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10.15252/embj.201694966 http://scihub22266oqcxt.onion/10.15252/embj.201694966 C5350561!5350561!28242756     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       EMBO+J 2017 ; 36 (6): 736-50 Nephropedia Template TP {{tp|p=28242756|t=2017. ZRF1 is a novel S6 kinase substrate that drives the senescence programme |pdf=|usr=}}{{28242756}} gab.com Text ZRF1 is a novel S6 kinase substrate that drives the senescence programme JO: EMBO J http://www.kidney.de/pget.php?&tw=1&pmid=28242756 #FOAvip The inactivation of S6 kinases mimics several aspects of caloric restriction, including small body size, increased insulin sensitivity and longevity. However, the impact of S6 kinase activity on cellular senescence remains to be established. Here, we show that the constitutive activation of mammalian target of rapamycin complex 1 (mTORC1) by tuberous sclerosis complex (TSC) mutations induces a premature senescence programme in fibroblasts that relies on S6 kinases. To determine novel molecular targets linking S6 kinase activation to the control of senescence, we set up a chemical genetic screen, leading to the identification of the nuclear epigenetic factor ZRF1 (also known as DNAJC2, MIDA1, Mpp11). S6 kinases phosphorylate ZRF1 on Ser47 in cultured cells and in mammalian tissues in vivo. Knock?down of ZRF1 or expression of a phosphorylation mutant is sufficient to blunt the S6 kinase?dependent senescence programme. This is traced by a sharp alteration in p16 levels, the cell cycle inhibitor and a master regulator of senescence. Our findings reveal a mechanism by which nutrient sensing pathways impact on cell senescence through the activation of mTORC1?S6 kinases and the phosphorylation of ZRF1. Twit Text FOAVip ZRF1 is a novel S6 kinase substrate that drives the senescence programme ????EMBO J http://www.kidney.de/pget.php?&tw=1&pmid=28242756 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28242756 #FOAvip English Wikipedia <ref>{{Cite pmid|28242756}}</ref> ZRF1 is a novel S6 kinase substrate that drives the senescence programme #MMPMID28242756 Barilari M; Bonfils G; Treins C; Koka V; De Villeneuve D; Fabrega S; Pende M EMBO J 2017[Mar]; 36 (6): 736-50 PMID28242756show ga The inactivation of S6 kinases mimics several aspects of caloric restriction, including small body size, increased insulin sensitivity and longevity. However, the impact of S6 kinase activity on cellular senescence remains to be established. Here, we show that the constitutive activation of mammalian target of rapamycin complex 1 (mTORC1) by tuberous sclerosis complex (TSC) mutations induces a premature senescence programme in fibroblasts that relies on S6 kinases. To determine novel molecular targets linking S6 kinase activation to the control of senescence, we set up a chemical genetic screen, leading to the identification of the nuclear epigenetic factor ZRF1 (also known as DNAJC2, MIDA1, Mpp11). S6 kinases phosphorylate ZRF1 on Ser47 in cultured cells and in mammalian tissues in vivo. Knock?down of ZRF1 or expression of a phosphorylation mutant is sufficient to blunt the S6 kinase?dependent senescence programme. This is traced by a sharp alteration in p16 levels, the cell cycle inhibitor and a master regulator of senescence. Our findings reveal a mechanism by which nutrient sensing pathways impact on cell senescence through the activation of mTORC1?S6 kinases and the phosphorylation of ZRF1. äZRF1 is a novel S6 kinase substrate that drives the senescence program(epmc).pdf DeepDyve Pubget Overpricing