SIRT2 is a negative regulator of anoxia-reoxygenation tolerance via regulation of 14-3-3 ζ and BAD in H9c2 cells

被引：68

作者：

Lynn, Edward G. ^{[1
]}

McLeod, Christopher J. ^{[1
]}

Gordon, Jeffrey P. ^{[1
]}

Bao, Jianjun ^{[1
]}

Sack, Michael N. ^{[1
]}

机构：

[1] NHLBI, Translat Med Branch, NIH, Bethesda, MD 20892 USA

来源：

FEBS LETTERS | 2008年 / 582卷 / 19期

基金：

美国国家卫生研究院;

关键词：

SIRT2; BAD; 14-3-3; zeta; H9c2; cells; anoxia-reoxygenation;

D O I：

10.1016/j.febslet.2008.07.016

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Knockdown or inhibition of SIRT2 enhances biological stress-tolerance. We extend this phenotype showing that SIRT2 knockdown reduces anoxia-reoxygenation injury in H9c2 cells. Gene array analysis following SIRT2 siRNA knockdown identifies 14-3-3 zeta as the most robustly induced gene. SIRT2 knockdown evokes induction of this chaperone, facilitating cytosolic sequestration of BAD with a corresponding reduction in mitochondrial BAD localization. Concurrent siRNA against SIRT2 and 14-3-3 zeta abolishes the SIRT2-depleted cytoprotective phenotype. SIRT2 functions to moderate cellular stress-tolerance, in part, by modulating the levels of 14-3-3 zeta with the concordant control of BAD subcellular localization. Published by Elsevier B. V. on behalf of the Federation of European Biochemical Societies.

引用

页码：2857 / 2862

页数：6

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