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http://purl.uniprot.org/citations/12496418http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/12496418http://www.w3.org/2000/01/rdf-schema#comment"TWEAK, a TNF family member, is produced by IFN-gamma-stimulated monocytes and induces multiple pathways of cell death, including caspase-dependent apoptosis, cathepsin B-dependent necrosis, and endogenous TNF-alpha-mediated cell death, in a cell type-specific manner. However, the TWEAK receptor(s) that mediates these multiple death pathways remains to be identified. Recently, fibroblast growth factor-inducible 14 (Fn14) has been identified to be a TWEAK receptor, which was responsible for TWEAK-induced proliferation of endothelial cells and angiogenesis. Because Fn14 lacks the cytoplasmic death domain, it remains unclear whether Fn14 can also mediate the TWEAK-induced cell death. In this study, we demonstrated that TWEAK could induce apoptotic cell death in Fn14 transfectants. A pan-caspase inhibitor, benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone, rather sensitized the Fn14 transfectants to TWEAK-induced cell death by necrosis via reactive oxygen intermediates and cathepsin B-dependent pathway. By using newly generated agonistic anti-Fn14 mAbs, we also observed that Fn14 is constitutively expressed on the cell surface of all TWEAK-sensitive tumor cell lines, and can transmit the multiple death signals. Moreover, an anti-Fn14 mAb that blocks TWEAK-Fn14 interaction could totally abrogate TWEAK binding and TWEAK-induced cell death in all TWEAK-sensitive tumor cell lines. These results revealed that the multiple pathways of TWEAK-induced cell death are solely mediated by Fn14."xsd:string
http://purl.uniprot.org/citations/12496418http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.170.1.341"xsd:string
http://purl.uniprot.org/citations/12496418http://purl.uniprot.org/core/author"Nakayama M."xsd:string
http://purl.uniprot.org/citations/12496418http://purl.uniprot.org/core/author"Okumura K."xsd:string
http://purl.uniprot.org/citations/12496418http://purl.uniprot.org/core/author"Kojima Y."xsd:string
http://purl.uniprot.org/citations/12496418http://purl.uniprot.org/core/author"Harada N."xsd:string
http://purl.uniprot.org/citations/12496418http://purl.uniprot.org/core/author"Kominami E."xsd:string
http://purl.uniprot.org/citations/12496418http://purl.uniprot.org/core/author"Yagita H."xsd:string
http://purl.uniprot.org/citations/12496418http://purl.uniprot.org/core/author"Ishidoh K."xsd:string
http://purl.uniprot.org/citations/12496418http://purl.uniprot.org/core/date"2003"xsd:gYear
http://purl.uniprot.org/citations/12496418http://purl.uniprot.org/core/name"J Immunol"xsd:string
http://purl.uniprot.org/citations/12496418http://purl.uniprot.org/core/pages"341-348"xsd:string
http://purl.uniprot.org/citations/12496418http://purl.uniprot.org/core/title"Fibroblast growth factor-inducible 14 mediates multiple pathways of TWEAK-induced cell death."xsd:string
http://purl.uniprot.org/citations/12496418http://purl.uniprot.org/core/volume"170"xsd:string
http://purl.uniprot.org/citations/12496418http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/12496418
http://purl.uniprot.org/citations/12496418http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/12496418
http://purl.uniprot.org/uniprot/#_A0A0U5J5F5-mappedCitation-12496418http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/12496418
http://purl.uniprot.org/uniprot/#_C0H5Y4-mappedCitation-12496418http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/12496418
http://purl.uniprot.org/uniprot/#_O43508-mappedCitation-12496418http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/12496418
http://purl.uniprot.org/uniprot/#_Q4ACW9-mappedCitation-12496418http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/12496418
http://purl.uniprot.org/uniprot/#_Q9NP84-mappedCitation-12496418http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/12496418
http://purl.uniprot.org/uniprot/A0A0U5J5F5http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/12496418
http://purl.uniprot.org/uniprot/Q9NP84http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/12496418
http://purl.uniprot.org/uniprot/C0H5Y4http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/12496418