Calorie restriction alters mitochondrial protein acetylation

被引：208

作者：

Schwer, Bjoern ^{[1
,2
]}

Eckersdorff, Mark ^{[3
]}

Li, Yu ^{[5
]}

Silva, Jeffrey C. ^{[5
]}

Fermin, Damian ^{[3
]}

Kurtev, Martin V. ^{[6
]}

Giallourakis, Cosmas ^{[1
,2
]}

Comb, Michael J. ^{[5
]}

Alt, Frederick W. ^{[1
,2
]}

Lombard, David B. ^{[1
,2
,3
,4
]}

机构：

[1] Childrens Hosp, Howard Hughes Med Inst, Program Cellular & Mol Med, Boston, MA 02115 USA

[2] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA

[3] Univ Michigan, Dept Pathol, Ann Arbor, MI 48109 USA

[4] Univ Michigan, Inst Gerontol, Ann Arbor, MI 48109 USA

[5] Cell Signaling Technol, Danvers, MA 01923 USA

[6] Harvard Univ, Sch Med, Dept Neurobiol, Boston, MA 02115 USA

来源：

AGING CELL | 2009年 / 8卷 / 05期

关键词：

calorie restriction; longevity; mass spectrometry; metabolism; mitochondria; sirtuins; LYSINE ACETYLATION; CELLS; LIVER;

D O I：

10.1111/j.1474-9726.2009.00503.x

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

P>Calorie restriction (CR) increases lifespan in organisms ranging from budding yeast through mammals. Mitochondrial adaptation represents a key component of the response to CR. Molecular mechanisms underlying this adaptation are largely unknown. Here we show that lysine acetylation of mitochondrial proteins is altered during CR in a tissue-specific fashion. Via large-scale mass spectrometry screening, we identify 72 candidate proteins involved in a variety of metabolic pathways with altered acetylation during CR. Mitochondrial acetylation changes may play an important role in the pro-longevity CR response.

引用

页码：604 / 606

页数：3

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