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http://purl.uniprot.org/citations/28723569http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/28723569http://www.w3.org/2000/01/rdf-schema#comment"X-linked Inhibitor of Apoptosis (XIAP) deficiency predisposes people to pathogen-associated hyperinflammation. Upon XIAP loss, Toll-like receptor (TLR) ligation triggers RIPK3-caspase-8-mediated IL-1β activation and death in myeloid cells. How XIAP suppresses these events remains unclear. Here, we show that TLR-MyD88 causes the proteasomal degradation of the related IAP, cIAP1, and its adaptor, TRAF2, by inducing TNF and TNF Receptor 2 (TNFR2) signaling. Genetically, we define that myeloid-specific cIAP1 loss promotes TLR-induced RIPK3-caspase-8 and IL-1β activity in the absence of XIAP. Importantly, deletion of TNFR2 in XIAP-deficient cells limited TLR-MyD88-induced cIAP1-TRAF2 degradation, cell death, and IL-1β activation. In contrast to TLR-MyD88, TLR-TRIF-induced interferon (IFN)β inhibited cIAP1 loss and consequent cell death. These data reveal how, upon XIAP deficiency, a TLR-TNF-TNFR2 axis drives cIAP1-TRAF2 degradation to allow TLR or TNFR1 activation of RIPK3-caspase-8 and IL-1β. This mechanism may explain why XIAP-deficient patients can exhibit symptoms reminiscent of patients with activating inflammasome mutations."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.org/dc/terms/identifier"doi:10.1016/j.celrep.2017.06.073"xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/author"Hall C."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/author"Pang K.C."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/author"Schroder K."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/author"Zhan Y."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/author"Nguyen T.A."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/author"Chen K.W."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/author"Vaux D.L."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/author"Vince J.E."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/author"Lawlor K.E."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/author"Yabal M."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/author"Silke J."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/author"D'Silva D.B."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/author"Jost P.J."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/author"Feltham R."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/author"Conos S.A."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/author"Chatfield S.M."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/author"Grass C."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/author"Vince A.J."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/author"Ziehe S."xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/date"2017"xsd:gYear
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/name"Cell Rep"xsd:string
http://purl.uniprot.org/citations/28723569http://purl.uniprot.org/core/pages"668-682"xsd:string