| pubmed-article:8473495 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8473495 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:8473495 | lifeskim:mentions | umls-concept:C0021756 | lld:lifeskim |
| pubmed-article:8473495 | lifeskim:mentions | umls-concept:C0085828 | lld:lifeskim |
| pubmed-article:8473495 | lifeskim:mentions | umls-concept:C0288011 | lld:lifeskim |
| pubmed-article:8473495 | lifeskim:mentions | umls-concept:C0521447 | lld:lifeskim |
| pubmed-article:8473495 | lifeskim:mentions | umls-concept:C0017337 | lld:lifeskim |
| pubmed-article:8473495 | lifeskim:mentions | umls-concept:C0017710 | lld:lifeskim |
| pubmed-article:8473495 | lifeskim:mentions | umls-concept:C0205160 | lld:lifeskim |
| pubmed-article:8473495 | lifeskim:mentions | umls-concept:C1158770 | lld:lifeskim |
| pubmed-article:8473495 | lifeskim:mentions | umls-concept:C2346501 | lld:lifeskim |
| pubmed-article:8473495 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:8473495 | pubmed:dateCreated | 1993-5-14 | lld:pubmed |
| pubmed-article:8473495 | pubmed:abstractText | IL-2 gene transcription is affected by several nuclear proteins. We asked whether dexamethasone (Dex) and cyclosporin A (CsA) inhibit IL-2 gene transcription by interfering with the activity of nuclear proteins that bind to the IL-2 promoter. Nuclear extracts from primary human T lymphocytes were analyzed by electrophoretic DNA mobility shift assays. Both Dex and CsA inhibited the binding of transcription factors AP-1 and NF-AT, but not of NF-kB and OCT-1/OAF, to their corresponding sites on the IL-2 gene promoter. To correlate changes in nuclear factor binding in vitro with transcriptional activity in vivo and define the structural requirements for IL-2 promoter repression, we used transient DNA transfections. Jurkat cells were transfected with plasmids containing either the intact IL-2 promoter or its AP-1, NF-AT, and NF-kB motifs. Dex inhibited the IL-2 promoter and the AP-1, but not the NF-AT and NF-kB plasmids. In contrast, CsA inhibited the IL-2 promoter and the NF-AT, but not the AP-1 and NF-kB plasmids. These results suggest that in human T lymphocytes both Dex and CsA inhibited IL-2 gene transcription through interference with transcription factors AP-1 and NF-AT. We propose that, while maximum inhibition may involve interaction with both transcription factors, AP-1 is the primary target of Dex. | lld:pubmed |
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| pubmed-article:8473495 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8473495 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8473495 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:8473495 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8473495 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:8473495 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:8473495 | pubmed:author | pubmed-author:AhujaS SSS | lld:pubmed |
| pubmed-article:8473495 | pubmed:author | pubmed-author:NajjarS MSM | lld:pubmed |
| pubmed-article:8473495 | pubmed:author | pubmed-author:BoumpasD TDT | lld:pubmed |
| pubmed-article:8473495 | pubmed:author | pubmed-author:PaliogianniFF | lld:pubmed |
| pubmed-article:8473495 | pubmed:author | pubmed-author:RaptisAA | lld:pubmed |
| pubmed-article:8473495 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8473495 | pubmed:volume | 91 | lld:pubmed |
| pubmed-article:8473495 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8473495 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8473495 | pubmed:pagination | 1481-9 | lld:pubmed |
| pubmed-article:8473495 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:8473495 | pubmed:year | 1993 | lld:pubmed |
| pubmed-article:8473495 | pubmed:articleTitle | Negative transcriptional regulation of human interleukin 2 (IL-2) gene by glucocorticoids through interference with nuclear transcription factors AP-1 and NF-AT. | lld:pubmed |
| pubmed-article:8473495 | pubmed:affiliation | Kidney Disease Section, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892. | lld:pubmed |
| pubmed-article:8473495 | pubmed:publicationType | Journal Article | lld:pubmed |
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