| http://purl.uniprot.org/citations/12663502 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/12663502 | http://www.w3.org/2000/01/rdf-schema#comment | "Mutational activation of beta-catenin and cyclin D1 over-expression are a frequent change in mouse hepatic tumors. Although activated beta-catenin may bind to T cell factor (TCF) family members and transcriptionally activate the cyclin D1 gene, either beta-catenin or cyclin D1 may be activated by various pathways independently of beta-catenin mutations. In this study, we investigated beta-catenin activation and mutations, cyclin D1 expression, H-ras mutations and phosphorylation of extracellular signal regulated protein kinases 1/2 (ERK1/2), Akt and glycogen synthetase kinase 3beta (GSK3 beta) in mouse hepatic carcinogenesis. Nuclear/cytoplasmic staining of beta-catenin, a sign of beta-catenin activation, was frequently observed in association with the high nuclear cyclin D1 labeling index in the hepatic tumors at the late stage of carcinogenesis. The beta-catenin activation was further suggested by the fact that all hepatocellular carcinoma (HCC) cell lines examined showed the nuclear beta-catenin/TCF4 complex together with cyclin D1 over-expression. However, the fact that only 31.8% (7/22) of the lesions with the nuclear/cytoplasmic beta-catenin staining showed beta-catenin mutations indicated that beta-catenin was activated not only by its own mutations but also by other reason(s). On the other hand, there was no correlation between the beta-catenin/cyclin D1 activation and the H-ras mutations or phosphorylation of Akt, GSK3 beta and ERK1/2, although GSK3 beta was frequently over-expressed in the tumors. These results indicate that, although beta-catenin and cyclin D1 activation are well correlated, the Akt/GSK3 beta and ras/ERK1/2 pathways may not play a major role in the beta-catenin/cyclin D1 activation."xsd:string |
| http://purl.uniprot.org/citations/12663502 | http://purl.org/dc/terms/identifier | "doi:10.1093/carcin/24.3.435"xsd:string |
| http://purl.uniprot.org/citations/12663502 | http://purl.uniprot.org/core/author | "Ogawa K."xsd:string |
| http://purl.uniprot.org/citations/12663502 | http://purl.uniprot.org/core/author | "Kasai S."xsd:string |
| http://purl.uniprot.org/citations/12663502 | http://purl.uniprot.org/core/author | "Obata M."xsd:string |
| http://purl.uniprot.org/citations/12663502 | http://purl.uniprot.org/core/author | "Gotoh J."xsd:string |
| http://purl.uniprot.org/citations/12663502 | http://purl.uniprot.org/core/author | "Yoshie M."xsd:string |
| http://purl.uniprot.org/citations/12663502 | http://purl.uniprot.org/core/date | "2003"xsd:gYear |
| http://purl.uniprot.org/citations/12663502 | http://purl.uniprot.org/core/name | "Carcinogenesis"xsd:string |
| http://purl.uniprot.org/citations/12663502 | http://purl.uniprot.org/core/pages | "435-442"xsd:string |
| http://purl.uniprot.org/citations/12663502 | http://purl.uniprot.org/core/title | "Cyclin D1 over-expression correlates with beta-catenin activation, but not with H-ras mutations, and phosphorylation of Akt, GSK3 beta and ERK1/2 in mouse hepatic carcinogenesis."xsd:string |
| http://purl.uniprot.org/citations/12663502 | http://purl.uniprot.org/core/volume | "24"xsd:string |
| http://purl.uniprot.org/citations/12663502 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/12663502 |
| http://purl.uniprot.org/citations/12663502 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/12663502 |
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