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
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.