| pubmed-article:8186461 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8186461 | lifeskim:mentions | umls-concept:C0079460 | lld:lifeskim |
| pubmed-article:8186461 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:8186461 | lifeskim:mentions | umls-concept:C0054450 | lld:lifeskim |
| pubmed-article:8186461 | lifeskim:mentions | umls-concept:C0024297 | lld:lifeskim |
| pubmed-article:8186461 | lifeskim:mentions | umls-concept:C1333104 | lld:lifeskim |
| pubmed-article:8186461 | lifeskim:mentions | umls-concept:C0013879 | lld:lifeskim |
| pubmed-article:8186461 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:8186461 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:8186461 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:8186461 | pubmed:dateCreated | 1994-6-20 | lld:pubmed |
| pubmed-article:8186461 | pubmed:abstractText | Granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-2 (IL-2) are produced by stimulation with phorbol-12-myristate acetate (PMA) and calcium ionophore (A23187) in human T cell leukemia Jurkat cells. The expression of GM-CSF and IL-2 is inhibited by immunosuppressive drugs such as cyclosporin A (CsA) and FK506. Earlier studies on the IL-2 gene expression showed that overexpression of calcineurin (CN), a Ca2+/calmodulin-dependent protein phosphatase, can stimulate transcription from the IL-2 promoter through the NF-AT-binding site. In this study, we obtained evidence that transfection of the cDNAs for CN A (catalytic) and CN B (regulatory) subunits also augments transcription from the GM-CSF promoter and recovers the transcription inhibited by CsA. The constitutively active type of the CN A subunit, which lacks the auto-inhibitory and calmodulin-binding domains, acts in synergy with PMA to activate transcription from the GM-CSF promoter. We also found that the active CN partially replaces calcium ionophore in synergy with PMA to induce expression of endogenous GM-CSF and IL-2. By multimerizing the regulatory elements of the GM-CSF promoter, we found that one of the target sites for the CN action is the conserved lymphokine element 0 (CLE0), located at positions between -54 and -40. Mobility shift assays showed that the CLE0 sequence has an AP1-binding site and is associated with an NF-AT-like factor, termed NF-CLE0 gamma. NF-CLE0 gamma binding is induced by PMA/A23187 and is inhibited by treatment with CsA. These results suggest that CN is involved in the coordinated induction of the GM-CSF and IL-2 genes and that the CLE0 sequence of the GM-CSF gene is a functional analogue of the NF-AT-binding site in the IL-2 promoter, which mediates signals downstream of T cell activation. | lld:pubmed |
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| pubmed-article:8186461 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8186461 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8186461 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8186461 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:8186461 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8186461 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:8186461 | pubmed:issn | 1059-1524 | lld:pubmed |
| pubmed-article:8186461 | pubmed:author | pubmed-author:NaitoYY | lld:pubmed |
| pubmed-article:8186461 | pubmed:author | pubmed-author:AraiKK | lld:pubmed |
| pubmed-article:8186461 | pubmed:author | pubmed-author:AraiNN | lld:pubmed |
| pubmed-article:8186461 | pubmed:author | pubmed-author:TsuboiAA | lld:pubmed |
| pubmed-article:8186461 | pubmed:author | pubmed-author:TokumitsuHH | lld:pubmed |
| pubmed-article:8186461 | pubmed:author | pubmed-author:MasudaE SES | lld:pubmed |
| pubmed-article:8186461 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8186461 | pubmed:volume | 5 | lld:pubmed |
| pubmed-article:8186461 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8186461 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8186461 | pubmed:pagination | 119-28 | lld:pubmed |
| pubmed-article:8186461 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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