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http://purl.uniprot.org/citations/22365665http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22365665http://www.w3.org/2000/01/rdf-schema#comment"Interleukin-1β (IL-1β) is a potent inflammatory cytokine that is usually cleaved and activated by inflammasome-associated caspase-1. To determine whether IL-1β activation is regulated by inhibitor of apoptosis (IAP) proteins, we treated macrophages with an IAP-antagonist "Smac mimetic" compound or genetically deleted the genes that encode the three IAP family members cIAP1, cIAP2, and XIAP. After Toll-like receptor priming, IAP inhibition triggered cleavage of IL-1β that was mediated not only by the NLRP3-caspase-1 inflammasome, but also by caspase-8 in a caspase-1-independent manner. In the absence of IAPs, rapid and full generation of active IL-1β by the NLRP3-caspase-1 inflammasome, or by caspase-8, required the kinase RIP3 and reactive oxygen species production. These results demonstrate that activation of the cell death-inducing ripoptosome platform and RIP3 can generate bioactive IL-1β and implicate them as additional targets for the treatment of pathological IL-1-driven inflammatory responses."xsd:string
http://purl.uniprot.org/citations/22365665http://purl.org/dc/terms/identifier"doi:10.1016/j.immuni.2012.01.012"xsd:string
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/author"Ma S."xsd:string
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/author"Tschopp J."xsd:string
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/author"O'Reilly L."xsd:string
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/author"Wong W.W."xsd:string
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/author"Gross O."xsd:string
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/author"Vince J.E."xsd:string
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/author"Castillo R."xsd:string
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/author"Guarda G."xsd:string
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/author"Lawlor K.E."xsd:string
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/author"Silke J."xsd:string
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/author"Mason K."xsd:string
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/author"Anderton H."xsd:string
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/author"Gentle I."xsd:string
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/author"Allam R."xsd:string
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/author"Hacker G."xsd:string
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/name"Immunity"xsd:string
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/pages"215-227"xsd:string
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/title"Inhibitor of apoptosis proteins limit RIP3 kinase-dependent interleukin-1 activation."xsd:string
http://purl.uniprot.org/citations/22365665http://purl.uniprot.org/core/volume"36"xsd:string
http://purl.uniprot.org/citations/22365665http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/22365665
http://purl.uniprot.org/citations/22365665http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/22365665