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http://purl.uniprot.org/citations/15696195http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15696195http://www.w3.org/2000/01/rdf-schema#comment"Rap1b, an abundant small GTPase in platelets, becomes rapidly activated upon stimulation with agonists. Though it has been implicated to act downstream from G protein-coupled receptors (GPCRs) and upstream of integrin alpha IIbbeta3, the precise role of Rap1b in platelet function has been elusive. Here we report the generation of a murine rap1b knockout and show that Rap1b deficiency results in a bleeding defect due to defective platelet function. Aggregation of Rap1b-null platelets is reduced in response to stimulation with both GPCR-linked and GPCR-independent agonists. Underlying the defective Rap1b-null platelet function is decreased activation of integrin alphaIIbbeta3 in response to stimulation with agonists and signaling downstream from the integrin alpha IIbbeta3. In vivo, Rap1b-null mice are protected from arterial thrombosis. These data provide genetic evidence that Rap1b is involved in a common pathway of integrin activation, is required for normal hemostasis in vivo, and may be a clinically relevant antithrombotic therapy target."xsd:string
http://purl.uniprot.org/citations/15696195http://purl.org/dc/terms/identifier"doi:10.1172/jci22973"xsd:string
http://purl.uniprot.org/citations/15696195http://purl.uniprot.org/core/author"Schoenwaelder S.M."xsd:string
http://purl.uniprot.org/citations/15696195http://purl.uniprot.org/core/author"Smyth S.S."xsd:string
http://purl.uniprot.org/citations/15696195http://purl.uniprot.org/core/author"White G.C."xsd:string
http://purl.uniprot.org/citations/15696195http://purl.uniprot.org/core/author"Fischer T.H."xsd:string
http://purl.uniprot.org/citations/15696195http://purl.uniprot.org/core/author"Chrzanowska-Wodnicka M."xsd:string
http://purl.uniprot.org/citations/15696195http://purl.uniprot.org/core/date"2005"xsd:gYear
http://purl.uniprot.org/citations/15696195http://purl.uniprot.org/core/name"J Clin Invest"xsd:string
http://purl.uniprot.org/citations/15696195http://purl.uniprot.org/core/pages"680-687"xsd:string
http://purl.uniprot.org/citations/15696195http://purl.uniprot.org/core/title"Rap1b is required for normal platelet function and hemostasis in mice."xsd:string
http://purl.uniprot.org/citations/15696195http://purl.uniprot.org/core/volume"115"xsd:string
http://purl.uniprot.org/citations/15696195http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/15696195
http://purl.uniprot.org/citations/15696195http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/15696195
http://purl.uniprot.org/uniprot/#_A0A1W2P777-mappedCitation-15696195http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15696195
http://purl.uniprot.org/uniprot/#_Q99JI6-mappedCitation-15696195http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15696195
http://purl.uniprot.org/uniprot/#_Q52L50-mappedCitation-15696195http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15696195
http://purl.uniprot.org/uniprot/Q99JI6http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/15696195
http://purl.uniprot.org/uniprot/A0A1W2P777http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/15696195
http://purl.uniprot.org/uniprot/Q52L50http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/15696195