Nuclear respiratory factor 2 induces SIRT3 expression

被引：71
作者：
Satterstrom, F. Kyle [1 ,2 ]
Swindell, William R. [3 ,4 ]
Laurent, Gaelle [2 ]
Vyas, Sejal [2 ]
Bulyk, Martha L. [3 ,4 ,5 ]
Haigis, Marcia C. [2 ]
机构：
[1] Harvard Univ, Sch Engn & Appl Sci, Cambridge, MA 02138 USA
[2] Harvard Univ, Sch Med, Dept Cell Biol, Boston, MA 02115 USA
[3] Brigham & Womens Hosp, Dept Med, Div Genet, Boston, MA 02115 USA
[4] Harvard Univ, Sch Med, Boston, MA 02115 USA
[5] Brigham & Womens Hosp, Dept Pathol, Boston, MA 02115 USA
来源：
AGING CELL | 2015年 / 14卷 / 05期
关键词：
calorie restriction; dietary restriction; microarray analysis; nuclear respiratory factor 2; SIRT3; FATTY-ACID OXIDATION; TRANSCRIPTION FACTOR; CALORIE RESTRICTION; GENE-EXPRESSION; BINDING-SITES; GABP; ALPHA; IDENTIFICATION; DEACETYLASE; DEFICIENCY;
D O I：
10.1111/acel.12360
中图分类号：
Q2 [细胞生物学];
学科分类号：
071009 ; 090102 ;
摘要：
The mitochondrial deacetylase SIRT3 regulates several important metabolic processes. SIRT3 is transcriptionally upregulated in multiple tissues during nutrient stresses such as dietary restriction and fasting, but the molecular mechanism of this induction is unclear. We conducted a bioinformatic study to identify transcription factor(s) involved in SIRT3 induction. Our analysis identified an enrichment of binding sites for nuclear respiratory factor 2 (NRF-2), a transcription factor known to play a role in the expression of mitochondrial genes, in the DNA sequences of SIRT3 and genes with closely correlated expression patterns. Invitro, knockdown or overexpression of NRF-2 modulated SIRT3 levels, and the NRF-2 subunit directly bound to the SIRT3 promoter. Our results suggest that NRF-2 is a regulator of SIRT3expression and may shed light on how SIRT3 is upregulated during nutrient stress.
引用
收藏
页码：818 / 825
页数：8
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