| http://purl.uniprot.org/citations/15220191 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15220191 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15220191 | http://www.w3.org/2000/01/rdf-schema#comment | "Insulinoma-associated protein (IA)-2beta, also known as phogrin, is an enzymatically inactive member of the transmembrane protein tyrosine phosphatase family and is located in dense-core secretory vesicles. In patients with type 1 diabetes, autoantibodies to IA-2beta appear years before the development of clinical disease. The genomic structure and function of IA-2beta, however, is not known. In the present study, we determined the genomic structure of IA-2beta and found that both human and mouse IA-2beta consist of 23 exons and span approximately 1,000 and 800 kb, respectively. With this information, we prepared a targeting construct and inactivated the mouse IA-2beta gene as demonstrated by lack of IA-2beta mRNA and protein expression. The IA-2beta(-/-) mice, in contrast to wild-type controls, showed mild glucose intolerance and impaired glucose-stimulated insulin secretion. Knockout of the IA-2beta gene in NOD mice, the most widely studied animal model for human type 1 diabetes, failed to prevent the development of cyclophosphamide-induced diabetes. We conclude that IA-2beta is involved in insulin secretion, but despite its importance as a major autoantigen in human type 1 diabetes, it is not required for the development of diabetes in NOD mice."xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.org/dc/terms/identifier | "doi:10.2337/diabetes.53.7.1684"xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.org/dc/terms/identifier | "doi:10.2337/diabetes.53.7.1684"xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/author | "Nakamura S."xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/author | "Nakamura S."xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/author | "Gross S."xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/author | "Gross S."xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/author | "Zhu M."xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/author | "Zhu M."xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/author | "Saeki K."xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/author | "Saeki K."xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/author | "Kubosaki A."xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/author | "Kubosaki A."xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/author | "Hendriks W."xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/author | "Hendriks W."xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/author | "Miura J."xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/author | "Miura J."xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/author | "Notkins A.L."xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/author | "Notkins A.L."xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/name | "Diabetes"xsd:string |
| http://purl.uniprot.org/citations/15220191 | http://purl.uniprot.org/core/name | "Diabetes"xsd:string |