SIRT1


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Related to SIRT1: SIRT2

SIRT1

A gene on chromosome 10q21.3 that encodes a widely expressed NAD-dependent protein deacetylase, which links transcriptional regulation to intracellular energetics and co-ordinates distinct cellular functions such as cell cycle, response to DNA damage, metabolism, apoptosis and autophagy. SIRT1 can modulate chromatin function by deacetylating histones and altering the methylation of histones and DNA, leading to transcriptional repression. It deacetylates a broad range of transcription factors and co-regulators, up- and downregulating target gene expression.
References in periodicals archive ?
Relative expression of miR142 was normalized with U6, and the relative expression of Sirt1 mRNA was normalized to GAPDH.
Guarente said he believes that NR is likely acting through a pathway that his lab previously identified, in which boosting NAD turns on not only SIRT1 but another gene called mTORC1, which stimulates protein synthesis in cells and helps them to proliferate.
SIRT1 overexpression is reportedly associated with cancer development through the triggering of DNA repair impairment and cell proliferation.
Dissecting systemic control of metabolism and aging in the NAD World: the importance of SIRT1 and NAMPT-mediated NAD biosynthesis.
To further verify that FOXL2 regulated gene, StAR and SIRT1 expression, we performed RT-PCR analyses to measure the endogenous mRNA expression of the StAR and SIRT1 gene following stimulation with both the WT and mutant FOXL2 proteins.
Oral NaB group showed decreased genetic expression of AMPK (0.04 fold, p<0.001), mTOR (0.30 fold, p=0.04), Akt (0.29 fold, p=0.67) and Sirt1 (0.83 fold, p=0.18).
That is, when glycolysis-dependent hyperinflammation was initiated, nuclear SIRT1 levels decreased, and when glycolysis shifted to fatty acid oxidation, levels of SIRT1 were restored [17].
It is well established that the expression of SIRT1 is negatively regulated by miR-34a [16].
Our previous work demonstrated that CD38 deficiency protects against obesity, hypertrophy, and myocardial ischemia/reperfusion injury through activating Sirt1 [11-13].
We pioneered the concept that [NAD.sup.+] redox and intermediary metabolism sensors sirtuin1 (SIRT1) and sirtuin6 (SIRT6) epigenetically reprogram the universal attributes of resistance to tolerance in monocytes by shifting glycolysis and glucose oxidation high energy use to the low energy state lipolysis by generating silent heterochromatin at selective sets of immune and metabolism fueling gene sets (TNF[alpha]) [4, 5] and maintaining open euchromatin at reciprocally functioning gene sets [6-8].
Several studies reported that FoxO1 interacts with Akt [22] and Sirtuin 1 (SIRT1) [23], affecting hepatic AdipoR1/R2 gene expression [24,25].