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J Biol Chem. 2012 Dec 14;287(51):42436-43. doi: 10.1074/jbc.R112.404863. Epub 2012 Oct 18.

Mitochondrial protein acylation and intermediary metabolism: regulation by sirtuins and implications for metabolic disease.

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1
Gladstone Institute of Virology and Immunology, San Francisco, California 94158, USA.

Abstract

The sirtuins are a family of NAD(+)-dependent protein deacetylases that regulate cell survival, metabolism, and longevity. Three sirtuins, SIRT3-5, localize to mitochondria. Expression of SIRT3 is selectively activated during fasting and calorie restriction. SIRT3 regulates the acetylation level and enzymatic activity of key metabolic enzymes, such as acetyl-CoA synthetase, long-chain acyl-CoA dehydrogenase, and 3-hydroxy-3-methylglutaryl-CoA synthase 2, and enhances fat metabolism during fasting. SIRT5 exhibits demalonylase/desuccinylase activity, and lysine succinylation and malonylation are abundant mitochondrial protein modifications. No convincing enzymatic activity has been reported for SIRT4. Here, we review the emerging role of mitochondrial sirtuins as metabolic sensors that respond to changes in the energy status of the cell and modulate the activities of key metabolic enzymes via protein deacylation.

PMID:
23086951
PMCID:
PMC3522244
DOI:
10.1074/jbc.R112.404863
[Indexed for MEDLINE]
Free PMC Article
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