SIRT6

SIRT6

A gene on chromosome 19p13.3 that encodes an NAD-dependent protein deacetylase that acts on Lys-9 of histone H3 at NF-kappaB target promoters, downregulating a subset of NF-kappaB target genes. Its deacetylation of nucleosomes interferes with RELA binding to target DNA. It may be required for the association of WRN with telomeres during S-phase and for normal telomere maintenance and genomic stability. It is required for normal IGF1 serum levels and glucose homeostasis. SIRT 6 modulates cell senescence and apoptosis and regulates TNF production.
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References in periodicals archive ?
On the April 11, (https://science.sciencemag.org/content/early/2019/04/10/science.aax4558) Science released a notice  declaring that it is retracting the report after a series of investigations conducted by the University of Cambridge on the paper entitled "Human SIRT6 promotes DNA end resection through CtIP deacetylation."
The RF current, like SIRT6, upregulates Sirtuin genes while downregulating SIRT1, 3, 5, and 7, resulting in new collagen formation and increased fibroblast survival.
These increase the function of the enzyme sirtuin 6 (SIRT6) in cancer cells, regulation of this enzyme could open up new avenues for cancer treatment, revealed the researchers from the University of Eastern Finland
SIRT1 and SIRT6 are mainly located in the nucleus, whereas SIRT2 is mainly present in the cytoplasm.
Similarly, in Sirt6-knockout ESCs, the expression of Oct4, Sox2, and Nanog (the downstream of Sirt6) is inhibited and the upregulation of Tet enzymes and the significant increase of DNA 5hmC are found, resulting in ESC skewed development towards neuroectoderm [68].
Lappas, "SIRT6 is decreased with preterm labor and regulates key terminal effector pathways of human labor in fetal membranes," Biology of Reproduction, vol.
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].
demonstrated that SIRT6 protein expression is downregulated in atherosclerotic plaques of diabetics, and this defect is linked to the chronic oxidative stress condition [6].
SIRT6 promotes DNA repair under stress by activating PARP1.
In contrast, SIRT6 protein levels are reported to be moderately increased in the same arthritis experimental model (12).
A similar method has been used to determine the binding constants for several flavonoids with the histone deacetylase SIRT6 and to characterize the ability of these agents to displace quercetin from SIRT6 (35).