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http://purl.uniprot.org/citations/19265110http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19265110http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/19265110http://www.w3.org/2000/01/rdf-schema#comment"PTPN22 is a gene encoding the protein tyrosine phosphatase Lyp. A missense mutation changing residue 1858 from cytosine to thymidine (1858C/T) is associated with multiple autoimmune disorders. Studies have demonstrated that Lyp has an inhibitory effect on TCR signaling; however, the presence of autoantibodies in all of the diseases associated with the 1858T variant and recent evidence that Ca(2+) flux is altered in B cells of 1858T carriers indicate a role for Lyp in B cell signaling. In this study we show that B cell signal transduction is impaired in individuals who express the variant. This defect in signaling is characterized by a deficit in proliferation, a decrease in phosphorylation of key signaling proteins, and is reversed by inhibition of Lyp. These findings suggest that the PTPN22 1858T variant alters BCR signaling and implicate B cells in the mechanism by which the PTPN22 1858T variant contributes to autoimmunity."xsd:string
http://purl.uniprot.org/citations/19265110http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.0713370"xsd:string
http://purl.uniprot.org/citations/19265110http://purl.org/dc/terms/identifier"doi:10.4049/jimmunol.0713370"xsd:string
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/author"Funk A."xsd:string
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/author"Funk A."xsd:string
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/author"He Y."xsd:string
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/author"He Y."xsd:string
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/author"Zhang X."xsd:string
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/author"Zhang X."xsd:string
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/author"Zhang Z.Y."xsd:string
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/author"Zhang Z.Y."xsd:string
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/author"Habib T."xsd:string
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/author"Habib T."xsd:string
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/author"Buckner J.H."xsd:string
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/author"Buckner J.H."xsd:string
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/author"Arechiga A.F."xsd:string
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/author"Arechiga A.F."xsd:string
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/date"2009"xsd:gYear
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/name"J. Immunol."xsd:string
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/name"J. Immunol."xsd:string
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/pages"3343-3347"xsd:string
http://purl.uniprot.org/citations/19265110http://purl.uniprot.org/core/pages"3343-3347"xsd:string