| http://purl.uniprot.org/citations/12118252 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/12118252 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/12118252 | http://www.w3.org/2000/01/rdf-schema#comment | "The autoimmune disease type 1 diabetes mellitus (insulin-dependent diabetes mellitus, IDDM) has a multifactorial etiology. So far, the major histocompatibility complex (MHC) is the only major susceptibility locus that has been identified for this disease and its animal models. The Komeda diabetes-prone (KDP) rat is a spontaneous animal model of human type 1 diabetes in which the major susceptibility locus Iddm/kdp1 accounts, in combination with MHC, for most of the genetic predisposition to diabetes. Here we report the positional cloning of Iddm/kdp1 and identify a nonsense mutation in Cblb, a member of the Cbl/Sli family of ubiquitin-protein ligases. Lymphocytes of the KDP rat infiltrate into pancreatic islets and several tissues including thyroid gland and kidney, indicating autoimmunity. Similar findings in Cblb-deficient mice are caused by enhanced T-cell activation. Transgenic complementation with wildtype Cblb significantly suppresses development of the KDP phenotype. Thus, Cblb functions as a negative regulator of autoimmunity and Cblb is a major susceptibility gene for type 1 diabetes in the rat. Impairment of the Cblb signaling pathway may contribute to human autoimmune diseases, including type 1 diabetes."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.org/dc/terms/identifier | "doi:10.1038/ng927"xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.org/dc/terms/identifier | "doi:10.1038/ng927"xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Saitoh Y."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Saitoh Y."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Yasuda K."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Yasuda K."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Wang H.-Y."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Wang H.-Y."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Seino S."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Seino S."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Yokoi N."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Yokoi N."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Yano H."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Yano H."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Kitada K."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Kitada K."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Serikawa T."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Serikawa T."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Seino Y."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Seino Y."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Komeda K."xsd:string |
| http://purl.uniprot.org/citations/12118252 | http://purl.uniprot.org/core/author | "Komeda K."xsd:string |