| http://purl.uniprot.org/citations/12031967 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/12031967 | http://www.w3.org/2000/01/rdf-schema#comment | "To test the hypothesis that c-Myc plays an important role in beta-cell growth and differentiation, we generated transgenic mice overexpressing c-Myc in beta-cells under control of the rat insulin II promoter. F(1) transgenic mice from two founders developed neonatal diabetes (associated with reduced plasma insulin levels) and died of hyperglycemia 3 days after birth. In pancreata of transgenic mice, marked hyperplasia of cells with an altered phenotype and amorphous islet organization was displayed: islet volume was increased threefold versus wild-type littermates. Apoptotic nuclei were increased fourfold in transgenic versus wild-type mice, suggesting an increased turnover of beta-cells. Very few cells immunostained for insulin; pancreatic insulin mRNA and content were markedly reduced. GLUT2 mRNA was decreased, but other beta-cell-associated genes (IAPP [islet amyloid pancreatic polypeptide], PDX-1 [pancreatic and duodenal homeobox-1], and BETA2/NeuroD) were expressed at near-normal levels. Immunostaining for both GLUT2 and Nkx6.1 was mainly cytoplasmic. The defect in beta-cell phenotype in transgenic embryos (embryonic days 17-18) and neonates (days 1-2) was similar and, therefore, was not secondary to overt hyperglycemia. When pancreata were transplanted under the kidney capsules of athymic mice to analyze the long-term effects of c-Myc activation, beta-cell depletion was found, suggesting that, ultimately, apoptosis predominates over proliferation. In conclusion, these studies demonstrate that activation of c-Myc in beta-cells leads to 1) increased proliferation and apoptosis, 2) initial hyperplasia with amorphous islet organization, and 3) selective downregulation of insulin gene expression and the development of overt diabetes."xsd:string |
| http://purl.uniprot.org/citations/12031967 | http://purl.org/dc/terms/identifier | "doi:10.2337/diabetes.51.6.1793"xsd:string |
| http://purl.uniprot.org/citations/12031967 | http://purl.uniprot.org/core/author | "Sharma A."xsd:string |
| http://purl.uniprot.org/citations/12031967 | http://purl.uniprot.org/core/author | "Bonner-Weir S."xsd:string |
| http://purl.uniprot.org/citations/12031967 | http://purl.uniprot.org/core/author | "Palmiter R.D."xsd:string |
| http://purl.uniprot.org/citations/12031967 | http://purl.uniprot.org/core/author | "Weir G.C."xsd:string |
| http://purl.uniprot.org/citations/12031967 | http://purl.uniprot.org/core/author | "Laybutt D.R."xsd:string |
| http://purl.uniprot.org/citations/12031967 | http://purl.uniprot.org/core/author | "Kaneto H."xsd:string |
| http://purl.uniprot.org/citations/12031967 | http://purl.uniprot.org/core/author | "Lebet J."xsd:string |
| http://purl.uniprot.org/citations/12031967 | http://purl.uniprot.org/core/date | "2002"xsd:gYear |
| http://purl.uniprot.org/citations/12031967 | http://purl.uniprot.org/core/name | "Diabetes"xsd:string |
| http://purl.uniprot.org/citations/12031967 | http://purl.uniprot.org/core/pages | "1793-1804"xsd:string |
| http://purl.uniprot.org/citations/12031967 | http://purl.uniprot.org/core/title | "Overexpression of c-Myc in beta-cells of transgenic mice causes proliferation and apoptosis, downregulation of insulin gene expression, and diabetes."xsd:string |
| http://purl.uniprot.org/citations/12031967 | http://purl.uniprot.org/core/volume | "51"xsd:string |
| http://purl.uniprot.org/citations/12031967 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/12031967 |
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| http://purl.uniprot.org/uniprot/#_O88594-mappedCitation-12031967 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/12031967 |
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