Please use this identifier to cite or link to this item:
https://ahro.austin.org.au/austinjspui/handle/1/17044
Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Tanzer, Maria C | - |
dc.contributor.author | Khan, Nufail | - |
dc.contributor.author | Rickard, James A | - |
dc.contributor.author | Etemadi, Nima | - |
dc.contributor.author | Lalaoui, Najoua | - |
dc.contributor.author | Spall, Sukhdeep Kaur | - |
dc.contributor.author | Hildebrand, Joanne M | - |
dc.contributor.author | Segal, David | - |
dc.contributor.author | Miasari, Maria | - |
dc.contributor.author | Chau, Diep | - |
dc.contributor.author | Wong, WendyWei-Lynn | - |
dc.contributor.author | McKinlay, Mark | - |
dc.contributor.author | Chunduru, Srinivas K | - |
dc.contributor.author | Benetatos, Christopher A | - |
dc.contributor.author | Condon, Stephen M | - |
dc.contributor.author | Vince, James E | - |
dc.contributor.author | Herold, Marco J | - |
dc.contributor.author | Silke, John | - |
dc.date | 2017 | - |
dc.date.accessioned | 2018-01-21T22:17:14Z | - |
dc.date.available | 2018-01-21T22:17:14Z | - |
dc.date.issued | 2017-03 | - |
dc.identifier.citation | Cell death and differentiation 2017; 24(3): 481-491 | - |
dc.identifier.uri | https://ahro.austin.org.au/austinjspui/handle/1/17044 | - |
dc.description.abstract | 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-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.iso | eng | - |
dc.title | Combination of IAP antagonist and IFNγ activates novel caspase-10- and RIPK1-dependent cell death pathways. | - |
dc.type | Journal Article | - |
dc.identifier.journaltitle | Cell death and differentiation | - |
dc.identifier.affiliation | Cell Signalling and Cell Death, The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria, Australia | - |
dc.identifier.affiliation | Olivia Newton-John Cancer Research Institute, Heidelberg, Victoria, Australia | - |
dc.identifier.affiliation | School of Cancer Medicine, La Trobe University, Melbourne, Victoria, Australia | - |
dc.identifier.affiliation | Institute of Experimental Immunology, University of Zurich, Zurich 8057, Switzerland | - |
dc.identifier.affiliation | TetraLogic Pharmaceuticals Corporation, Malvern, PA, USA | - |
dc.identifier.pubmeduri | https://pubmed.ncbi.nlm.nih.gov/28106882 | - |
dc.identifier.doi | 10.1038/cdd.2016.147 | - |
dc.identifier.pubmedid | 28106882 | - |
dc.type.austin | Journal Article | - |
item.openairetype | Journal Article | - |
item.fulltext | No Fulltext | - |
item.cerifentitytype | Publications | - |
item.openairecristype | http://purl.org/coar/resource_type/c_18cf | - |
item.grantfulltext | none | - |
item.languageiso639-1 | en | - |
Appears in Collections: | Journal articles |
Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.