Abstract
p73 and p63 are evolving members of the p53 tumor suppressor family. TAp73 is a p73 isoform with a potent transcriptional activation domain, and loss of TAp73 predisposes mice to tumor development. In this issue of Genes & Development, Rufini and colleagues (pp. 2009-2014) discuss how TAp73-null mice display an aging phenotype that is due to mitochondrial dysfunction. Specifically, decreased levels of cytochrome C oxidase subunit 4 isoform 1 (Cox4i1) impair cytochrome C oxidase (COX) function, the multimeric enzyme that executes the last step in aerobic respiration. An emerging theme is that defects in metabolism account for both cancer and aging.
Original language | English (US) |
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Pages (from-to) | 1997-2000 |
Number of pages | 4 |
Journal | Genes and Development |
Volume | 26 |
Issue number | 18 |
DOIs | |
State | Published - Sep 15 2012 |
Keywords
- Aging
- Metabolism
- Mitochondria
- P53
- ROS
- Senescence
- p73
ASJC Scopus subject areas
- Genetics
- Developmental Biology