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10.1016/j.redox.2015.08.019 http://scihub22266oqcxt.onion/10.1016/j.redox.2015.08.019 C4600855!4600855!26448396     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       Redox+Biol 2015 ; 6 (ä): 507-15 Nephropedia Template TP {{tp|p=26448396|t=2015. S-nitrosylation in TNF superfamily signaling pathway: Implication in cancer? |pdf=|usr=}}{{26448396}} gab.com Text S-nitrosylation in TNF superfamily signaling pathway: Implication in cancer JO: Redox Biol http://www.kidney.de/pget.php?&tw=1&pmid=26448396 #FOAvip One of the key features of tumor cells is the acquisition of resistance to apoptosis. Thus, novel therapeutic strategies that circumvent apoptotic resistance and result in tumor elimination are needed. One strategy to induce apoptosis is to activate death receptor signaling pathways. In the tumor microenvironment, stimulation of Fas, Death receptor 4 (DR4) and tumor necrosis factor receptor 1 (TNFR1) can initiate multiple signaling pathways driving either tumor promotion or elimination. Nitric oxide (NO) is an important signaling molecule now understood to play a dual role in cancer biology. More and more attention is directed toward the role displayed by S-nitrosylation, the incorporation of an NO moiety to a cysteine thiol group, in promoting cell death in tumor cells. Protein post-translation modification by S-nitrosylation has decisive roles in regulating signal-transduction pathways. In this review, we summarize several examples of protein modification by S-nitrosylation that regulate signaling pathways engaged by members of the TNF superfamily (Fas ligand (FasL), Tumor-necrosis-factor-related apoptosis inducing ligand (TRAIL) and TNFalpha (TNF?)) and the way it influences cell fate decisions. Twit Text FOAVip S-nitrosylation in TNF superfamily signaling pathway: Implication in cancer ????Redox Biol http://www.kidney.de/pget.php?&tw=1&pmid=26448396 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26448396 #FOAvip English Wikipedia <ref>{{Cite pmid|26448396}}</ref> S-nitrosylation in TNF superfamily signaling pathway: Implication in cancer? #MMPMID26448396 Plenchette S; Romagny S; Laurens V; Bettaieb A Redox Biol 2015[Dec]; 6 (ä): 507-15 PMID26448396show ga One of the key features of tumor cells is the acquisition of resistance to apoptosis. Thus, novel therapeutic strategies that circumvent apoptotic resistance and result in tumor elimination are needed. One strategy to induce apoptosis is to activate death receptor signaling pathways. In the tumor microenvironment, stimulation of Fas, Death receptor 4 (DR4) and tumor necrosis factor receptor 1 (TNFR1) can initiate multiple signaling pathways driving either tumor promotion or elimination. Nitric oxide (NO) is an important signaling molecule now understood to play a dual role in cancer biology. More and more attention is directed toward the role displayed by S-nitrosylation, the incorporation of an NO moiety to a cysteine thiol group, in promoting cell death in tumor cells. Protein post-translation modification by S-nitrosylation has decisive roles in regulating signal-transduction pathways. In this review, we summarize several examples of protein modification by S-nitrosylation that regulate signaling pathways engaged by members of the TNF superfamily (Fas ligand (FasL), Tumor-necrosis-factor-related apoptosis inducing ligand (TRAIL) and TNFalpha (TNF?)) and the way it influences cell fate decisions. äS-nitrosylation in TNF superfamily signaling pathway: Implication in c(epmc).pdf DeepDyve Pubget Overpricing