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10.1038/ncomms10274 http://scihub22266oqcxt.onion/10.1038/ncomms10274 C4738349!4738349!26817517     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2016 ; 7 (ä): ä Nephropedia Template TP {{tp|p=26817517|t=2016. Cytotoxicity of crystals involves RIPK3-MLKL-mediated necroptosis |pdf=|usr=}}{{26817517}} gab.com Text Cytotoxicity of crystals involves RIPK3-MLKL-mediated necroptosis JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=26817517 #FOAvip Crystals cause injury in numerous disorders, and induce inflammation via the NLRP3 inflammasome, however, it remains unclear how crystals induce cell death. Here we report that crystals of calcium oxalate, monosodium urate, calcium pyrophosphate dihydrate and cystine trigger caspase-independent cell death in five different cell types, which is blocked by necrostatin-1. RNA interference for receptor-interacting protein kinase 3 (RIPK3) or mixed lineage kinase domain like (MLKL), two core proteins of the necroptosis pathway, blocks crystal cytotoxicity. Consistent with this, deficiency of RIPK3 or MLKL prevents oxalate crystal-induced acute kidney injury. The related tissue inflammation drives TNF-?-related necroptosis. Also in human oxalate crystal-related acute kidney injury, dying tubular cells stain positive for phosphorylated MLKL. Furthermore, necrostatin-1 and necrosulfonamide, an inhibitor for human MLKL suppress crystal-induced cell death in human renal progenitor cells. Together, TNF-?/TNFR1, RIPK1, RIPK3 and MLKL are molecular targets to limit crystal-induced cytotoxicity, tissue injury and organ failure. Twit Text FOAVip Cytotoxicity of crystals involves RIPK3-MLKL-mediated necroptosis ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=26817517 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26817517 #FOAvip English Wikipedia <ref>{{Cite pmid|26817517}}</ref> Cytotoxicity of crystals involves RIPK3-MLKL-mediated necroptosis #MMPMID26817517 Mulay SR; Desai J; Kumar SV; Eberhard JN; Thomasova D; Romoli S; Grigorescu M; Kulkarni OP; Popper B; Vielhauer V; Zuchtriegel G; Reichel C; Bräsen JH; Romagnani P; Bilyy R; Munoz LE; Herrmann M; Liapis H; Krautwald S; Linkermann A; Anders HJ Nat Commun 2016[]; 7 (ä): ä PMID26817517show ga Crystals cause injury in numerous disorders, and induce inflammation via the NLRP3 inflammasome, however, it remains unclear how crystals induce cell death. Here we report that crystals of calcium oxalate, monosodium urate, calcium pyrophosphate dihydrate and cystine trigger caspase-independent cell death in five different cell types, which is blocked by necrostatin-1. RNA interference for receptor-interacting protein kinase 3 (RIPK3) or mixed lineage kinase domain like (MLKL), two core proteins of the necroptosis pathway, blocks crystal cytotoxicity. Consistent with this, deficiency of RIPK3 or MLKL prevents oxalate crystal-induced acute kidney injury. The related tissue inflammation drives TNF-?-related necroptosis. Also in human oxalate crystal-related acute kidney injury, dying tubular cells stain positive for phosphorylated MLKL. Furthermore, necrostatin-1 and necrosulfonamide, an inhibitor for human MLKL suppress crystal-induced cell death in human renal progenitor cells. Together, TNF-?/TNFR1, RIPK1, RIPK3 and MLKL are molecular targets to limit crystal-induced cytotoxicity, tissue injury and organ failure. äCytotoxicity of crystals involves RIPK3-MLKL-mediated necroptosis (epmc).pdf DeepDyve Pubget Overpricing