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10.1016/j.cell.2016.04.012 http://scihub22266oqcxt.onion/10.1016/j.cell.2016.04.012 C4889222!4889222!27133168     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell 2016 ; 165 (5): 1209-23 Nephropedia Template TP {{tp|p=27133168|t=2016. Two Conserved Histone Demethylases Regulate Mitochondrial Stress-Induced Longevity |pdf=|usr=}}{{27133168}} gab.com Text Two Conserved Histone Demethylases Regulate Mitochondrial Stress-Induced Longevity JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=27133168 #FOAvip Across eukaryotic species, mild mitochondrial stress can have beneficial effects on the lifespan of organisms. Mitochondrial dysfunction activates an unfolded protein response (UPRmt), a stress signaling mechanism designed to ensure mitochondrial homeostasis. Perturbation of mitochondria during larval development in C. elegans not only delays aging but also maintains UPRmt signaling, suggesting an epigenetic mechanism that modulates both longevity and mitochondrial proteostasis throughout life. We identify the conserved histone lysine demethylases jmjd-1.2/PHF8 and jmjd-3.1/JMJD3 as positive regulators of lifespan in response to mitochondrial dysfunction across species. Reduction-of-function of the demethylases potently suppresses longevity and UPRmt induction while gain-of-function is sufficient to extend lifespan in an UPRmt-dependent manner. A systems genetics approach in the BXD mouse reference population further indicates conserved roles of the mammalian orthologs in longevity and UPRmt signaling. These findings illustrate an evolutionary conserved epigenetic mechanism that determines the rate of aging downstream of mitochondrial perturbations. Twit Text FOAVip Two Conserved Histone Demethylases Regulate Mitochondrial Stress-Induced Longevity ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=27133168 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27133168 #FOAvip English Wikipedia <ref>{{Cite pmid|27133168}}</ref> Two Conserved Histone Demethylases Regulate Mitochondrial Stress-Induced Longevity #MMPMID27133168 Merkwirth C; Jovaisaite V; Durieux J; Matilainen O; Jordan SD; Quiros PM; Steffen KK; Williams EG; Mouchiroud L; Uhlein SN; Murillo V; Wolff SC; Shaw RJ; Auwerx J; Dillin A Cell 2016[May]; 165 (5): 1209-23 PMID27133168show ga Across eukaryotic species, mild mitochondrial stress can have beneficial effects on the lifespan of organisms. Mitochondrial dysfunction activates an unfolded protein response (UPRmt), a stress signaling mechanism designed to ensure mitochondrial homeostasis. Perturbation of mitochondria during larval development in C. elegans not only delays aging but also maintains UPRmt signaling, suggesting an epigenetic mechanism that modulates both longevity and mitochondrial proteostasis throughout life. We identify the conserved histone lysine demethylases jmjd-1.2/PHF8 and jmjd-3.1/JMJD3 as positive regulators of lifespan in response to mitochondrial dysfunction across species. Reduction-of-function of the demethylases potently suppresses longevity and UPRmt induction while gain-of-function is sufficient to extend lifespan in an UPRmt-dependent manner. A systems genetics approach in the BXD mouse reference population further indicates conserved roles of the mammalian orthologs in longevity and UPRmt signaling. These findings illustrate an evolutionary conserved epigenetic mechanism that determines the rate of aging downstream of mitochondrial perturbations. äTwo Conserved Histone Demethylases Regulate Mitochondrial Stress-Induc(epmc).pdf DeepDyve Pubget Overpricing