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http://purl.uniprot.org/citations/9382840http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/9382840http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/9382840http://www.w3.org/2000/01/rdf-schema#comment"Apo2 ligand (Apo2L [1], also called TRAIL for tumor necrosis factor (TNF)-related apoptosis-inducing ligand [2]) belongs to the TNF family and activates apoptosis in tumor cells. Three closely related receptors bind Apo2L: DR4 and DR5, which contain cytoplasmic death domains and signal apoptosis, and DcR1, a decoy receptor that lacks a cytoplasmic tail and inhibits Apo2L function [3-5]. By cross-hybridization with DcR1, we have identified a fourth Apo2L receptor, which contains a cytoplasmic region with a truncated death domain. We subsequently named this protein decoy receptor 2 (DcR2). The DcR2 gene mapped to human chromosome 8p21, as did the genes encoding DR4, DR5 and DcR1. A single DcR2 mRNA transcript showed a unique expression pattern in human tissues and was particularly abundant in fetal liver and adult testis. Upon overexpression, DcR2 did not activate apoptosis or nuclear factor-kappaB; however, it substantially reduced cellular sensitivity to Apo2L-induced apoptosis. These results suggest that DcR2 functions as an inhibitory Apo2L receptor."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.org/dc/terms/identifier"doi:10.1016/s0960-9822(06)00422-2"xsd:string
http://purl.uniprot.org/citations/9382840http://purl.org/dc/terms/identifier"doi:10.1016/s0960-9822(06)00422-2"xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Baldwin D."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Baldwin D."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Goddard A.D."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Goddard A.D."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Huang A."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Huang A."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Yuan J."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Yuan J."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Ashkenazi A."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Ashkenazi A."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Godowski P."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Godowski P."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Gurney A."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Gurney A."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Marsters S.A."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Marsters S.A."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Pitti R.M."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Pitti R.M."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Sheridan J.P."xsd:string
http://purl.uniprot.org/citations/9382840http://purl.uniprot.org/core/author"Sheridan J.P."xsd:string