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

MeSH terms

  • Apoptosis / physiology*
  • Cytochromes c / metabolism
  • Humans
  • Mitochondria / genetics
  • Mitochondria / metabolism*
  • Neoplasms / genetics
  • Neoplasms / metabolism*
  • Protein Isoforms / genetics
  • Protein Isoforms / metabolism
  • Protein Transport / physiology
  • Stress, Physiological / genetics
  • Stress, Physiological / metabolism*
  • Tumor Suppressor Protein p53 / genetics
  • Tumor Suppressor Protein p53 / metabolism*
  • bcl-2 Homologous Antagonist-Killer Protein / metabolism

Substances

  • BAK1 protein, human
  • Protein Isoforms
  • Tumor Suppressor Protein p53
  • bcl-2 Homologous Antagonist-Killer Protein
  • Cytochromes c