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rdf:type |
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lifeskim:mentions |
umls-concept:C0014912,
umls-concept:C0017262,
umls-concept:C0021467,
umls-concept:C0021469,
umls-concept:C0034804,
umls-concept:C0035143,
umls-concept:C0040648,
umls-concept:C0079904,
umls-concept:C0209548,
umls-concept:C0441655,
umls-concept:C1704829
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pubmed:issue |
1
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pubmed:dateCreated |
1997-7-8
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pubmed:abstractText |
The cytokine interleukin-6 (IL-6), a key mediator of immune and acute phase responses of the liver, has also been implicated in uterine functions. Estrogens are potent repressors of IL-6 production by uterine stromal cells. In the endometrial adenocarcinoma cell line Ishikawa, phorbol ester-induced activation of the IL-6 promoter was inhibited to basal levels by 17 beta-estradiol (E2) in a wild-type receptor-dependent fashion. Although tamoxifen has been shown to have estrogenic effects on the endometrium, it did not inhibit induction of the IL-6 promoter. We previously showed that inhibition of IL-6 gene expression by E2 does not involve high-affinity binding of the estrogen receptor (ER) to IL-6 DNA. We now report that the ER can directly interact with the transcription factors NF-IL6 and NF-kappa B and can inhibit their ability to bind DNA which might be the molecular basis for repression of IL-6 gene expression by estrogens.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/CCAAT-Enhancer-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Drug Combinations,
http://linkedlifedata.com/resource/pubmed/chemical/Estradiol,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-6,
http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B,
http://linkedlifedata.com/resource/pubmed/chemical/Nuclear Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Estrogen,
http://linkedlifedata.com/resource/pubmed/chemical/Tamoxifen,
http://linkedlifedata.com/resource/pubmed/chemical/Tetradecanoylphorbol Acetate
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0014-5793
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
2
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pubmed:volume |
409
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
79-85
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:9199508-Adenocarcinoma,
pubmed-meshheading:9199508-CCAAT-Enhancer-Binding Proteins,
pubmed-meshheading:9199508-DNA-Binding Proteins,
pubmed-meshheading:9199508-Drug Combinations,
pubmed-meshheading:9199508-Endometrial Neoplasms,
pubmed-meshheading:9199508-Estradiol,
pubmed-meshheading:9199508-Female,
pubmed-meshheading:9199508-Gene Expression Regulation,
pubmed-meshheading:9199508-Humans,
pubmed-meshheading:9199508-Interleukin-6,
pubmed-meshheading:9199508-NF-kappa B,
pubmed-meshheading:9199508-Nuclear Proteins,
pubmed-meshheading:9199508-Promoter Regions, Genetic,
pubmed-meshheading:9199508-Receptors, Estrogen,
pubmed-meshheading:9199508-Structure-Activity Relationship,
pubmed-meshheading:9199508-Tamoxifen,
pubmed-meshheading:9199508-Tetradecanoylphorbol Acetate,
pubmed-meshheading:9199508-Tumor Cells, Cultured
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pubmed:year |
1997
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pubmed:articleTitle |
Repression of interleukin-6 gene expression by 17 beta-estradiol: inhibition of the DNA-binding activity of the transcription factors NF-IL6 and NF-kappa B by the estrogen receptor.
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pubmed:affiliation |
Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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