Sirtuins, metabolism, and DNA repair

被引：107

作者：

Choi, Jee-Eun ^{[1
,2
]}

Mostoslavsky, Raul ^{[2
]}

机构：

[1] Harvard Univ, Biol & Biomed Sci Grad Program, Sch Med, Boston, MA 02115 USA

[2] Harvard Univ, Massachusetts Gen Hosp, Ctr Canc, Sch Med, Boston, MA 02114 USA

来源：

CURRENT OPINION IN GENETICS & DEVELOPMENT | 2014年 / 26卷

关键词：

FATTY-ACID OXIDATION; HISTONE DEACETYLASE SIRT6; TUMOR-SUPPRESSOR; CALORIE RESTRICTION; GENOMIC INSTABILITY; SKELETAL-MUSCLE; GENE-EXPRESSION; PROTEIN-KINASE; CONSERVED ROLE; CHROMATIN;

D O I：

10.1016/j.gde.2014.05.005

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Cells evolve to actively coordinate nutrient availability with cellular activity in order to maintain metabolic homeostasis. In addition, active pathways to repair DNA damage are crucial to avoid deleterious genomic instability. In recent years, it has become increasingly clear that availability of intermediate metabolites may play an important role in DNA repair, suggesting that these two seemingly distant cellular activities may be highly coordinated. The sirtuin family of proteins now described as deacylases (they can also remove acyl groups other than acetyl moieties), it appears to have evolved to control both metabolism and DNA repair. In this review, we discuss recent advances that lay the foundation to understanding the role of sirtuins in these two biological processes, and the potential crosstalk to coordinate them.

引用

页码：24 / 32

页数：9

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