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10.1016/j.cell.2016.05.017 http://scihub22266oqcxt.onion/10.1016/j.cell.2016.05.017 C4893198!4893198!27259148     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       Cell 2016 ; 165 (6): 1361-74 Nephropedia Template TP {{tp|p=27259148|t=2016. Repression of the antioxidant NRF2 pathway in premature aging |pdf=|usr=}}{{27259148}} gab.com Text Repression of the antioxidant NRF2 pathway in premature aging JO: Cell http://www.kidney.de/pget.php?&tw=1&pmid=27259148 #FOAvip Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare, invariably fatal premature aging disorder. The disease is caused by constitutive production of progerin, a mutant form of the nuclear architectural protein lamin A, leading, through unknown mechanisms, to diverse morphological, epigenetic and genomic damage and to mesenchymal stem cell (MSC) attrition in vivo. Using a high-throughput siRNA screen we identify the NRF2 antioxidant pathway as a driver mechanism in HGPS. Progerin sequesters NRF2 and thereby causes its subnuclear mislocalization, resulting in impaired NRF2 transcriptional activity and consequently increased chronic oxidative stress. Suppressed NRF2 activity or increased oxidative stress are sufficient to recapitulate HGPS aging defects whereas re-activation of NRF2 activity in HGPS patient cells reverses progerin-associated nuclear aging defects and restores in vivo viability of MSCs in an animal model. These findings identify repression of the NRF2-mediated antioxidative response as a key contributor to the premature aging phenotype. Twit Text FOAVip Repression of the antioxidant NRF2 pathway in premature aging ????Cell http://www.kidney.de/pget.php?&tw=1&pmid=27259148 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27259148 #FOAvip English Wikipedia <ref>{{Cite pmid|27259148}}</ref> Repression of the antioxidant NRF2 pathway in premature aging #MMPMID27259148 Kubben N; Zhang W; Wang L; Voss TC; Yang J; Qu J; Liu GH; Misteli T Cell 2016[Jun]; 165 (6): 1361-74 PMID27259148show ga Hutchinson-Gilford Progeria Syndrome (HGPS) is a rare, invariably fatal premature aging disorder. The disease is caused by constitutive production of progerin, a mutant form of the nuclear architectural protein lamin A, leading, through unknown mechanisms, to diverse morphological, epigenetic and genomic damage and to mesenchymal stem cell (MSC) attrition in vivo. Using a high-throughput siRNA screen we identify the NRF2 antioxidant pathway as a driver mechanism in HGPS. Progerin sequesters NRF2 and thereby causes its subnuclear mislocalization, resulting in impaired NRF2 transcriptional activity and consequently increased chronic oxidative stress. Suppressed NRF2 activity or increased oxidative stress are sufficient to recapitulate HGPS aging defects whereas re-activation of NRF2 activity in HGPS patient cells reverses progerin-associated nuclear aging defects and restores in vivo viability of MSCs in an animal model. These findings identify repression of the NRF2-mediated antioxidative response as a key contributor to the premature aging phenotype. äRepression of the antioxidant NRF2 pathway in premature aging (epmc).pdf DeepDyve Pubget Overpricing