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http://purl.uniprot.org/citations/11911831http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11911831http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11911831http://www.w3.org/2000/01/rdf-schema#comment"DR3 is a death domain-containing receptor that is upregulated during T cell activation and whose overexpression induces apoptosis and NF-kappaB activation in cell lines. Here we show that an endothelial cell-derived TNF-like factor, TL1A, is a ligand for DR3 and decoy receptor TR6/DcR3 and that its expression is inducible by TNF and IL-1alpha. TL1A induces NF-kappaB activation and apoptosis in DR3-expressing cell lines, while TR6-Fc protein antagonizes these signaling events. Interestingly, in T cells, TL1A acts as a costimulator that increases IL-2 responsiveness and secretion of proinflammatory cytokines both in vitro and in vivo. Our data suggest that interaction of TL1A with DR3 promotes T cell expansion during an immune response, whereas TR6 has an opposing effect."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.org/dc/terms/identifier"doi:10.1016/s1074-7613(02)00283-2"xsd:string
http://purl.uniprot.org/citations/11911831http://purl.org/dc/terms/identifier"doi:10.1016/s1074-7613(02)00283-2"xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Chen C."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Chen C."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Hu B."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Hu B."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Hu G."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Hu G."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Liu D."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Liu D."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Kim S."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Kim S."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Luo X."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Luo X."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Ni J."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Ni J."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Feng P."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Feng P."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Zhang J."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Zhang J."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Zhuang L."xsd:string
http://purl.uniprot.org/citations/11911831http://purl.uniprot.org/core/author"Zhuang L."xsd:string