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General information | Expression | Regulation | Mutation | Interaction |
Basic Information |
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Gene ID | 23410 |
Name | SIRT3 |
Synonymous | SIR2L3;sirtuin 3;SIRT3;sirtuin 3 |
Definition | NAD-dependent deacetylase sirtuin-3, mitochondrial|SIR2-like protein 3|mitochondrial nicotinamide adenine dinucleotide-dependent deacetylase|silent mating type information regulation 2, S.cerevisiae, homolog 3|sir2-like 3|sirtuin type 3 |
Position | 11p15.5 |
Gene type | protein-coding |
Source | Count: 1; Generif |
Sentence |
Abstract |
"These results identify SIRT3 as a genomically expressed, mitochondria-localized tumor suppressor." | The sirtuin gene family (SIRT) is hypothesized to regulate the aging process and play a role in cellular repair. This work demonstrates that SIRT3(-/-) mouse embryonic fibroblasts (MEFs) exhibit abnormal mitochondrial physiology as well as increases in stress-induced superoxide levels and genomic instability. expression of a single oncogene (Myc or Ras) in SIRT3(-/-) MEFs results in in vitro transformation and altered intracellular metabolism. Superoxide dismutase prevents transformation by a single oncogene in SIRT3(-/-) MEFs and reverses the tumor-permissive phenotype as well as stress-induced genomic instability. In addition, SIRT3(-/-) mice develop ER/PR-positive mammary tumors. Finally, human breast and other human cancer specimens exhibit reduced SIRT3 levels. These results identify SIRT3 as a genomically expressed, mitochondria-localized tumor suppressor.CI - Copyright (c) 2010 Elsevier Inc. All rights reserved. |
"These results identify SIRT3 as a genomically expressed, mitochondria-localized tumor suppressor." | The sirtuin gene family (SIRT) is hypothesized to regulate the aging process and play a role in cellular repair. This work demonstrates that SIRT3(-/-) mouse embryonic fibroblasts (MEFs) exhibit abnormal mitochondrial physiology as well as increases in stress-induced superoxide levels and genomic instability. expression of a single oncogene (Myc or Ras) in SIRT3(-/-) MEFs results in in vitro transformation and altered intracellular metabolism. Superoxide dismutase prevents transformation by a single oncogene in SIRT3(-/-) MEFs and reverses the tumor-permissive phenotype as well as stress-induced genomic instability. In addition, SIRT3(-/-) mice develop ER/PR-positive mammary tumors. Finally, human breast and other human cancer specimens exhibit reduced SIRT3 levels. These results identify SIRT3 as a genomically expressed, mitochondria-localized tumor suppressor.CI - Copyright (c) 2010 Elsevier Inc. All rights reserved. |
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