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 ?
Hydrogen sulfide prevents H2O2-induced senescence in human umbilical vein endothelial cells through SIRT1 activation.
The activation of the SIRT1 gene in humans implies this could be a potential mechanism for supplements to reduce aortic stiffness.
SIRT1 gene also knowns as 'longevity gene', products a protein deacetylase that has been reported to suppress cardiovascular pathologies such as myocardial infarction via anti-apoptosis, anti-inflammation, or increasing mitochondrial biogenesis in model organisms.
10) demonstrated that SIRT1 modulates the activity of RA SFs.
Of the selected candidate genes, only SIRT1 expression was significantly correlated with telomere length, mtDNA content, and annual [PM.
Due to its ability to enhance SIRT1, (4-6) which is called the longevity enzyme, resveratrol has been extensively studied for its wide array of benefits.
The role of SIRT1 is well understood in hypertrophy but not in hyperplasia, which is where Dr Mazloum's research was focused.
It has been reported that SIRT1 can regulate autophagy through the deacetylation of Atg5, Atg7, Atg8, and other autophagy mediators, which in turn plays an important role in the regulation of proliferation, metabolism, and stress resistance in different cells [17].
In recent years, resveratrol has been reported widely to be an activator of SIRT1 [7] and has been shown to reduce ischemia-reperfusion injury in kidneys [8].
We also assessed the effects of NOS inhibition on SIRT1 protein expression and metabolic modifications in skeletal muscle.
Their past work on the hypothalamus also had shown that SIRT1 function is dependent on energy levels in cells.