Nuclear and mitochondrial apoptotic pathways of p53

Ute M. Moll, Alexander Zaika

Research output: Contribution to journalShort survey

163 Citations (Scopus)

Abstract

In contrast to p53-mediated cell cycle arrest, the mechanisms of p53-mediated apoptosis in response to cellular stresses such as DNA damage, hypoxia and oncogenic signals still remain poorly understood. Elucidating these pathways is all the more pressing since there is good evidence that the activation of apoptosis rather than cell cycle arrest is crucial in p53 tumor suppression. Moreover, the therapeutic interest in p53 as the molecular target of anticancer intervention rests mainly on its powerful apoptotic capability. This puzzling elusiveness suggests that p53 not only engages a plethora of downstream pathways but itself might possess a biochemical flexibility that goes beyond its role as a mere transcription factor. Recent evidence of a direct pro-apoptotic role of p53 protein at mitochondria suggests a synergistic effect with its transcriptional activation function and brings an unexpected new level of complexity into p53 apoptotic pathways.

Original languageEnglish (US)
Pages (from-to)65-69
Number of pages5
JournalFEBS Letters
Volume493
Issue number2-3
DOIs
StatePublished - Mar 30 2001
Externally publishedYes

Fingerprint

Cell Cycle Checkpoints
Chemical activation
Cells
Apoptosis
Mitochondria
Transcriptional Activation
DNA Damage
Tumors
Transcription Factors
DNA
Neoplasms
Proteins
Therapeutics
Hypoxia

Keywords

  • Apoptosis
  • Mitochondrial localization
  • p53
  • Stress-induced
  • Transcription factor

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Nuclear and mitochondrial apoptotic pathways of p53. / Moll, Ute M.; Zaika, Alexander.

In: FEBS Letters, Vol. 493, No. 2-3, 30.03.2001, p. 65-69.

Research output: Contribution to journalShort survey

Moll, Ute M. ; Zaika, Alexander. / Nuclear and mitochondrial apoptotic pathways of p53. In: FEBS Letters. 2001 ; Vol. 493, No. 2-3. pp. 65-69.
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