| pubmed-article:8524816 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8524816 | lifeskim:mentions | umls-concept:C0018894 | lld:lifeskim |
| pubmed-article:8524816 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
| pubmed-article:8524816 | lifeskim:mentions | umls-concept:C0021467 | lld:lifeskim |
| pubmed-article:8524816 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
| pubmed-article:8524816 | lifeskim:mentions | umls-concept:C0021469 | lld:lifeskim |
| pubmed-article:8524816 | lifeskim:mentions | umls-concept:C1519516 | lld:lifeskim |
| pubmed-article:8524816 | lifeskim:mentions | umls-concept:C1515021 | lld:lifeskim |
| pubmed-article:8524816 | pubmed:issue | 25 | lld:pubmed |
| pubmed-article:8524816 | pubmed:dateCreated | 1996-1-24 | lld:pubmed |
| pubmed-article:8524816 | pubmed:abstractText | Activation of individual CD4+ T cells results in differential lymphokine expression: interleukin 2 (IL-2) is preferentially produced by T helper type 1 (TH1) cells, which are involved in cell-mediated immune responses, whereas IL-4 is synthesized by TH2 cells, which are essential for humoral immunity. The Ca(2+)-dependent factor NF-ATp plays a key role in the inducible transcription of both these lymphokine genes. However, while IL2 expression requires the contribution of Ca(2+)- and protein kinase C-dependent signals, we report that activation of human IL4 transcription through the Ca(2+)-dependent pathway is diminished by protein kinase C stimulation in Jurkat T cells. This phenomenon is due to mutually exclusive binding of NF-ATp and NF-kappa B to the P sequence, an element located 69 bp upstream of the IL4 transcription initiation site. Human IL4 promoter-mediated transcription is downregulated in Jurkat cells stimulated with the NF-kappa B-activating cytokine tumor necrosis factor alpha and suppressed in RelA-overexpressing cells. In contrast, protein kinase C stimulation or RelA overexpression does not affect the activity of a human IL4 promoter containing a mouse P sequence, which is a higher-affinity site for NF-ATp and a lower-affinity site for RelA. Thus, competition between two general transcriptional activators, RelA and NF-ATp, mediates the inhibitory effect of protein kinase C stimulation on IL4 expression and may contribute to differential gene expression in TH cells. | lld:pubmed |
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| pubmed-article:8524816 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8524816 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8524816 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8524816 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8524816 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:8524816 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:8524816 | pubmed:author | pubmed-author:CasolaroVV | lld:pubmed |
| pubmed-article:8524816 | pubmed:author | pubmed-author:SongZZ | lld:pubmed |
| pubmed-article:8524816 | pubmed:author | pubmed-author:ThanosDD | lld:pubmed |
| pubmed-article:8524816 | pubmed:author | pubmed-author:GeorasS NSN | lld:pubmed |
| pubmed-article:8524816 | pubmed:author | pubmed-author:OnoS JSJ | lld:pubmed |
| pubmed-article:8524816 | pubmed:author | pubmed-author:AbdulkadirS... | lld:pubmed |
| pubmed-article:8524816 | pubmed:author | pubmed-author:ZubkoffI DID | lld:pubmed |
| pubmed-article:8524816 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8524816 | pubmed:day | 5 | lld:pubmed |
| pubmed-article:8524816 | pubmed:volume | 92 | lld:pubmed |
| pubmed-article:8524816 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8524816 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8524816 | pubmed:pagination | 11623-7 | lld:pubmed |
| pubmed-article:8524816 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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