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10.1038/cdd.2016.147 http://scihub22266oqcxt.onion/10.1038/cdd.2016.147 C5344208!5344208 !28106882     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28106882 &cmd=llinks): Failed to open stream: HTTP request failed! 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Combination of IAP antagonist and IFN? activates novel caspase-10- and RIPK1-dependent cell death pathways |pdf=|usr=}}{{28106882 }} gab.com Text Combination of IAP antagonist and IFN activates novel caspase-10- and RIPK1-dependent cell death pathways JO: Cell Death Differ http://www.kidney.de/pget.php?&tw=1&pmid=28106882 #FOAvip Peptido-mimetic inhibitor of apoptosis protein (IAP) antagonists (Smac mimetics (SMs)) can kill tumour cells by depleting endogenous IAPs and thereby inducing tumour necrosis factor (TNF) production. We found that interferon-? (IFN?) synergises with SMs to kill cancer cells independently of TNF- and other cell death receptor signalling pathways. Surprisingly, CRISPR/Cas9 HT29 cells doubly deficient for caspase-8 and the necroptotic pathway mediators RIPK3 or MLKL were still sensitive to IFN?/SM-induced killing. Triple CRISPR/Cas9-knockout HT29 cells lacking caspase-10 in addition to caspase-8 and RIPK3 or MLKL were resistant to IFN?/SM killing. Caspase-8 and RIPK1 deficiency was, however, sufficient to protect cells from IFN?/SM-induced cell death, implying a role for RIPK1 in the activation of caspase-10. These data show that RIPK1 and caspase-10 mediate cell death in HT29 cells when caspase-8-mediated apoptosis and necroptosis are blocked and help to clarify how SMs operate as chemotherapeutic agents. Twit Text FOAVip Combination of IAP antagonist and IFN activates novel caspase-10- and RIPK1-dependent cell death pathways ????Cell Death Differ http://www.kidney.de/pget.php?&tw=1&pmid=28106882 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28106882 #FOAvip English Wikipedia <ref>{{Cite pmid|28106882 }}</ref> Combination of IAP antagonist and IFN? activates novel caspase-10- and RIPK1-dependent cell death pathways #MMPMID28106882 Tanzer MC ; Khan N ; Rickard JA ; Etemadi N ; Lalaoui N ; Spall SK ; Hildebrand JM ; Segal D ; Miasari M ; Chau D ; Wong WL ; McKinlay M ; Chunduru SK ; Benetatos CA ; Condon SM ; Vince JE ; Herold MJ ; Silke J Cell Death Differ 2017[Mar]; 24 (3 ): 481-491 PMID28106882 show ga Peptido-mimetic inhibitor of apoptosis protein (IAP) antagonists (Smac mimetics (SMs)) can kill tumour cells by depleting endogenous IAPs and thereby inducing tumour necrosis factor (TNF) production. We found that interferon-? (IFN?) synergises with SMs to kill cancer cells independently of TNF- and other cell death receptor signalling pathways. Surprisingly, CRISPR/Cas9 HT29 cells doubly deficient for caspase-8 and the necroptotic pathway mediators RIPK3 or MLKL were still sensitive to IFN?/SM-induced killing. Triple CRISPR/Cas9-knockout HT29 cells lacking caspase-10 in addition to caspase-8 and RIPK3 or MLKL were resistant to IFN?/SM killing. Caspase-8 and RIPK1 deficiency was, however, sufficient to protect cells from IFN?/SM-induced cell death, implying a role for RIPK1 in the activation of caspase-10. These data show that RIPK1 and caspase-10 mediate cell death in HT29 cells when caspase-8-mediated apoptosis and necroptosis are blocked and help to clarify how SMs operate as chemotherapeutic agents. |Animals [MESH] |Apoptosis/*drug effects [MESH] |CRISPR-Cas Systems/genetics [MESH] |Caspase 10/chemistry/genetics/*metabolism [MESH] |Caspase 8/chemistry/genetics/metabolism [MESH] |Caspase Inhibitors/pharmacology [MESH] |Cell Line [MESH] |Cytokine TWEAK/pharmacology [MESH] |Drug Synergism [MESH] |HT29 Cells [MESH] |Humans [MESH] |Inhibitor of Apoptosis Proteins/antagonists & inhibitors/*metabolism [MESH] |Interferon-gamma/genetics/metabolism/*pharmacology [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Pentanoic Acids/pharmacology [MESH] |Protein Kinases/deficiency/metabolism [MESH] |Receptor-Interacting Protein Serine-Threonine Kinases/deficiency/genetics/*metabolism [MESH] |Receptors, Tumor Necrosis Factor, Type I/deficiency/genetics/metabolism [MESH]Combination of IAP antagonist and IFN? activates novel caspase-10- and(epmc).pdf DeepDyve Pubget Overpricing