| http://purl.uniprot.org/citations/19036881 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/19036881 | http://www.w3.org/2000/01/rdf-schema#comment | "Implicated in the pathogenesis of breast cancer, prolactin (PRL) mediates its function in part through the prolactin receptor (PRLr)-associated Janus kinase 2 (Jak2)/signal transducer and activator of transcription 5 (Stat5) signaling complex. To delineate the mechanisms of Stat5a regulation in breast cancer, transcription factor-transcription factor (TF-TF) array analysis was employed to identify associated transcriptional regulators. These analyses revealed a PRL-inducible association of Stat5a with the transcription factor and protooncogene c-Myb. Confirmatory co-immunoprecipitation studies using lysates from both T47D and MCF7 breast cancer cells revealed a PRL-inducible association between these transcription factors. Ectopic expression of c-Myb enhanced the PRL-induced expression from both composite and synthetic Stat5a-responsive luciferase reporters. Chromatin immunoprecipitation assays also revealed a PRL-inducible association between c-Myb and endogenous Stat5a-responsive CISH promoter, which was associated with an enhanced expression of CISH gene product at the RNA and protein levels. Small interfering RNA-mediated c-Myb knockdown impaired the PRL-induced mRNA expression of five Stat5-responsive genes. DNA binding-defective mutants of c-Myb, incapable of activating expression from a c-Myb-responsive reporter, maintained their ability to enhance a Stat5a-responsive reporter. At a cellular level, ectopic expression of c-Myb resulted in an increase in T47D proliferation. Taken together, these results indicate that c-Myb potentiates Stat5a-driven gene expression, possibly functioning as a Stat5a coactivator, in human breast cancer."xsd:string |
| http://purl.uniprot.org/citations/19036881 | http://purl.org/dc/terms/identifier | "doi:10.1210/en.2008-1079"xsd:string |
| http://purl.uniprot.org/citations/19036881 | http://purl.uniprot.org/core/author | "Fang F."xsd:string |
| http://purl.uniprot.org/citations/19036881 | http://purl.uniprot.org/core/author | "Clevenger C.V."xsd:string |
| http://purl.uniprot.org/citations/19036881 | http://purl.uniprot.org/core/author | "Rycyzyn M.A."xsd:string |
| http://purl.uniprot.org/citations/19036881 | http://purl.uniprot.org/core/date | "2009"xsd:gYear |
| http://purl.uniprot.org/citations/19036881 | http://purl.uniprot.org/core/name | "Endocrinology"xsd:string |
| http://purl.uniprot.org/citations/19036881 | http://purl.uniprot.org/core/pages | "1597-1606"xsd:string |
| http://purl.uniprot.org/citations/19036881 | http://purl.uniprot.org/core/title | "Role of c-Myb during prolactin-induced signal transducer and activator of transcription 5a signaling in breast cancer cells."xsd:string |
| http://purl.uniprot.org/citations/19036881 | http://purl.uniprot.org/core/volume | "150"xsd:string |
| http://purl.uniprot.org/citations/19036881 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/19036881 |
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| http://purl.uniprot.org/uniprot/#_Q708E1-mappedCitation-19036881 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/19036881 |
| http://purl.uniprot.org/uniprot/#_Q708E2-mappedCitation-19036881 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/19036881 |
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| http://purl.uniprot.org/uniprot/#_Q708E8-mappedCitation-19036881 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/19036881 |
| http://purl.uniprot.org/uniprot/#_Q708E9-mappedCitation-19036881 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/19036881 |
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| http://purl.uniprot.org/uniprot/#_Q708J0-mappedCitation-19036881 | http://www.w3.org/1999/02/22-rdf-syntax-ns#object | http://purl.uniprot.org/citations/19036881 |