The interaction between FOXO and SIRT1: tipping the balance towards survival
The interaction between FOXO and SIRT1: tipping the balance towards survival
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DOI：
10.1016/j.tcb.2004.07.006
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发表时间：
2004-08-01
影响因子：
19
通讯作者：
Partridge, L
中科院分区：
文献类型：
--
作者：
Giannakou, ME;Partridge, L
当过表达时，NAD依赖性蛋白脱乙酰基酶Sir 2延长芽殖酵母和线虫线虫的寿命。在蠕虫中，这种寿命的延长需要FOXO转录因子daf-16。最近的三篇文章集中在哺乳动物同源的Sir 2和FOXO强调了产生这种遗传相互作用的机制。哺乳动物SIRT 1使FOXO 3和/或FbXO 4脱乙酰基，从而减弱FOXO诱导的细胞凋亡并增强FOXO诱导的细胞周期停滞。SIRT 1可能通过将FOXO依赖性反应从细胞死亡转移到细胞存活来延长寿命。
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.