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http://purl.uniprot.org/citations/16120603http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/16120603http://www.w3.org/2000/01/rdf-schema#comment"In contrast to hormone-dependent breast cancer, steroid hormone-induced proliferation in the normal mammary gland does not occur in the steroid-receptor positive cells but rather in adjacent cells via paracrine signaling involving several local growth factors. To help elucidate the mechanisms involved in the block in proliferation in hormone-receptor positive cells, we have utilized a CCAAT/enhancer binding protein (C/EBPbeta)-null mouse model. Loss of this transcription factor results in increased steroid and prolactin receptor expression concomitant with a 10-fold decrease in proliferation in response to pregnancy hormones. To determine the basis for this decrease, several markers of cell cycle progression were analyzed in wild type and C/EBPbeta-null mammary epithelial cells (MECs). These studies indicated that cell cycle progression in C/EBPbeta-null MECs is blocked at the G1/S transition. C/EBPbeta-null mammary glands display substantially increased levels of the activated form of transforming growth factor beta, a potent inhibitor of epithelial cell proliferation, as well as increased downstream Smad2 expression and signaling. While cyclin D1 levels were equivalent, cyclin E expression was markedly reduced in C/EBPbeta-null as compared with wildtype MECs. In addition, increased p27 stability and retention in the nucleus and decreased levels of the cdc25a phosphatase contributed to a significant loss of cdk2 kinase activity. Collectively, these changes prevent C/EBPbeta-null mammary epithelial cells from responding to hormone-induced proliferative signals."xsd:string
http://purl.uniprot.org/citations/16120603http://purl.org/dc/terms/identifier"doi:10.1074/jbc.m508167200"xsd:string
http://purl.uniprot.org/citations/16120603http://purl.uniprot.org/core/author"Contreras A."xsd:string
http://purl.uniprot.org/citations/16120603http://purl.uniprot.org/core/author"Rosen J.M."xsd:string
http://purl.uniprot.org/citations/16120603http://purl.uniprot.org/core/author"Grimm S.L."xsd:string
http://purl.uniprot.org/citations/16120603http://purl.uniprot.org/core/author"Barcellos-Hoff M.H."xsd:string
http://purl.uniprot.org/citations/16120603http://purl.uniprot.org/core/date"2005"xsd:gYear
http://purl.uniprot.org/citations/16120603http://purl.uniprot.org/core/name"J Biol Chem"xsd:string
http://purl.uniprot.org/citations/16120603http://purl.uniprot.org/core/pages"36301-36309"xsd:string
http://purl.uniprot.org/citations/16120603http://purl.uniprot.org/core/title"Cell cycle defects contribute to a block in hormone-induced mammary gland proliferation in CCAAT/enhancer-binding protein (C/EBPbeta)-null mice."xsd:string
http://purl.uniprot.org/citations/16120603http://purl.uniprot.org/core/volume"280"xsd:string
http://purl.uniprot.org/citations/16120603http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/16120603
http://purl.uniprot.org/citations/16120603http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/16120603
http://purl.uniprot.org/uniprot/#_P28033-mappedCitation-16120603http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16120603
http://purl.uniprot.org/uniprot/#_Q3UGB9-mappedCitation-16120603http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16120603
http://purl.uniprot.org/uniprot/#_O70192-mappedCitation-16120603http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16120603
http://purl.uniprot.org/uniprot/#_Q3U6X7-mappedCitation-16120603http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16120603
http://purl.uniprot.org/uniprot/#_P97377-mappedCitation-16120603http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16120603
http://purl.uniprot.org/uniprot/#_Q3U307-mappedCitation-16120603http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16120603
http://purl.uniprot.org/uniprot/#_Q3UPN9-mappedCitation-16120603http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16120603
http://purl.uniprot.org/uniprot/#_Q6LD68-mappedCitation-16120603http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/16120603
http://purl.uniprot.org/uniprot/P28033http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/16120603
http://purl.uniprot.org/uniprot/Q3UPN9http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/16120603
http://purl.uniprot.org/uniprot/Q6LD68http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/16120603