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10.1089/dna.2016.3396 http://scihub22266oqcxt.onion/10.1089/dna.2016.3396 C4939383!4939383!27341284     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       DNA+Cell+Biol 2016 ; 35 (7): 311-3 Nephropedia Template TP {{tp|p=27341284|t=2016. NOD1 and NOD2: New Functions Linking Endoplasmic Reticulum Stress and Inflammation |pdf=|usr=}}{{27341284}} gab.com Text NOD1 and NOD2: New Functions Linking Endoplasmic Reticulum Stress and Inflammation JO: DNA Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27341284 #FOAvip Although viruses have long been known to subvert the endoplasmic reticulum (ER) for their replication, recent work has shown that this strategy is also used by bacterial pathogens and parasites to promote their intracellular growth. The ensuing disruption of cellular processes triggers a condition known as ER stress, which activates the host cell's unfolded protein response (UPR) to restore homeostasis. Recent work has linked the UPR, in particular the arm of this response that depends on the ER-resident sensor IRE1, to innate immunity and inflammation. Surprisingly, two intracellular innate immune receptors, NOD1 and NOD2, previously shown to sense bacterial peptidoglycan, were found to transduce ER stress signals to elicit inflammation. Given the known roles of both ER stress and NOD2 in chronic inflammatory diseases, including inflammatory bowel disease and type 2 diabetes, this new link has important implications for understanding the basis for these pathologies. Twit Text FOAVip NOD1 and NOD2: New Functions Linking Endoplasmic Reticulum Stress and Inflammation ????DNA Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27341284 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27341284 #FOAvip English Wikipedia <ref>{{Cite pmid|27341284}}</ref> NOD1 and NOD2: New Functions Linking Endoplasmic Reticulum Stress and Inflammation #MMPMID27341284 Byndloss MX; Keestra-Gounder AM; Bäumler AJ; Tsolis RM DNA Cell Biol 2016[Jul]; 35 (7): 311-3 PMID27341284show ga Although viruses have long been known to subvert the endoplasmic reticulum (ER) for their replication, recent work has shown that this strategy is also used by bacterial pathogens and parasites to promote their intracellular growth. The ensuing disruption of cellular processes triggers a condition known as ER stress, which activates the host cell's unfolded protein response (UPR) to restore homeostasis. Recent work has linked the UPR, in particular the arm of this response that depends on the ER-resident sensor IRE1, to innate immunity and inflammation. Surprisingly, two intracellular innate immune receptors, NOD1 and NOD2, previously shown to sense bacterial peptidoglycan, were found to transduce ER stress signals to elicit inflammation. Given the known roles of both ER stress and NOD2 in chronic inflammatory diseases, including inflammatory bowel disease and type 2 diabetes, this new link has important implications for understanding the basis for these pathologies. äNOD1 and NOD2: New Functions Linking Endoplasmic Reticulum Stress and (epmc).pdf DeepDyve Pubget Overpricing