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http://purl.uniprot.org/citations/15056731http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15056731http://www.w3.org/2000/01/rdf-schema#comment"Estrogen receptor alpha (ERalpha) negative breast tumors often present with enhanced expression and/or activation of growth factor receptors, resulting in increased growth factor signaling and hyperactivation of MAPK (ERK1 and ERK2). We have pre-viously shown that ERalpha(+) MCF-7 cells with elevated growth factor signaling lose expression of ERalpha without any ligand-independent transcriptional activation, and this is a reversible effect attributable to ERK1/2 hyperactivation. Here, we show that down-regulation of ERalpha is not mediated by a specific ERK-1 vs. ERK-2 substrate. Despite up-regulated activator protein-1 activity in response to ERK1/2 activation, and in ERalpha(-) and hormone-independent breast cancers, we find that increased activator protein-1 activity is not responsible for ERalpha down-regulation. Interestingly, our findings implicate a cytoplasmic substrate of ERK1/2. However, RSK1, the best-characterized cytoplasmic ERK1/2 substrate, does not down-regulate ERalpha in our models. On the other hand, inhibition of nuclear factor-kappaB (which is linked to chemoresistance in cancer in general and has elevated activity in hormone-independent and ERalpha-breast cancer) significantly enhances ERalpha activity, suggesting that indirect elevation in nuclear factor-kappaB activity (due to hyperactive ERK1/2) is at least partially responsible for ERalpha down-regulation in these cell line models."xsd:string
http://purl.uniprot.org/citations/15056731http://purl.org/dc/terms/identifier"doi:10.1210/me.2004-0048"xsd:string
http://purl.uniprot.org/citations/15056731http://purl.uniprot.org/core/author"Murthy S."xsd:string
http://purl.uniprot.org/citations/15056731http://purl.uniprot.org/core/author"El-Ashry D."xsd:string
http://purl.uniprot.org/citations/15056731http://purl.uniprot.org/core/author"Holloway J.N."xsd:string
http://purl.uniprot.org/citations/15056731http://purl.uniprot.org/core/date"2004"xsd:gYear
http://purl.uniprot.org/citations/15056731http://purl.uniprot.org/core/name"Mol Endocrinol"xsd:string
http://purl.uniprot.org/citations/15056731http://purl.uniprot.org/core/pages"1396-1410"xsd:string
http://purl.uniprot.org/citations/15056731http://purl.uniprot.org/core/title"A cytoplasmic substrate of mitogen-activated protein kinase is responsible for estrogen receptor-alpha down-regulation in breast cancer cells: the role of nuclear factor-kappaB."xsd:string
http://purl.uniprot.org/citations/15056731http://purl.uniprot.org/core/volume"18"xsd:string
http://purl.uniprot.org/citations/15056731http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/15056731
http://purl.uniprot.org/citations/15056731http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/15056731
http://purl.uniprot.org/uniprot/#_A0A125SXW0-mappedCitation-15056731http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15056731
http://purl.uniprot.org/uniprot/#_A0A125SXW1-mappedCitation-15056731http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15056731
http://purl.uniprot.org/uniprot/#_Q14268-mappedCitation-15056731http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15056731
http://purl.uniprot.org/uniprot/#_A0A125SXV8-mappedCitation-15056731http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15056731
http://purl.uniprot.org/uniprot/#_A0A125SXV9-mappedCitation-15056731http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15056731
http://purl.uniprot.org/uniprot/#_A0A125SXW2-mappedCitation-15056731http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15056731
http://purl.uniprot.org/uniprot/#_A0A125SXW3-mappedCitation-15056731http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15056731
http://purl.uniprot.org/uniprot/#_B6DU68-mappedCitation-15056731http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15056731
http://purl.uniprot.org/uniprot/#_B6DU69-mappedCitation-15056731http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15056731
http://purl.uniprot.org/uniprot/#_A0A125SXV6-mappedCitation-15056731http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15056731
http://purl.uniprot.org/uniprot/#_A0A125SXV7-mappedCitation-15056731http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15056731
http://purl.uniprot.org/uniprot/#_A0A4R1-mappedCitation-15056731http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/15056731