2018年5月2日 · Molecularly, ATM phosphorylates SIRT6 deacetylase and thus prevents MDM2-mediated ubiquitination and proteasomal degradation. Extra copies of Sirt6 extend lifespan in Atm-/-mice, with restored metabolic homeostasis. Moreover, the treatment with CQ remarkably extends lifespan of Caenorhabditis elegans, but not the ATM-1 mutants. In a progeria ...

2018年5月2日 · Molecularly, ATM phosphorylates SIRT6 deacetylase and thus prevents MDM2-mediated ubiquitination and proteasomal degradation. Extra copies of Sirt6 extend lifespan in Atm-/- mice, with restored metabolic homeostasis. Moreover, the treatment with CQ remarkably extends lifespan of Caenorhabditis elegans, but not the ATM-1 mutants.

2015年12月29日 · H2AX stabilization is mediated by the ATM kinase, sirtuin protein SIRT6, and ISWI family chromatin remodeler SNF2H. This enables efficient γH2AX foci formation and DSB repair even in the quiescent cellular state in which cells rarely express H2AX.

2019年5月21日 · Sirt6 transgenic mice show reduced fat mass, lower LDL cholesterol and triglyceride levels, and improved glucose tolerance, and these effects are mediated by suppression of PPARγ target genes 19....

2015年12月29日 · Our results reveal a pathway controlled by ATM, SIRT6, and SNF2H to block HUWE1, which stabilizes H2AX and induces its incorporation into chromatin only when cells are damaged.

2019年10月30日 · Another study in C. elegans deficient for the DNA repair factor Atm, which display reduced lifespan, increased copies of Sirt6 restore lifespan and metabolic homeostasis . Mechanistically, ATM phosphorylates SIRT6, thus preventing MDM2-mediated degradation.

Sirtuin6(SIRT6)是一种组蛋白去乙酰化酶，可参与调控DNA损伤修复。 已有研究报道，SIRT6可以通过减轻血管平滑肌细胞的DNA损伤缓解小鼠动脉粥样硬化。 然而，目前关于SIRT6是否通过影响DNA损伤调控血管钙化尚不清楚。

2021年5月28日 · Here, we show that SIRT6 overexpression leads to a reduction in frailty and lifespan extension in both male and female B6 mice. A combination of physiological assays, in vivo multi-omics analyses...

2015年12月29日 · H2AX Ser139, the ATM phosphorylation site, was essential for H2AX stabilization upon DSB formation. Our results reveal a pathway controlled by ATM, SIRT6, and SNF2H to block HUWE1, which stabilizes H2AX and induces its incorporation into chromatin only when cells are damaged.

Our results reveal a pathway controlled by ATM, SIRT6, and SNF2H to block HUWE1, which stabilizes H2AX and induces its incorporation into chromatin only when cells are damaged.