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http://purl.uniprot.org/citations/30397201http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/30397201http://www.w3.org/2000/01/rdf-schema#comment"The interaction between natural killer (NK) cell inhibitory receptors and their cognate ligands constitutes a key mechanism by which healthy tissues are protected from NK cell-mediated lysis. However, self-ligand recognition remains poorly understood within the prototypical NKR-P1 receptor family. Here we report the structure of the inhibitory NKR-P1B receptor bound to its cognate host ligand, Clr-b. NKR-P1B and Clr-b interact via a head-to-head docking mode through an interface that includes a large array of polar interactions. NKR-P1B:Clr-b recognition is extremely sensitive to mutations at the heterodimeric interface, with most mutations severely impacting both Clr-b binding and NKR-P1B receptor function to implicate a low affinity interaction. Within the structure, two NKR-P1B:Clr-b complexes are cross-linked by a non-classic NKR-P1B homodimer, and the disruption of homodimer formation abrogates Clr-b recognition. These data provide an insight into a fundamental missing-self recognition system and suggest an avidity-based mechanism underpins NKR-P1B receptor function."xsd:string
http://purl.uniprot.org/citations/30397201http://purl.org/dc/terms/identifier"doi:10.1038/s41467-018-06989-2"xsd:string
http://purl.uniprot.org/citations/30397201http://purl.uniprot.org/core/author"Fu Z."xsd:string
http://purl.uniprot.org/citations/30397201http://purl.uniprot.org/core/author"Tanaka M."xsd:string
http://purl.uniprot.org/citations/30397201http://purl.uniprot.org/core/author"Rossjohn J."xsd:string
http://purl.uniprot.org/citations/30397201http://purl.uniprot.org/core/author"Lanier L.L."xsd:string
http://purl.uniprot.org/citations/30397201http://purl.uniprot.org/core/author"Berry R."xsd:string
http://purl.uniprot.org/citations/30397201http://purl.uniprot.org/core/author"Carlyle J.R."xsd:string
http://purl.uniprot.org/citations/30397201http://purl.uniprot.org/core/author"Gully B.S."xsd:string
http://purl.uniprot.org/citations/30397201http://purl.uniprot.org/core/author"Aguilar O.A."xsd:string
http://purl.uniprot.org/citations/30397201http://purl.uniprot.org/core/author"Balaji G.R."xsd:string
http://purl.uniprot.org/citations/30397201http://purl.uniprot.org/core/author"Shingu-Vazquez M.A."xsd:string
http://purl.uniprot.org/citations/30397201http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/30397201http://purl.uniprot.org/core/name"Nat Commun"xsd:string
http://purl.uniprot.org/citations/30397201http://purl.uniprot.org/core/pages"4623"xsd:string
http://purl.uniprot.org/citations/30397201http://purl.uniprot.org/core/title"Recognition of host Clr-b by the inhibitory NKR-P1B receptor provides a basis for missing-self recognition."xsd:string
http://purl.uniprot.org/citations/30397201http://purl.uniprot.org/core/volume"9"xsd:string
http://purl.uniprot.org/citations/30397201http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/30397201
http://purl.uniprot.org/citations/30397201http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/30397201
http://purl.uniprot.org/uniprot/#_Q99JB4-mappedCitation-30397201http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30397201
http://purl.uniprot.org/uniprot/#_Q91V08-mappedCitation-30397201http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/30397201
http://purl.uniprot.org/uniprot/Q99JB4http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/30397201
http://purl.uniprot.org/uniprot/Q91V08http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/30397201