| pubmed-article:8413215 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8413215 | lifeskim:mentions | umls-concept:C0079633 | lld:lifeskim |
| pubmed-article:8413215 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
| pubmed-article:8413215 | lifeskim:mentions | umls-concept:C0086860 | lld:lifeskim |
| pubmed-article:8413215 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:8413215 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:8413215 | pubmed:dateCreated | 1993-10-26 | lld:pubmed |
| pubmed-article:8413215 | pubmed:abstractText | Interleukin-8 (IL-8), a chemotactic cytokine for T lymphocytes and neutrophils, is induced in several cell types by a variety of stimuli including the inflammatory cytokines IL-1 and tumor necrosis factor alpha TNF-alpha. Several cis elements, including a binding site for the inducible transcription factor NF-kappa B, have been identified in the regulatory region of the IL-8 gene. We have examined the ability of various NF-kappa B subunits to bind to, and activate transcription from, the IL-8 promoter. A nuclear complex was induced in phorbol myristate acetate-treated Jurkat T cells which bound specifically to the kappa B site of the IL-8 promoter and was inhibited by addition of purified I kappa B alpha to the reaction mixture. Only antibody to RelA (p65), but not to NFKB1 (p50), NFKB2 (p50B), c-Rel, or RelB was able to abolish binding, suggesting that RelA is a major component in these kappa B binding complexes. Gel mobility shift analysis with in vitro-translated and purified proteins indicated that whereas the kappa B element in the human immunodeficiency virus type 1 long terminal repeat bound to all members of the kappa B/Rel family examined, the IL-8 kappa B site bound only to RelA and to c-Rel and NFKB2 homodimers, but not to NFKB1 homodimers or heterodimers of NFKB1-RelA. Transient transfection analysis demonstrated a kappa B-dependent expression of the IL-8 promoter in a human fibrosarcoma cell line (8387) and in Jurkat T lymphocytes. Cotransfection with various NF-kappa B subunits indicated that RelA and c-Rel, but neither NFKB1 nor heterodimeric NFKB1-RelA, was able to activate transcription from the IL-8 promoter. Furthermore, cotransfection of NFKB1 and RelA, although able to support activation from the human immunodeficiency virus type 1 long terminal repeat, failed to activate expression from the IL-8 promoter. Antisense oligonucleotides to RelA, but not NFKB1, inhibited phorbol myristate acetate-induced IL-8 production in Jurkat T lymphocytes. These data demonstrate the differential ability of members of the kappa B/Rel family to bind to, and activate transcription from, the IL-8 promoter. Furthermore, while providing a novel example of a kappa B-regulated promoter in which the classical NF-kappa B complex is unable to activate transcription from the kappa B element, these data provide direct evidence for the role of RelA in regulation of IL-8 gene expression. | lld:pubmed |
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| pubmed-article:8413215 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8413215 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8413215 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8413215 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:8413215 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8413215 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:8413215 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:8413215 | pubmed:author | pubmed-author:RosenC ACA | lld:pubmed |
| pubmed-article:8413215 | pubmed:author | pubmed-author:KunschCC | lld:pubmed |
| pubmed-article:8413215 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8413215 | pubmed:volume | 13 | lld:pubmed |
| pubmed-article:8413215 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8413215 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8413215 | pubmed:pagination | 6137-46 | lld:pubmed |
| pubmed-article:8413215 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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