RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/23781148http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23781148http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23781148http://www.w3.org/2000/01/rdf-schema#comment"DOC-1R (deleted in oral cancer-1 related) is a novel putative tumor suppressor. This study investigated DOC-1R antitumor activity and the underlying molecular mechanisms. Cell phenotypes were assessed using flow cytometry, BrdU incorporation and CDK2 kinase assays in DOC-1R overexpressing HeLa cells. In addition, RT-PCR and Western blot assays were used to detect underlying molecular changes in these cells. The interaction between DOC-1R and CDK2 proteins was assayed by GST pull-down and immunoprecipitation-Western blot assays. The data showed that DOC-1R overexpression inhibited G1/S phase transition, DNA replication and suppressed CDK2 activity. Molecularly, DOC-1R inhibited CDK2 expression at the mRNA and protein levels, and there were decreased levels of G1-phase cyclins (cyclin D1 and E) and elevated levels of p21, p27, and p53 proteins. Meanwhile, DOC-1R associated with CDK2 and inhibited CDK2 activation by obstructing its association with cyclin E and A. In conclusion, the antitumor effects of DOC-1R may be mediated by negatively regulating G1 phase progression and G1/S transition through inhibiting CDK2 expression and activation."xsd:string
http://purl.uniprot.org/citations/23781148http://purl.org/dc/terms/identifier"doi:10.7150/ijbs.5763"xsd:string
http://purl.uniprot.org/citations/23781148http://purl.org/dc/terms/identifier"doi:10.7150/ijbs.5763"xsd:string
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/author"Hu X."xsd:string
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/author"Hu X."xsd:string
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/author"Liu Q."xsd:string
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/author"Liu Q."xsd:string
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/author"Gao J."xsd:string
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/author"Gao J."xsd:string
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/author"Luo Y."xsd:string
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/author"Luo Y."xsd:string
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/author"Liu X."xsd:string
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/author"Liu X."xsd:string
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/author"Shi X."xsd:string
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/author"Shi X."xsd:string
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/author"Wang S."xsd:string
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/author"Wang S."xsd:string
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/name"Int. J. Biol. Sci."xsd:string
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/name"Int. J. Biol. Sci."xsd:string
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/pages"541-549"xsd:string
http://purl.uniprot.org/citations/23781148http://purl.uniprot.org/core/pages"541-549"xsd:string