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http://purl.uniprot.org/citations/17572677http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17572677http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/17572677http://www.w3.org/2000/01/rdf-schema#comment"B1 cells are an important cell population for the production of natural antibodies and for antibacterial immunoglobulin responses. Here we identified the mouse protein Siglec-G as a B1 cell inhibitory receptor. Siglec-G was expressed in a B cell-restricted way, with large amounts present in B1 cells. When overexpressed, Siglec-G inhibited B cell receptor-mediated calcium signaling. Siglec-G-deficient mice had massive expansion of the B1a cell population, which began early in development and was B cell intrinsic. Siglec-G-deficient mice had higher titers of natural IgM antibodies but not a higher penetrance of IgG autoantibodies. Siglec-G-deficient B1 cells showed a strongly enhanced calcium signaling. Our results demonstrate that Siglec-G-dependent negative regulation exists in B1 cells, which may explain the naturally muted signaling response of B1 cells."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.org/dc/terms/identifier"doi:10.1038/ni1480"xsd:string
http://purl.uniprot.org/citations/17572677http://purl.org/dc/terms/identifier"doi:10.1038/ni1480"xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Zhang J."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Zhang J."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Crocker P.R."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Crocker P.R."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Hoffmann A."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Hoffmann A."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Winkler T.H."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Winkler T.H."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Nitschke L."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Nitschke L."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Jellusova J."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Jellusova J."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Wellmann U."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Wellmann U."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Kerr S."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Kerr S."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Kneitz B."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Kneitz B."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Weisel F."xsd:string
http://purl.uniprot.org/citations/17572677http://purl.uniprot.org/core/author"Weisel F."xsd:string