Journal
JOURNAL OF CELL SCIENCE
Volume 126, Issue 1, Pages 274-288Publisher
COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.115188
Keywords
Sirtuin-3; Mitochondria; Hexokinase-2; Bak; Bax; Apoptosis; Cisplatin
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Funding
- National Institutes of Health [5R01CA118356, 5R01AA01287]
- NATIONAL CANCER INSTITUTE [R01CA118356] Funding Source: NIH RePORTER
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Sirtuin-3 exhibits properties of a tumor suppressor partly emanating from its ability to control the state of mitochondrial metabolism, with depletion of sirt-3 increasing tumor cell survival. In the present study we demonstrate that depletion of sirtuin-3 brings about an anti-apoptotic phenotype via stimulating cyclophilin-D activity, which promotes the binding of hexokinase II to the mitochondria, thereby preventing Bak/Bax dependent mitochondrial injury and cell death. By contrast, increased expression of sirtuin-3 decreases cyclophilin-D activity, resulting in detachment of hexokinase II from the mitochondria and potentiation of Bak- and Bax-induced mitochondrial injury and loss of cell viability.
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