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10.1038/cdd.2013.195 http://scihub22266oqcxt.onion/10.1038/cdd.2013.195 C3950326!3950326!24440909     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Differ 2014 ; 21 (4): 634-44 Nephropedia Template TP {{tp|p=24440909|t=2014. A novel role for the apoptosis inhibitor ARC in suppressing TNF?-induced regulated necrosis |pdf=|usr=}}{{24440909}} gab.com Text A novel role for the apoptosis inhibitor ARC in suppressing TNF -induced regulated necrosis JO: Cell Death Differ http://www.kidney.de/pget.php?&tw=1&pmid=24440909 #FOAvip TNF? signaling can promote apoptosis or a regulated form of necrosis. ARC (apoptosis repressor with CARD (caspase recruitment domain)) is an endogenous inhibitor of apoptosis that antagonizes both the extrinsic (death receptor) and intrinsic (mitochondrial/ER) apoptosis pathways. We discovered that ARC blocks not only apoptosis but also necrosis. TNF?-induced necrosis was abrogated by overexpression of wild-type ARC but not by a CARD mutant that is also defective for inhibition of apoptosis. Conversely, knockdown of ARC exacerbated TNF?-induced necrosis, an effect that was rescued by reconstitution with wild-type, but not CARD-defective, ARC. Similarly, depletion of ARC in vivo exacerbated necrosis caused by infection with vaccinia virus, which elicits severe tissue damage through this pathway, and sensitized mice to TNF?-induced systemic inflammatory response syndrome. The mechanism underlying these effects is an interaction of ARC with TNF receptor 1 that interferes with recruitment of RIP1, a critical mediator of TNF?-induced regulated necrosis. These findings extend the role of ARC from an apoptosis inhibitor to a regulator of the TNF? pathway and an inhibitor of TNF?-mediated regulated necrosis. Twit Text FOAVip A novel role for the apoptosis inhibitor ARC in suppressing TNF -induced regulated necrosis ????Cell Death Differ http://www.kidney.de/pget.php?&tw=1&pmid=24440909 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24440909 #FOAvip English Wikipedia <ref>{{Cite pmid|24440909}}</ref> A novel role for the apoptosis inhibitor ARC in suppressing TNF?-induced regulated necrosis #MMPMID24440909 Kung G; Dai P; Deng L; Kitsis RN Cell Death Differ 2014[Apr]; 21 (4): 634-44 PMID24440909show ga TNF? signaling can promote apoptosis or a regulated form of necrosis. ARC (apoptosis repressor with CARD (caspase recruitment domain)) is an endogenous inhibitor of apoptosis that antagonizes both the extrinsic (death receptor) and intrinsic (mitochondrial/ER) apoptosis pathways. We discovered that ARC blocks not only apoptosis but also necrosis. TNF?-induced necrosis was abrogated by overexpression of wild-type ARC but not by a CARD mutant that is also defective for inhibition of apoptosis. Conversely, knockdown of ARC exacerbated TNF?-induced necrosis, an effect that was rescued by reconstitution with wild-type, but not CARD-defective, ARC. Similarly, depletion of ARC in vivo exacerbated necrosis caused by infection with vaccinia virus, which elicits severe tissue damage through this pathway, and sensitized mice to TNF?-induced systemic inflammatory response syndrome. The mechanism underlying these effects is an interaction of ARC with TNF receptor 1 that interferes with recruitment of RIP1, a critical mediator of TNF?-induced regulated necrosis. These findings extend the role of ARC from an apoptosis inhibitor to a regulator of the TNF? pathway and an inhibitor of TNF?-mediated regulated necrosis. äA novel role for the apoptosis inhibitor ARC in suppressing TNF?-induc(epmc).pdf DeepDyve Pubget Overpricing