title: Stressed SIRT7: facing a crossroad of senescence and immortality.
abstract: 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 GABPβ1, in decision making between the choices of inducing cell aging and immortality.
authors.affiliation: Institute of Aging Research, Hangzhou Normal University School of Medicine, Hangzhou, Zhejiang, China.|Department of Immunology of Monash University, Hudson Institute of Medical Research, Melbourne, Vic., Australia.
authors.forename: Jun-Ping
authors.initials: JP
authors.lastname: Liu
authors.affiliation: Institute of Aging Research, Hangzhou Normal University School of Medicine, Hangzhou, Zhejiang, China.
authors.forename: Ruping
authors.initials: R
authors.lastname: Chen
mesh_terms: D000818:Animals; D016922:Cellular Senescence / Q000502:physiology*; D057809:HEK293 Cells; D006412:Hematopoietic Stem Cells / Q000378:metabolism*; D006801:Humans; D018384:Oxidative Stress / Q000502:physiology*; D037761:Sirtuins / Q000096:biosynthesis*
chemical_list: C510661:SIRT7 protein, human; D037761:Sirtuins
keywords: ageing; cancer; hematopoietic stem cells; immortality; longevity; senescence