Stressed SIRT7: facing a crossroad of senescence and immortality

被引：7
|
作者：
Liu, Jun-Ping [1 ,2 ,3 ]
Chen, Ruping [1 ]
机构：
[1] Hangzhou Normal Univ, Sch Med, Inst Aging Res, Hangzhou, Zhejiang, Peoples R China
[2] Monash Univ, Dept Immunol, Melbourne, Vic 3004, Australia
[3] Hudson Inst Med Res, Melbourne, Vic, Australia
来源：
CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY | 2015年 / 42卷 / 06期
关键词：
ageing; cancer; hematopoietic stem cells; immortality; longevity; senescence;
D O I：
10.1111/1440-1681.12423
中图分类号：
R9 [药学];
学科分类号：
1007 ;
摘要：
SIRT7 with coenzyme NAD catalyzes protein de-acetylation. In stress response, SIRT7 regulates protein folding in mitochondria with unknown mechanisms. Decreases in SIRT7 entrain hematopoietic stem cell senescence, but increasing SIRT7 causes elevation of hematopoietic stem cell regenerative function. We discuss the recent findings on SIRT7 and its binding proteins, NRF1 and GABP1, in decision making between the choices of inducing cell aging and immortality.
引用
收藏
页码：567 / 569
页数：3
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