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 (sûr′to͞o-ĭn, -tyo͞o-)
Any of a family of enzymes that occur in all living organisms and are thought to regulate cellular aging, apoptosis, and resistance to stress in more complex eukaryotic organisms.

[Alteration of Sir2, name of the first gene coding for the synthesis of such enzymes to be isolated (short for s(ilent mating-type) i(nformation) r(egulation) 2, so called because the gene silences the expression of genes relating to the two mating types of the yeast from which it was isolated ) + -in.]


a protein that regulates cell metabolism and ageing
References in periodicals archive ?
Relationship between mitochondrial DNA copy number and SIRT1 expression in porcine oocytes.
full) premature aging of the arteries by activating SIRT1 - a gene that slows down the aging.
MicroRNA-target interactions databases confirm that miR-373-3p has experimentally validated strong relation to SIRT1 gene which has multiple cardioprotective functions.
It has also been documented that the inhibition of SIRT1 and SIRT2 decreases the toll-like receptor (TLR)-induced activation of macrophages and the production of pro-inflammatory cytokines and other mediators by blocking the activation of mitogen-activated protein kinase (MAPK) and MAPK/extracellular signal-regulated kinase (9).
Formal mediation analysis was performed to explore the role of SIRT1 and telomere length as mediators of the association between exposure to particulate air pollution and markers of aging.
The deacetylase activity of SIRT1 largely depends on nicotinamide adenine dinucleotide (NAD+) and nicotinamide phosphoribosyltransferase (NAMPT) is the rate limiting enzyme in the biosynthesis of NAD+ (Preyat and Leo 2013).
Sirtuin1 or simply SIRT1 is a gene involved in the regulation of cellular energy metabolism and functions as a cellular supervisor by preventing DNA damage and regulating gene transcription.
For this reason we wanted to understand more about the precise mechanisms by which SIRT1 affects metabolism.
Several reports have shown that SIRT1 expression is a prognostic indicator for many cancers including GC [18-20].
dependent histone deacetylase, and the p53 gene was the first SIRT1 deacetylation nonhistone target to be discovered [4, 5].
In skeletal muscle cells, SIRT1 regulates mitochondrial biogenesis and fatty acid oxidation via deacetylation and activation of PGC-1[alpha] (Gerhart-Hines et al.
They showed that increasing the expression of a protein called SIRT1 in the mouse hypothalamus increased the mouse lifespan, mimicking the effects of a calorie-restricted diet.