Calorie Restriction Promotes Mammalian Cell Survival by Inducing the SIRT1 Deacetylase | Zendy

Haim Cohen | Zendy; Christine Miller | Zendy; Kevin J. Bitterman | Zendy; Nathan R. Wall | Zendy; Brian Hekking | Zendy; Benedikt M. Kessler | Zendy; Konrad T. Howitz | Zendy; Myriam Gorospe | Zendy; Rafael de Cabo | Zendy; David Sinclair | Zendy

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Calorie Restriction Promotes Mammalian Cell Survival by Inducing the SIRT1 Deacetylase

Author(s) -

Haim Cohen,

Christine Miller,

Kevin J. Bitterman,

Nathan R. Wall,

Brian Hekking,

Benedikt M. Kessler,

Konrad T. Howitz,

Myriam Gorospe,

Rafael de Cabo,

David Sinclair

Publication year - 2004

Publication title -

science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 12.556

H-Index - 1186

eISSN - 1095-9203

pISSN - 0036-8075

DOI - 10.1126/science.1099196

Subject(s) - calorie restriction , apoptosis , microbiology and biotechnology , programmed cell death , ku70 , biology , growth factor , endocrinology , chemistry , medicine , cancer research , dna damage , biochemistry , dna , receptor

A major cause of aging is thought to result from the cumulative effects of cell loss over time. In yeast, caloric restriction (CR) delays aging by activating the Sir2 deacetylase. Here we show that expression of mammalian Sir2 (SIRT1) is induced in CR rats as well as in human cells that are treated with serum from these animals. Insulin and insulin-like growth factor 1 (IGF-1) attenuated this response. SIRT1 deacetylates the DNA repair factor Ku70, causing it to sequester the proapoptotic factor Bax away from mitochondria, thereby inhibiting stress-induced apoptotic cell death. Thus, CR could extend life-span by inducing SIRT1 expression and promoting the long-term survival of irreplaceable cells.

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