Journal
TRENDS IN BIOCHEMICAL SCIENCES
Volume 32, Issue 1, Pages 1-4Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tibs.2006.11.002
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Funding
- NIA NIH HHS [R01 AG019972-01, R01 AG028730, R01 AG019972, R01 AG019972-03, T32 AG023480, R01 AG028730-01A1, R01 AG019719-05, R01 AG019972-02, R01 AG019972-04, T32 AG023480-05, P01 AG027916-010003, R01 AG019719-04, R01 AG019972-05, R01 AG019719, P01 AG027916] Funding Source: Medline
- NIGMS NIH HHS [R01 GM068072, R01 GM068072-01] Funding Source: Medline
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM068072] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG019972, T32AG023480, R01AG028730, P01AG027916, R01AG019719] Funding Source: NIH RePORTER
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Bacterial acetyl-coenzyme A (acetyl-CoA) synthetase (AceCS), an evolutionarily conserved enzyme that converts acetate to acetyl-CoA, is activated by sirtuin-mediated deacetylation. Two recent studies show that this mechanism of regulation is also crucial for mammalian AceCS activity, indicating that control of metabolism at the step of converting acetate to acetyl-CoA is conserved. These findings highlight a metabolic regulatory network controlled by sirtuins that has implications for the mechanisms of calorie restriction and modulation of mammalian lifespan.
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