| pubmed-article:11397794 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:11397794 | lifeskim:mentions | umls-concept:C0085828 | lld:lifeskim |
| pubmed-article:11397794 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:11397794 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:11397794 | lifeskim:mentions | umls-concept:C1540075 | lld:lifeskim |
| pubmed-article:11397794 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:11397794 | pubmed:issue | 31 | lld:pubmed |
| pubmed-article:11397794 | pubmed:dateCreated | 2001-7-30 | lld:pubmed |
| pubmed-article:11397794 | pubmed:abstractText | The immunosuppressive effects of glucocorticoids arise largely by inhibition of cytokine gene expression, which has been ascribed to interference between the glucocorticoid receptor and transcription factors such as AP-1 and NF-kappa B as well as by competition for common coactivators. Here we show that glucocorticoid-induced inhibition of interleukin-2 mRNA expression in activated normal T cells required new protein synthesis, suggesting that this phenomenon is secondary to expression of glucocorticoid-regulated genes. One of the most prominent glucocorticoid-induced genes is glucocorticoid-induced leucine zipper (GILZ), which has been reported to inhibit activation-induced up-regulation of Fas ligand (FasL) mRNA. Indeed, transient expression of GILZ in Jurkat T cells blocked induction of a reporter construct driven by the FasL promoter. This could be accounted for by GILZ-mediated inhibition of Egr-2 and Egr-3, NFAT/AP-1-inducible transcription factors that bind a regulatory element in the FasL promoter and up-regulate FasL expression. GILZ also potently inhibited AP-1-driven and IL-2 promoter-driven reporter constructs, and recombinant GILZ specifically interacted with c-Fos and c-Jun in vitro and inhibited the binding of active AP-1 to its target DNA. Whereas homodimerization of GILZ required the presence of its leucine zipper, the interaction with c-Fos and c-Jun occurred through the N-terminal 60-amino acid region of GILZ. Thus, GILZ represents a glucocorticoid-induced gene product that can inhibit a variety of activation-induced events, at least in part by direct interference with AP-1, and is therefore a candidate for a mediator of glucocorticoid-induced immunosuppression. | lld:pubmed |
| pubmed-article:11397794 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:11397794 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:11397794 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:11397794 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:11397794 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:11397794 | pubmed:author | pubmed-author:AshwellJ DJD | lld:pubmed |
| pubmed-article:11397794 | pubmed:author | pubmed-author:MittelstadtP... | lld:pubmed |
| pubmed-article:11397794 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:11397794 | pubmed:day | 3 | lld:pubmed |
| pubmed-article:11397794 | pubmed:volume | 276 | lld:pubmed |
| pubmed-article:11397794 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:11397794 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:11397794 | pubmed:pagination | 29603-10 | lld:pubmed |
| pubmed-article:11397794 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:11397794 | pubmed:year | 2001 | lld:pubmed |
| pubmed-article:11397794 | pubmed:articleTitle | Inhibition of AP-1 by the glucocorticoid-inducible protein GILZ. | lld:pubmed |
| pubmed-article:11397794 | pubmed:affiliation | Laboratory of Immune Cell Biology, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA. | lld:pubmed |
| pubmed-article:11397794 | pubmed:publicationType | Journal Article | lld:pubmed |
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