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PMID: 19007744 Published · ppublish English Journal Article Review

The mitochondrial p53 pathway.

Biochimica et biophysica acta ·Vol. 1787 ·No. 5 ·2009-05-00 ·Pages 414-20

Vaseva AV, Moll UM

Abstract

p53 is one of the most mutated tumor suppressors in human cancers and as such has been intensively studied for a long time. p53 is a major orchestrator of the cellular response to a broad array of stress types by regulating apoptosis, cell cycle arrest, senescence, DNA repair and genetic stability. For a long time it was thought that these functions of p53 solely rely on its function as a transcription factor, and numerous p53 target genes have been identified [1]. In the last 8 years however, a novel transcription-independent proapoptotic function mediated by the cytoplasmic pool of p53 has been revealed. p53 participates directly in the intrinsic apoptosis pathway by interacting with the multidomain members of the Bcl-2 family to induce mitochondrial outer membrane permeabilization. Our review will discuss these studies, focusing on recent advances in the field.

MeSH Terms
Apoptosis/genetics Brain Ischemia/pathology Cell Death Gene Expression Regulation, Neoplastic Genes, Tumor Suppressor Genes, bcl-2 Humans Kidney Diseases/pathology,physiopathology Mitochondria/physiology Neoplasms/genetics Protein Transport/physiology Reperfusion Injury/physiopathology Transcription, Genetic Tumor Suppressor Protein p53/genetics,metabolism,physiology
Chemicals
Tumor Suppressor Protein p53
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Vaseva Angelina V
Department of Pathology, Stony Brook University, Stony Brook, NY 11794, USA.
Moll Ute M
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Article Info
Journal
Biochimica et biophysica acta
Abbr.
Biochim Biophys Acta
ISSN
0006-3002
Published
2009-05-00
Epub
2008-00-25
Pages
414-20
Language
English
Region
Netherlands
NLM ID
0217513
PMCID
PMC2819081
Subset
IM
Grants
NCI NIH HHS · R01 CA060664 · United States
NCI NIH HHS · R01 CA060664-14A1 · United States
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