| pubmed-article:12595566 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12595566 | lifeskim:mentions | umls-concept:C0029016 | lld:lifeskim |
| pubmed-article:12595566 | lifeskim:mentions | umls-concept:C1333214 | lld:lifeskim |
| pubmed-article:12595566 | lifeskim:mentions | umls-concept:C0162493 | lld:lifeskim |
| pubmed-article:12595566 | lifeskim:mentions | umls-concept:C0443264 | lld:lifeskim |
| pubmed-article:12595566 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:12595566 | pubmed:dateCreated | 2003-2-21 | lld:pubmed |
| pubmed-article:12595566 | pubmed:abstractText | Cell differentiation and development are highly regulated processes at the transcriptional level. One of the main transcription factors that regulate these processes is AP-2alpha, a cell-type specific protein required for vertebrate development and embryogenesis. AP-2alpha also regulates apoptosis and cell-cycle specific events by interacting with the oncogene c-Myc. In searching for novel AP-2alpha- interacting factors, using an affinity chromatography approach, we have observed that oncoprotein DEK interacts with AP-2alpha in vitro. The existence of an interaction between AP-2alpha and DEK in cellular cultures was demonstrated by expression of a tagged AP-2alpha form followed by immunodetection. By transient co-expression experiments using a reporter for APOE promoter activity we have found that DEK stimulates the transactivation activity of AP-2alpha over APOE promoter. Finally, electrophoretic mobility shift assays suggested that DEK enhances the DNA-binding activity of AP-2alpha. Our data suggest a novel cellular function of DEK as a transcriptional co-activator. | lld:pubmed |
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| pubmed-article:12595566 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12595566 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12595566 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12595566 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:12595566 | pubmed:issn | 1362-4962 | lld:pubmed |
| pubmed-article:12595566 | pubmed:author | pubmed-author:VázquezJesúsJ | lld:pubmed |
| pubmed-article:12595566 | pubmed:author | pubmed-author:GarcíaMiguel... | lld:pubmed |
| pubmed-article:12595566 | pubmed:author | pubmed-author:ValdiviesoFer... | lld:pubmed |
| pubmed-article:12595566 | pubmed:author | pubmed-author:CampillosMóni... | lld:pubmed |
| pubmed-article:12595566 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:12595566 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:12595566 | pubmed:volume | 31 | lld:pubmed |
| pubmed-article:12595566 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12595566 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12595566 | pubmed:pagination | 1571-5 | lld:pubmed |
| pubmed-article:12595566 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:12595566 | pubmed:year | 2003 | lld:pubmed |
| pubmed-article:12595566 | pubmed:articleTitle | Transcriptional activation by AP-2alpha is modulated by the oncogene DEK. | lld:pubmed |
| pubmed-article:12595566 | pubmed:affiliation | Centro de Biología Molecular Severo Ochoa, CSIC-Universidad Autónoma de Madrid, 28049 Cantoblanco, Madrid, Spain. | lld:pubmed |
| pubmed-article:12595566 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12595566 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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