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http://purl.uniprot.org/citations/24813850http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24813850http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/24813850http://www.w3.org/2000/01/rdf-schema#comment"Receptor-interacting protein kinase (RIPK)-1 is involved in RIPK3-dependent and -independent signaling pathways leading to cell death and/or inflammation. Genetic ablation of ripk1 causes postnatal lethality, which was not prevented by deletion of ripk3, caspase-8, or fadd. However, animals that lack RIPK1, RIPK3, and either caspase-8 or FADD survived weaning and matured normally. RIPK1 functions in vitro to limit caspase-8-dependent, TNFR-induced apoptosis, and animals lacking RIPK1, RIPK3, and TNFR1 survive to adulthood. The role of RIPK3 in promoting lethality in ripk1(-/-) mice suggests that RIPK3 activation is inhibited by RIPK1 postbirth. Whereas TNFR-induced RIPK3-dependent necroptosis requires RIPK1, cells lacking RIPK1 were sensitized to necroptosis triggered by poly I:C or interferons. Disruption of TLR (TRIF) or type I interferon (IFNAR) signaling delayed lethality in ripk1(-/-)tnfr1(-/-) mice. These results clarify the complex roles for RIPK1 in postnatal life and provide insights into the regulation of FADD-caspase-8 and RIPK3-MLKL signaling by RIPK1."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.org/dc/terms/identifier"doi:10.1016/j.cell.2014.04.018"xsd:string
http://purl.uniprot.org/citations/24813850http://purl.org/dc/terms/identifier"doi:10.1016/j.cell.2014.04.018"xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Kanneganti T.D."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Kanneganti T.D."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Gong Y.N."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Gong Y.N."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Gurung P."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Gurung P."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Green D.R."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Green D.R."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Llambi F."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Llambi F."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Brewer T.L."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Brewer T.L."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Cripps J.G."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Cripps J.G."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Dillon C.P."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Dillon C.P."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Janke L.J."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Janke L.J."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Kelliher M.A."xsd:string
http://purl.uniprot.org/citations/24813850http://purl.uniprot.org/core/author"Kelliher M.A."xsd:string