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10.1073/pnas.1618773114 http://scihub22266oqcxt.onion/10.1073/pnas.1618773114 C5206521!5206521!27965388     free     free     free       Proc+Natl+Acad+Sci+U+S+A 2016 ; 113 (52): 15078-83 Nephropedia Template TP {{tp|p=27965388|t=2016. TIFA as a crucial mediator for NLRP3 inflammasome |pdf=|usr=}}{{27965388}} gab.com Text TIFA as a crucial mediator for NLRP3 inflammasome JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=27965388 #FOAvip Oxidative and inflammatory stresses (e.g., atheroprone flow and hyperlipidemia) induce innate immune responses in vascular endothelium, of which the assembly and activation of nucleotide oligomerization domain-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome constitute a core mechanism. We show that TNF-? receptor-associated factor-interacting protein with a forkhead-associated domain (TIFA) is a mediator of NLRP3 inflammasome in endothelium. The involved regulations include that sterol regulatory element-binding protein 2 transcriptionally induces TIFA (signal 1) and that phosphorylated TIFA causes higher-order assembly of NLRP3 inflammasome (signal 2). Given that sustained innate immune response/activation in endothelium is common to a variety of vascular impairments, TIFA-mediated NLRP3 inflammasome constitutes a pathway by which sustained oxidative and inflammatory stresses lead to dysfunctional endothelium. Twit Text FOAVip TIFA as a crucial mediator for NLRP3 inflammasome ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=27965388 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27965388 #FOAvip English Wikipedia <ref>{{Cite pmid|27965388}}</ref> TIFA as a crucial mediator for NLRP3 inflammasome #MMPMID27965388 Lin TY; Wei TYW; Li S; Wang SC; He M; Martin M; Zhang J; Shentu TP; Xiao H; Kang J; Wang KC; Chen Z; Chien S; Tsai MD; Shyy JYJ Proc Natl Acad Sci U S A 2016[Dec]; 113 (52): 15078-83 PMID27965388show ga Oxidative and inflammatory stresses (e.g., atheroprone flow and hyperlipidemia) induce innate immune responses in vascular endothelium, of which the assembly and activation of nucleotide oligomerization domain-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome constitute a core mechanism. We show that TNF-? receptor-associated factor-interacting protein with a forkhead-associated domain (TIFA) is a mediator of NLRP3 inflammasome in endothelium. The involved regulations include that sterol regulatory element-binding protein 2 transcriptionally induces TIFA (signal 1) and that phosphorylated TIFA causes higher-order assembly of NLRP3 inflammasome (signal 2). Given that sustained innate immune response/activation in endothelium is common to a variety of vascular impairments, TIFA-mediated NLRP3 inflammasome constitutes a pathway by which sustained oxidative and inflammatory stresses lead to dysfunctional endothelium. äTIFA as a crucial mediator for NLRP3 inflammasome (epmc).pdf DeepDyve Pubget Overpricing