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http://purl.uniprot.org/citations/22307329http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22307329http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/22307329http://www.w3.org/2000/01/rdf-schema#comment"Dysregulation of the G(1)/S transition in the cell cycle contributes to tumor development. The oncogenic transcription factors c-Jun and c-Myc are indispensable regulators at this transition, and their aberrant expression is associated with many malignancies. Degradation of c-Jun/c-Myc is a critical process for the G(1)/S transition, which is initiated upon phosphorylation by glycogen synthase kinase 3 β (GSK3β). However, a specific kinase or kinases responsible for priming phosphorylation events that precede this GSK3β modification has not been definitively identified. Here, we found that the dual-specificity tyrosine phosphorylation-regulated kinase DYRK2 functions as a priming kinase of c-Jun and c-Myc. Knockdown of DYRK2 in human cancer cells shortened the G(1) phase and accelerated cell proliferation due to escape of c-Jun and c-Myc from ubiquitination-mediated degradation. In concert with these results, silencing DYRK2 increased cell proliferation in human cancer cells, and this promotion was completely impeded by codeprivation of c-Jun or c-Myc in vivo. We also found marked attenuation of DYRK2 expression in multiple human tumor samples. Downregulation of DYRK2 correlated with high levels of unphosphorylated c-Jun and c-Myc and, importantly, with invasiveness of human breast cancers. These results reveal that DYRK2 regulates tumor progression through modulation of c-Jun and c-Myc."xsd:string
http://purl.uniprot.org/citations/22307329http://purl.org/dc/terms/identifier"doi:10.1172/jci60818"xsd:string
http://purl.uniprot.org/citations/22307329http://purl.org/dc/terms/identifier"doi:10.1172/jci60818"xsd:string
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/author"Kitagawa M."xsd:string
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/author"Kitagawa M."xsd:string
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/author"Miki Y."xsd:string
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/author"Miki Y."xsd:string
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/author"Yamaguchi T."xsd:string
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/author"Yamaguchi T."xsd:string
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/author"Yoshida K."xsd:string
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/author"Yoshida K."xsd:string
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/author"Kurata M."xsd:string
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/author"Kurata M."xsd:string
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/author"Taira N."xsd:string
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/author"Taira N."xsd:string
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/author"Mimoto R."xsd:string
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/author"Mimoto R."xsd:string
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/date"2012"xsd:gYear
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/name"J. Clin. Invest."xsd:string
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/name"J. Clin. Invest."xsd:string
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/pages"859-872"xsd:string
http://purl.uniprot.org/citations/22307329http://purl.uniprot.org/core/pages"859-872"xsd:string