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10.1080/15384101.2016.1152427

http://scihub22266oqcxt.onion/10.1080/15384101.2016.1152427
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C4889297!4889297!26940461
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suck abstract from ncbi


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pmid26940461      Cell+Cycle 2016 ; 15 (7): 1009-18
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  • Calorie restriction-induced SIRT6 activation delays aging by suppressing NF-?B signaling #MMPMID26940461
  • Zhang N; Li Z; Mu W; Li L; Liang Y; Lu M; Wang Z; Qiu Y; Wang Z
  • Cell Cycle 2016[]; 15 (7): 1009-18 PMID26940461show ga
  • Calorie restriction (CR) extends lifespan from yeast to mammals. SIRT6 is a member of the sirtuin family of NAD+-dependent histone deacetylases, which is responsible for mediating the effects of CR. The transcription factor NF-?B, which is involved in inflammation and aging, has been shown to be regulated by SIRT6. Here we describe the crucial role of SIRT6 in aging and inflammation. We show that CR had improved renal insufficiency and enhanced SIRT6 expression after 6-month treatment in aged mice. Culture cells in low glucose (LG) conditions also showed resistance to cell senescence and enhanced SIRT6 expression compared to normal glucose (NG) group, showing beneficial effects of the CR-mimic cultural conditions. Moreover, SIRT6 overexpression is sufficient to delay the replicative senescence of WI38 by attenuating NF-?B signaling, while SIRT6 knockdown results in accelerated cell senescence and overactive NF-?B signaling. These findings confirm the key status of CR and disclose the critical role of SIRT6 on aging and inflammation.
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