| pubmed-article:10454570 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10454570 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
| pubmed-article:10454570 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:10454570 | lifeskim:mentions | umls-concept:C0086282 | lld:lifeskim |
| pubmed-article:10454570 | lifeskim:mentions | umls-concept:C0042071 | lld:lifeskim |
| pubmed-article:10454570 | lifeskim:mentions | umls-concept:C0021755 | lld:lifeskim |
| pubmed-article:10454570 | lifeskim:mentions | umls-concept:C0752312 | lld:lifeskim |
| pubmed-article:10454570 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:10454570 | lifeskim:mentions | umls-concept:C0000975 | lld:lifeskim |
| pubmed-article:10454570 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:10454570 | lifeskim:mentions | umls-concept:C0920532 | lld:lifeskim |
| pubmed-article:10454570 | lifeskim:mentions | umls-concept:C0392337 | lld:lifeskim |
| pubmed-article:10454570 | lifeskim:mentions | umls-concept:C0070750 | lld:lifeskim |
| pubmed-article:10454570 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:10454570 | pubmed:dateCreated | 1999-9-10 | lld:pubmed |
| pubmed-article:10454570 | pubmed:abstractText | We have investigated the in vivo and in vitro regulation of the human urokinase-type plasminogen activator (uPA) gene by interleukin-1 (IL-1) and analyzed the transcription factors and signalling pathways involved in the response of the -2.0-kb uPA enhancer to IL-1 induction and to tetradecanoyl phorbol acetate (TPA) induction. Mutational analysis showed the cooperative activity of the Ets-binding site (EBS) and the two AP-1 elements of the enhancer. The results reveal that the EBS is required for the response to both inducers mediated by Ets-2, which is regulated at a level subsequent to DNA binding, by an IL-1- and phorbol ester-inducible transactivation domain. Both the IL-1 and the TPA-mediated induction result in a drastic increase of AP-1 binding to the downstream site of the enhancer (uPA 3' TPA-responsive element), while a mostly qualitative change, resulting from the interplay between ATF-2 homodimers and c-Jun-ATF-2 heterodimers, takes place at the upstream AP-1 element. The analysis of two distinct mitogen-activated protein kinase pathways shows that stress-activated protein kinase-Jun N-terminal kinase activation, resulting in the phosphorylation of ATF-2, c-Jun, and JunD, is required not only for the IL-1- but also for the TPA-dependent induction, while the extracellular signal-related kinase 1 (ERK-1) and ERK-2 activation is involved in the TPA- but not in the IL-1-dependent stimulation of the uPA enhancer. | lld:pubmed |
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| pubmed-article:10454570 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10454570 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10454570 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:10454570 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10454570 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:10454570 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:10454570 | pubmed:author | pubmed-author:CirilloGG | lld:pubmed |
| pubmed-article:10454570 | pubmed:author | pubmed-author:CaraccioloAA | lld:pubmed |
