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10.1016/j.cytogfr.2013.12.013 http://scihub22266oqcxt.onion/10.1016/j.cytogfr.2013.12.013 C3999177!3999177!24412261     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       Cytokine+Growth+Factor+Rev 2014 ; 25 (2): 167-74 Nephropedia Template TP {{tp|p=24412261|t=2014. Necrosis-Dependent and Independent Signaling of the RIP kinases in Inflammation |pdf=|usr=}}{{24412261}} gab.com Text Necrosis-Dependent and Independent Signaling of the RIP kinases in Inflammation JO: Cytokine Growth Factor Rev http://www.kidney.de/pget.php?&tw=1&pmid=24412261 #FOAvip It is now widely accepted that some forms of necrosis are controlled by a dedicated signaling pathway triggered by various cell surface and intracellular receptors. This regulated form of necrosis is mediated by the kinase activity of receptor-interacting protein kinase 1 (RIP1/RIPK1) and/or RIP3/RIPK3. A number of studies using the RIP1 kinase inhibitor Necrostatin-1 (Nec-1) and its derivatives, or RIP3-deficient mice demonstrated that RIP1 and RIP3 are involved in various infectious and sterile inflammatory diseases. As a consequence, these specific phenotypes were construed to depend on necrosis. However, emerging evidence indicates that the RIP1 kinase activity and RIP3 can also control apoptosis and inflammatory cytokine production independent of necrosis. Therefore, we may need to re-interpret conclusions drawn based on loss of RIP1 or RIP3 functions in in vivo models. We propose that studies of RIP1 and RIP3 in different inflammatory responses need to consider cell death-dependent and independent mechanisms of the RIP kinases. Twit Text FOAVip Necrosis-Dependent and Independent Signaling of the RIP kinases in Inflammation ????Cytokine Growth Factor Rev http://www.kidney.de/pget.php?&tw=1&pmid=24412261 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24412261 #FOAvip English Wikipedia <ref>{{Cite pmid|24412261}}</ref> Necrosis-Dependent and Independent Signaling of the RIP kinases in Inflammation #MMPMID24412261 Moriwaki K; Chan FK Cytokine Growth Factor Rev 2014[Apr]; 25 (2): 167-74 PMID24412261show ga It is now widely accepted that some forms of necrosis are controlled by a dedicated signaling pathway triggered by various cell surface and intracellular receptors. This regulated form of necrosis is mediated by the kinase activity of receptor-interacting protein kinase 1 (RIP1/RIPK1) and/or RIP3/RIPK3. A number of studies using the RIP1 kinase inhibitor Necrostatin-1 (Nec-1) and its derivatives, or RIP3-deficient mice demonstrated that RIP1 and RIP3 are involved in various infectious and sterile inflammatory diseases. As a consequence, these specific phenotypes were construed to depend on necrosis. However, emerging evidence indicates that the RIP1 kinase activity and RIP3 can also control apoptosis and inflammatory cytokine production independent of necrosis. Therefore, we may need to re-interpret conclusions drawn based on loss of RIP1 or RIP3 functions in in vivo models. We propose that studies of RIP1 and RIP3 in different inflammatory responses need to consider cell death-dependent and independent mechanisms of the RIP kinases. äNecrosis-Dependent and Independent Signaling of the RIP kinases in Inf(epmc).pdf DeepDyve Pubget Overpricing