| pubmed-article:19592671 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19592671 | lifeskim:mentions | umls-concept:C0052441 | lld:lifeskim |
| pubmed-article:19592671 | lifeskim:mentions | umls-concept:C0242275 | lld:lifeskim |
| pubmed-article:19592671 | lifeskim:mentions | umls-concept:C0035143 | lld:lifeskim |
| pubmed-article:19592671 | lifeskim:mentions | umls-concept:C0441655 | lld:lifeskim |
| pubmed-article:19592671 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
| pubmed-article:19592671 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:19592671 | pubmed:dateCreated | 2009-7-13 | lld:pubmed |
| pubmed-article:19592671 | pubmed:abstractText | The aryl hydrocarbon receptor (AHR) mediates most, if not all, of the many toxicological effects of the environmental pollutant 2,3,7,8-tetrachlorodibenzo- p-dioxin [(TCDD) or dioxin]. The "classical" pathway of AHR action involves dimerization of the liganded AHR with the aryl hydrocarbon nuclear translocator (ARNT) protein, and the AHR-ARNT dimer specifically associates with the enhancer regions of dioxin-responsive genes, leading to their increased transcription. Sutter and coworkers recently reported that epidermal growth factor (EGF) represses the dioxin-mediated induction of CYP1A1 in cultured normal human keratinocytes by inhibiting the recruitment of the transcriptional coactivator protein p300 to the CYP1A1 gene. EGF also inhibits the dioxin-dependent induction of certain parameters in keratinocytes that are reflective of dioxin-induced chloracne. These findings point to the potential usefulness of EGF for the treatment of chloracne and also describe a novel mechanism for repression of dioxin-induced gene transcription. | lld:pubmed |
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| pubmed-article:19592671 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19592671 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19592671 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:19592671 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19592671 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:19592671 | pubmed:issn | 1543-2548 | lld:pubmed |
| pubmed-article:19592671 | pubmed:author | pubmed-author:HankinsonOliv... | lld:pubmed |
| pubmed-article:19592671 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:19592671 | pubmed:volume | 9 | lld:pubmed |
| pubmed-article:19592671 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:19592671 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:19592671 | pubmed:pagination | 116-8 | lld:pubmed |
| pubmed-article:19592671 | pubmed:dateRevised | 2011-8-1 | lld:pubmed |
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| pubmed-article:19592671 | pubmed:year | 2009 | lld:pubmed |
| pubmed-article:19592671 | pubmed:articleTitle | Repression of aryl hydrocarbon receptor transcriptional activity by epidermal growth factor. | lld:pubmed |
| pubmed-article:19592671 | pubmed:affiliation | Department of Pathology and Laboratory Medicine, Jonsson Comprehensive Cancer Center, and Molecular Toxicology Program, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA. ohank@mednet.ucla.edu | lld:pubmed |
| pubmed-article:19592671 | pubmed:publicationType | Journal Article | lld:pubmed |
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