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http://purl.uniprot.org/citations/32428502http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/32428502http://www.w3.org/2000/01/rdf-schema#comment"Cell death pathways regulate various homeostatic processes. Autoimmune lymphoproliferative syndrome (ALPS) in humans and lymphoproliferative (LPR) disease in mice result from abrogated CD95-induced apoptosis. Because caspase-8 mediates CD95 signaling, we applied genetic approaches to dissect the roles of caspase-8 in cell death and inflammation. Here, we describe oligomerization-deficient Caspase-8F122GL123G/F122GL123G and non-cleavable Caspase-8D387A/D387A mutant mice with defective caspase-8-mediated apoptosis. Although neither mouse developed LPR disease, removal of the necroptosis effector Mlkl from Caspase-8D387A/D387A mice revealed an inflammatory role of caspase-8. Ablation of one allele of Fasl, Fadd, or Ripk1 prevented the pathology of Casp8D387A/D387AMlkl-/- animals. Removing both Fadd alleles from these mice resulted in early lethality prior to post-natal day 15 (P15), which was prevented by co-ablation of either Ripk1 or Caspase-1. Our results suggest an in vivo role of the inflammatory RIPK1-caspase-8-FADD (FADDosome) complex and reveal a FADD-independent inflammatory role of caspase-8 that involves activation of an inflammasome."xsd:string
http://purl.uniprot.org/citations/32428502http://purl.org/dc/terms/identifier"doi:10.1016/j.immuni.2020.04.010"xsd:string
http://purl.uniprot.org/citations/32428502http://purl.uniprot.org/core/author"Kanneganti T.D."xsd:string
http://purl.uniprot.org/citations/32428502http://purl.uniprot.org/core/author"Moretti J."xsd:string
http://purl.uniprot.org/citations/32428502http://purl.uniprot.org/core/author"Fitzgerald P."xsd:string
http://purl.uniprot.org/citations/32428502http://purl.uniprot.org/core/author"Pelletier S."xsd:string
http://purl.uniprot.org/citations/32428502http://purl.uniprot.org/core/author"Green D.R."xsd:string
http://purl.uniprot.org/citations/32428502http://purl.uniprot.org/core/author"Janke L.J."xsd:string
http://purl.uniprot.org/citations/32428502http://purl.uniprot.org/core/author"Rodriguez D.A."xsd:string
http://purl.uniprot.org/citations/32428502http://purl.uniprot.org/core/author"Guy C.S."xsd:string
http://purl.uniprot.org/citations/32428502http://purl.uniprot.org/core/author"Crawford J.C."xsd:string
http://purl.uniprot.org/citations/32428502http://purl.uniprot.org/core/author"Tummers B."xsd:string
http://purl.uniprot.org/citations/32428502http://purl.uniprot.org/core/author"Blander J.M."xsd:string
http://purl.uniprot.org/citations/32428502http://purl.uniprot.org/core/author"Ruhl S."xsd:string
http://purl.uniprot.org/citations/32428502http://purl.uniprot.org/core/author"Heckmann B.L."xsd:string
http://purl.uniprot.org/citations/32428502http://purl.uniprot.org/core/author"Mari L."xsd:string
http://purl.uniprot.org/citations/32428502http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/32428502http://purl.uniprot.org/core/name"Immunity"xsd:string
http://purl.uniprot.org/citations/32428502http://purl.uniprot.org/core/pages"994-1006.e8"xsd:string
http://purl.uniprot.org/citations/32428502http://purl.uniprot.org/core/title"Caspase-8-Dependent Inflammatory Responses Are Controlled by Its Adaptor, FADD, and Necroptosis."xsd:string
http://purl.uniprot.org/citations/32428502http://purl.uniprot.org/core/volume"52"xsd:string
http://purl.uniprot.org/citations/32428502http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/32428502
http://purl.uniprot.org/citations/32428502http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/32428502
http://purl.uniprot.org/uniprot/#_A0A087WQT6-mappedCitation-32428502http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/32428502