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10.1371/journal.pone.0163118 http://scihub22266oqcxt.onion/10.1371/journal.pone.0163118 C5025154!5025154!27631783     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       PLoS+One 2016 ; 11 (9): ä Nephropedia Template TP {{tp|p=27631783|t=2016. KLHDC10 Deficiency Protects Mice against TNF?-Induced Systemic Inflammation |pdf=|usr=}}{{27631783}} gab.com Text KLHDC10 Deficiency Protects Mice against TNF -Induced Systemic Inflammation JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=27631783 #FOAvip Systemic inflammatory response syndrome (SIRS) is a form of fatal acute inflammation for which there is no effective treatment. Here, we revealed that the ablation of Kelch domain containing 10 (KLHDC10), which we had originally identified as an activator of Apoptosis Signal-regulating Kinase 1 (ASK1), protects mice against TNF?-induced SIRS. The disease development of SIRS is mainly divided into two stages. The early stage is characterized by TNF?-induced systemic necroptosis, a regulated form of necrosis mediated by Receptor-interacting protein (RIP) 1/3 kinases. The later stage presents with an over-production of inflammatory cytokines induced by damage-associated molecular patterns (DAMPs), which are immunogenic cellular contents released from cells that underwent necroptosis. Analysis of TNF?-challenged mice revealed that KLHDC10-deficient mice show a reduction in the inflammatory response, but not in early systemic necroptosis. In vitro analysis suggested that the reduced inflammatory response observed in KLHDC10-deficient mice might be caused, in part, by enhanced necroptosis of inflammatory cells encountering DAMPs. Interestingly, the enhancement of necroptosis induced by KLHDC10 deficiency was selectively observed in inflammatory cells. Our results suggest that KLHDC10 is a cell-type specific regulator of necroptosis that ultimately contributes to the development of TNF?-induced SIRS. Twit Text FOAVip KLHDC10 Deficiency Protects Mice against TNF -Induced Systemic Inflammation ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=27631783 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27631783 #FOAvip English Wikipedia <ref>{{Cite pmid|27631783}}</ref> KLHDC10 Deficiency Protects Mice against TNF?-Induced Systemic Inflammation #MMPMID27631783 Yamaguchi N; Sekine S; Naguro I; Sekine Y; Ichijo H PLoS One 2016[]; 11 (9): ä PMID27631783show ga Systemic inflammatory response syndrome (SIRS) is a form of fatal acute inflammation for which there is no effective treatment. Here, we revealed that the ablation of Kelch domain containing 10 (KLHDC10), which we had originally identified as an activator of Apoptosis Signal-regulating Kinase 1 (ASK1), protects mice against TNF?-induced SIRS. The disease development of SIRS is mainly divided into two stages. The early stage is characterized by TNF?-induced systemic necroptosis, a regulated form of necrosis mediated by Receptor-interacting protein (RIP) 1/3 kinases. The later stage presents with an over-production of inflammatory cytokines induced by damage-associated molecular patterns (DAMPs), which are immunogenic cellular contents released from cells that underwent necroptosis. Analysis of TNF?-challenged mice revealed that KLHDC10-deficient mice show a reduction in the inflammatory response, but not in early systemic necroptosis. In vitro analysis suggested that the reduced inflammatory response observed in KLHDC10-deficient mice might be caused, in part, by enhanced necroptosis of inflammatory cells encountering DAMPs. Interestingly, the enhancement of necroptosis induced by KLHDC10 deficiency was selectively observed in inflammatory cells. Our results suggest that KLHDC10 is a cell-type specific regulator of necroptosis that ultimately contributes to the development of TNF?-induced SIRS. äKLHDC10 Deficiency Protects Mice against TNF?-Induced Systemic Inflamm(epmc).pdf DeepDyve Pubget Overpricing