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10.1007/s00018-016-2203-4 http://scihub22266oqcxt.onion/10.1007/s00018-016-2203-4 C4889460!4889460!27048814     free     free     free Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 219.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Mol+Life+Sci 2016 ; 73 (11-12): 2325-34 Nephropedia Template TP {{tp|p=27048814|t=2016. Necroptosis-independent signaling by the RIP kinases in inflammation |pdf=|usr=}}{{27048814}} gab.com Text Necroptosis-independent signaling by the RIP kinases in inflammation JO: Cell Mol Life Sci http://www.kidney.de/pget.php?&tw=1&pmid=27048814 #FOAvip Recent advances have identified a signaling cascade involving receptor interacting protein kinase 1 (RIPK1), RIPK3 and the pseudokinase mixed lineage kinase domain-like (MLKL) that is crucial for induction of necroptosis, a non-apoptotic form of cell death. RIPK1?RIPK3?MLKL-mediated necroptosis has been attributed to cause many inflammatory diseases through the release of cellular damage-associated molecular patterns (DAMPs). In addition to necroptosis, emerging evidence suggests that these necroptosis signal adaptors can also facilitate inflammation independent of cell death. In particular, the RIP kinases can drive NF-?B and inflammasome activation independent of cell death. In this review, we will discuss recent discoveries that led to this realization and present arguments why cell death-independent signaling by the RIP kinases may have a more important role in inflammation than necroptosis. Twit Text FOAVip Necroptosis-independent signaling by the RIP kinases in inflammation ????Cell Mol Life Sci http://www.kidney.de/pget.php?&tw=1&pmid=27048814 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27048814 #FOAvip English Wikipedia <ref>{{Cite pmid|27048814}}</ref> Necroptosis-independent signaling by the RIP kinases in inflammation #MMPMID27048814 Moriwaki K; Chan FKM Cell Mol Life Sci 2016[Jun]; 73 (11-12): 2325-34 PMID27048814show ga Recent advances have identified a signaling cascade involving receptor interacting protein kinase 1 (RIPK1), RIPK3 and the pseudokinase mixed lineage kinase domain-like (MLKL) that is crucial for induction of necroptosis, a non-apoptotic form of cell death. RIPK1?RIPK3?MLKL-mediated necroptosis has been attributed to cause many inflammatory diseases through the release of cellular damage-associated molecular patterns (DAMPs). In addition to necroptosis, emerging evidence suggests that these necroptosis signal adaptors can also facilitate inflammation independent of cell death. In particular, the RIP kinases can drive NF-?B and inflammasome activation independent of cell death. In this review, we will discuss recent discoveries that led to this realization and present arguments why cell death-independent signaling by the RIP kinases may have a more important role in inflammation than necroptosis. äNecroptosis-independent signaling by the RIP kinases in inflammation (epmc).pdf DeepDyve Pubget Overpricing