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10.1038/nature17631 http://scihub22266oqcxt.onion/10.1038/nature17631 C4869892!4869892!27007849     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nature 2016 ; 532 (7599): 394-7 Nephropedia Template TP {{tp|p=27007849|t=2016. NOD1/NOD2 signaling links ER stress with inflammation |pdf=|usr=}}{{27007849}} gab.com Text NOD1/NOD2 signaling links ER stress with inflammation JO: Nature http://www.kidney.de/pget.php?&tw=1&pmid=27007849 #FOAvip Endoplasmic reticulum (ER) stress is a major contributor to inflammatory diseases, such as Crohn?s disease and type 2 diabetes1,2. ER stress induces the unfolded protein response (UPR), which involves activation of three transmembrane receptors, ATF6 (activating transcription factor 6), PERK (protein kinase RNA-like endoplasmic reticulum kinase) and IRE1? (inositol-requiring enzyme 1?)3 (Extended Data figure 1a). Once activated, IRE1? recruits TRAF2 (TNF receptor-associated factor 2) to the ER membrane to initiate inflammatory responses via the nuclear factor kappa B (NF-?B) pathway4. Inflammation is commonly triggered when pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs) or nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs), detect tissue damage or microbial infection. However, it is not clear which PRRs play a major role in inducing inflammation during ER stress. Here we show that NOD1 and NOD2, two members of the NLR family of PRRs, are important mediators of ER stress-induced inflammation. The ER stress inducers thapsigargin and dithiothreitol (DTT) triggered production of the pro-inflammatory cytokine interleukin (IL)-6 in a NOD1/2-dependent fashion. Inflammation and IL-6 production triggered by infection with Brucella abortus, which induces ER stress by injecting the type IV secretion system (T4SS) effector protein VceC into host cells5, was TRAF2, NOD1/2 and RIP2-dependent and could be blunted by treatment with the ER-stress inhibitor tauroursodeoxycholate (TUDCA) or an IRE1? kinase inhibitor. The association of NOD1 and NOD2 with pro-inflammatory responses induced by the IRE1?/TRAF2 signaling pathway provides a novel link between innate immunity and ER stress-induced inflammation. Twit Text FOAVip NOD1/NOD2 signaling links ER stress with inflammation ????Nature http://www.kidney.de/pget.php?&tw=1&pmid=27007849 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27007849 #FOAvip English Wikipedia <ref>{{Cite pmid|27007849}}</ref> NOD1/NOD2 signaling links ER stress with inflammation #MMPMID27007849 Keestra-Gounder AM; Byndloss MX; Seyffert N; Young BM; Chávez-Arroyo A; Tsai AY; Cevallos SA; Winter MG; Pham OH; Tiffany CR; de Jong MF; Kerrinnes T; Ravindran R; Luciw PA; McSorley SJ; Bäumler AJ; Tsolis RM Nature 2016[Apr]; 532 (7599): 394-7 PMID27007849show ga Endoplasmic reticulum (ER) stress is a major contributor to inflammatory diseases, such as Crohn?s disease and type 2 diabetes1,2. ER stress induces the unfolded protein response (UPR), which involves activation of three transmembrane receptors, ATF6 (activating transcription factor 6), PERK (protein kinase RNA-like endoplasmic reticulum kinase) and IRE1? (inositol-requiring enzyme 1?)3 (Extended Data figure 1a). Once activated, IRE1? recruits TRAF2 (TNF receptor-associated factor 2) to the ER membrane to initiate inflammatory responses via the nuclear factor kappa B (NF-?B) pathway4. Inflammation is commonly triggered when pattern recognition receptors (PRRs), such as Toll-like receptors (TLRs) or nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs), detect tissue damage or microbial infection. However, it is not clear which PRRs play a major role in inducing inflammation during ER stress. Here we show that NOD1 and NOD2, two members of the NLR family of PRRs, are important mediators of ER stress-induced inflammation. The ER stress inducers thapsigargin and dithiothreitol (DTT) triggered production of the pro-inflammatory cytokine interleukin (IL)-6 in a NOD1/2-dependent fashion. Inflammation and IL-6 production triggered by infection with Brucella abortus, which induces ER stress by injecting the type IV secretion system (T4SS) effector protein VceC into host cells5, was TRAF2, NOD1/2 and RIP2-dependent and could be blunted by treatment with the ER-stress inhibitor tauroursodeoxycholate (TUDCA) or an IRE1? kinase inhibitor. The association of NOD1 and NOD2 with pro-inflammatory responses induced by the IRE1?/TRAF2 signaling pathway provides a novel link between innate immunity and ER stress-induced inflammation. äNOD1/NOD2 signaling links ER stress with inflammation (epmc).pdf DeepDyve Pubget Overpricing