Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/17044
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dc.contributor.authorTanzer, Maria C-
dc.contributor.authorKhan, Nufail-
dc.contributor.authorRickard, James A-
dc.contributor.authorEtemadi, Nima-
dc.contributor.authorLalaoui, Najoua-
dc.contributor.authorSpall, Sukhdeep Kaur-
dc.contributor.authorHildebrand, Joanne M-
dc.contributor.authorSegal, David-
dc.contributor.authorMiasari, Maria-
dc.contributor.authorChau, Diep-
dc.contributor.authorWong, WendyWei-Lynn-
dc.contributor.authorMcKinlay, Mark-
dc.contributor.authorChunduru, Srinivas K-
dc.contributor.authorBenetatos, Christopher A-
dc.contributor.authorCondon, Stephen M-
dc.contributor.authorVince, James E-
dc.contributor.authorHerold, Marco J-
dc.contributor.authorSilke, John-
dc.date2017-
dc.date.accessioned2018-01-21T22:17:14Z-
dc.date.available2018-01-21T22:17:14Z-
dc.date.issued2017-03-
dc.identifier.citationCell death and differentiation 2017; 24(3): 481-491-
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/17044-
dc.description.abstractPeptido-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-γ (IFNγ) 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 IFNγ/SM-induced killing. Triple CRISPR/Cas9-knockout HT29 cells lacking caspase-10 in addition to caspase-8 and RIPK3 or MLKL were resistant to IFNγ/SM killing. Caspase-8 and RIPK1 deficiency was, however, sufficient to protect cells from IFNγ/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.-
dc.language.isoeng-
dc.titleCombination of IAP antagonist and IFNγ activates novel caspase-10- and RIPK1-dependent cell death pathways.-
dc.typeJournal Article-
dc.identifier.journaltitleCell death and differentiation-
dc.identifier.affiliationCell Signalling and Cell Death, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia-
dc.identifier.affiliationOlivia Newton-John Cancer Research Institute, Heidelberg, Victoria, Australia-
dc.identifier.affiliationSchool of Cancer Medicine, La Trobe University, Melbourne, Victoria, Australia-
dc.identifier.affiliationInstitute of Experimental Immunology, University of Zurich, Zurich 8057, Switzerland-
dc.identifier.affiliationTetraLogic Pharmaceuticals Corporation, Malvern, PA, USA-
dc.identifier.pubmedurihttps://pubmed.ncbi.nlm.nih.gov/28106882-
dc.identifier.doi10.1038/cdd.2016.147-
dc.identifier.pubmedid28106882-
dc.type.austinJournal Article-
item.openairetypeJournal Article-
item.fulltextNo Fulltext-
item.cerifentitytypePublications-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.grantfulltextnone-
item.languageiso639-1en-
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