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10.1016/j.cell.2016.04.011 http://scihub22266oqcxt.onion/10.1016/j.cell.2016.04.011 C4889216!4889216!27133166     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell 2016 ; 165 (5): 1197-208 Nephropedia Template TP {{tp|p=27133166|t=2016. Mitochondrial stress induces chromatin reorganization to promote longevity and UPRmt |pdf=|usr=}}{{27133166}} gab.com Text Mitochondrial stress induces chromatin reorganization to promote longevity and UPRmt JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=27133166 #FOAvip Organisms respond to mitochondrial stress through the upregulation of an array of protective genes, often perpetuating an early response to metabolic dysfunction across a lifetime. We find that mitochondrial stress causes widespread changes in chromatin structure through histone H3K9 di-methylation marks traditionally associated with gene silencing. Mitochondrial stress response activation requires the di-methylation of histone H3K9 through the activity of the histone methyltransferase met-2 and the nuclear co-factor lin-65. While globally the chromatin becomes silenced by these marks, remaining portions of the chromatin open up, at which point the binding of canonical stress responsive factors such as DVE-1 occurs. Thus, a metabolic stress response is established and propagated into adulthood of animals through specific epigenetic modifications that allow for selective gene expression and lifespan extension. Twit Text FOAVip Mitochondrial stress induces chromatin reorganization to promote longevity and UPRmt ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=27133166 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27133166 #FOAvip English Wikipedia <ref>{{Cite pmid|27133166}}</ref> Mitochondrial stress induces chromatin reorganization to promote longevity and UPRmt #MMPMID27133166 Tian Y; Garcia G; Bian Q; Steffen KK; Joe L; Wolff S; Meyer BJ; Dillin A Cell 2016[May]; 165 (5): 1197-208 PMID27133166show ga Organisms respond to mitochondrial stress through the upregulation of an array of protective genes, often perpetuating an early response to metabolic dysfunction across a lifetime. We find that mitochondrial stress causes widespread changes in chromatin structure through histone H3K9 di-methylation marks traditionally associated with gene silencing. Mitochondrial stress response activation requires the di-methylation of histone H3K9 through the activity of the histone methyltransferase met-2 and the nuclear co-factor lin-65. While globally the chromatin becomes silenced by these marks, remaining portions of the chromatin open up, at which point the binding of canonical stress responsive factors such as DVE-1 occurs. Thus, a metabolic stress response is established and propagated into adulthood of animals through specific epigenetic modifications that allow for selective gene expression and lifespan extension. äMitochondrial stress induces chromatin reorganization to promote longe(epmc).pdf DeepDyve Pubget Overpricing