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http://purl.uniprot.org/citations/19213844 | http://www.w3.org/2000/01/rdf-schema#comment | "Pituitary tumor transforming gene (PTTG) encodes a securin protein critical in regulating chromosome separation. PTTG-null (PTTG(-/-)) mice exhibit pancreatic beta-cell hypoplasia and insulinopenic diabetes. We tested whether PTTG deletion causes beta-cell senescence, resulting in diminished beta-cell mass. We examined beta-cell mass, proliferation, apoptosis, neogenesis, cell size, and senescence in PTTG(-/-) and WT mice from embryo to young adulthood before diabetes is evident. The roles of cyclin-dependent kinase inhibitors and DNA damage in the pathogenesis of diabetes in PTTG(-/-) mice were also addressed. Relative beta-cell mass in PTTG(-/-) mice began to decrease at 2-3 wk, whereas beta-cell proliferation rate was initially normal but decreased in PTTG(-/-) mice beginning at 2 months. Apoptosis was also much more evident in PTTG(-/-) mice. At 1 month, beta-cell neogenesis was robust in wild-type mice but was absent in PTTG(-/-) mice. In addition, the size of beta-cells became larger and macronuclei were prominent in PTTG(-/-) animals. Senescence-associated beta-galactosidase was also active in PTTG(-/-) beta-cells at 1 month. Cyclin-dependent kinase inhibitor p21 was progressively up-regulated in PTTG(-/-) islets, and p21 deletion partially rescued PTTG(-/-) mice from development of diabetes. mRNA array showed that DNA damage-associated genes were activated in PTTG(-/-) islets. We conclude that beta-cell apoptosis and senescence contribute to the diminished beta-cell mass in PTTG(-/-) mice, likely secondary to DNA damage. Our results also suggest that ductal progenitor beta-cells are exhausted by excessive neogenesis induced by apoptosis in PTTG(-/-) mice."xsd:string |
http://purl.uniprot.org/citations/19213844 | http://purl.org/dc/terms/identifier | "doi:10.1210/en.2008-0972"xsd:string |
http://purl.uniprot.org/citations/19213844 | http://purl.uniprot.org/core/author | "Wong C."xsd:string |
http://purl.uniprot.org/citations/19213844 | http://purl.uniprot.org/core/author | "Yu R."xsd:string |
http://purl.uniprot.org/citations/19213844 | http://purl.uniprot.org/core/author | "Wawrowsky K."xsd:string |
http://purl.uniprot.org/citations/19213844 | http://purl.uniprot.org/core/author | "Chesnokova V."xsd:string |
http://purl.uniprot.org/citations/19213844 | http://purl.uniprot.org/core/author | "Ren S.G."xsd:string |
http://purl.uniprot.org/citations/19213844 | http://purl.uniprot.org/core/author | "Zonis S."xsd:string |
http://purl.uniprot.org/citations/19213844 | http://purl.uniprot.org/core/author | "Gruszka A."xsd:string |
http://purl.uniprot.org/citations/19213844 | http://purl.uniprot.org/core/author | "Benshlomo A."xsd:string |
http://purl.uniprot.org/citations/19213844 | http://purl.uniprot.org/core/date | "2009"xsd:gYear |
http://purl.uniprot.org/citations/19213844 | http://purl.uniprot.org/core/name | "Endocrinology"xsd:string |
http://purl.uniprot.org/citations/19213844 | http://purl.uniprot.org/core/pages | "2603-2610"xsd:string |
http://purl.uniprot.org/citations/19213844 | http://purl.uniprot.org/core/title | "Diminished pancreatic beta-cell mass in securin-null mice is caused by beta-cell apoptosis and senescence."xsd:string |
http://purl.uniprot.org/citations/19213844 | http://purl.uniprot.org/core/volume | "150"xsd:string |
http://purl.uniprot.org/citations/19213844 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/19213844 |
http://purl.uniprot.org/citations/19213844 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/19213844 |
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