期刊
TRENDS IN CELL BIOLOGY
卷 14, 期 8, 页码 408-412出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tcb.2004.07.006
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资金
- Biotechnology and Biological Sciences Research Council [SF19106] Funding Source: researchfish
- Biotechnology and Biological Sciences Research Council [SF19106] Funding Source: Medline
When overexpressed, the NAD-dependent protein deacetylase Sir2 extends the lifespan of both budding yeast and the nematode worm Caenorhabditis elegans. In the worm, this extension of lifespan requires the FOXO transcription factor daf-16. Three recent articles focusing on mammalian homologues of Sir2 and FOXO have highlighted the mechanisms that generate this genetic interaction. Mammalian SIRT1 deacetylates FOXO3 and/or FbXO4, thus attenuating FOXO-induced apoptosis and potentiating FOXO-induced cell-cycle arrest. SIRT1 might increase longevity by shifting FOXO dependent responses away from cell death and towards cell survival.
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