Bioinformatics and Systems Medicine Laboratory
General information | Expression | Regulation | Mutation | Interaction

Basic Information

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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