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http://purl.uniprot.org/citations/16618600http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16618600http://www.w3.org/2000/01/rdf-schema#comment"We previously reported that the mice deficient for SPA-1, a Rap1 GTPase-activating protein, developed hematopoietic stem cell disorders. Here, we demonstrate that SPA-1(-/-) mice show an age-dependent increase in B220(high) B1a cells producing anti-dsDNA antibody and lupus-like nephritis. SPA-1(-/-) peritoneal B1 cells revealed the altered Vkappa gene repertoire, including skewed Vkappa4 usage and the significant Igkappa/Iglambda isotype inclusion indicative of extensive receptor editing. Rap1GTP induced OcaB gene activation via p38MAPK-dependent Creb phosphorylation, and consistently, SPA-1(-/-) immature BM B cells showing high Rap1GTP exhibited the augmented expression of OcaB and Vkappa4 genes. SPA-1(-/-) BM cells could transfer the autoimmunity in association with the generation of peritoneal B220(high) B1a cells in Rag-2(-/-) recipients. Finally, a portion of SPA-1(-/-) mice developed B1 cell leukemia with hemolytic autoantibody. Present results suggest that the regulated Rap1 signal in the immature B cells plays a role in modifying the B cell receptor repertoire and in maintaining the self-tolerance."xsd:string
http://purl.uniprot.org/citations/16618600http://purl.org/dc/terms/identifier"doi:10.1016/j.immuni.2006.02.007"xsd:string
http://purl.uniprot.org/citations/16618600http://purl.uniprot.org/core/author"Hattori M."xsd:string
http://purl.uniprot.org/citations/16618600http://purl.uniprot.org/core/author"Kawai Y."xsd:string
http://purl.uniprot.org/citations/16618600http://purl.uniprot.org/core/author"Katayama Y."xsd:string
http://purl.uniprot.org/citations/16618600http://purl.uniprot.org/core/author"Minato N."xsd:string
http://purl.uniprot.org/citations/16618600http://purl.uniprot.org/core/author"Su L."xsd:string
http://purl.uniprot.org/citations/16618600http://purl.uniprot.org/core/author"Tamura A."xsd:string
http://purl.uniprot.org/citations/16618600http://purl.uniprot.org/core/author"Taniwaki M."xsd:string
http://purl.uniprot.org/citations/16618600http://purl.uniprot.org/core/author"Wang S.F."xsd:string
http://purl.uniprot.org/citations/16618600http://purl.uniprot.org/core/author"Hamazaki Y."xsd:string
http://purl.uniprot.org/citations/16618600http://purl.uniprot.org/core/author"Ishida D."xsd:string
http://purl.uniprot.org/citations/16618600http://purl.uniprot.org/core/date"2006"xsd:gYear
http://purl.uniprot.org/citations/16618600http://purl.uniprot.org/core/name"Immunity"xsd:string
http://purl.uniprot.org/citations/16618600http://purl.uniprot.org/core/pages"417-427"xsd:string
http://purl.uniprot.org/citations/16618600http://purl.uniprot.org/core/title"Rap1 signal controls B cell receptor repertoire and generation of self-reactive B1a cells."xsd:string
http://purl.uniprot.org/citations/16618600http://purl.uniprot.org/core/volume"24"xsd:string
http://purl.uniprot.org/citations/16618600http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/16618600
http://purl.uniprot.org/citations/16618600http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/16618600
http://purl.uniprot.org/uniprot/#_E9Q0Y4-mappedCitation-16618600http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16618600
http://purl.uniprot.org/uniprot/#_A0A494BAM3-mappedCitation-16618600http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16618600
http://purl.uniprot.org/uniprot/#_Q3U146-mappedCitation-16618600http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16618600
http://purl.uniprot.org/uniprot/#_P46062-mappedCitation-16618600http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16618600
http://purl.uniprot.org/uniprot/#_Q3UV58-mappedCitation-16618600http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16618600