| pubmed-article:8887554 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8887554 | lifeskim:mentions | umls-concept:C0038435 | lld:lifeskim |
| pubmed-article:8887554 | lifeskim:mentions | umls-concept:C0016026 | lld:lifeskim |
| pubmed-article:8887554 | lifeskim:mentions | umls-concept:C0056695 | lld:lifeskim |
| pubmed-article:8887554 | lifeskim:mentions | umls-concept:C1120843 | lld:lifeskim |
| pubmed-article:8887554 | lifeskim:mentions | umls-concept:C1366876 | lld:lifeskim |
| pubmed-article:8887554 | lifeskim:mentions | umls-concept:C0248446 | lld:lifeskim |
| pubmed-article:8887554 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:8887554 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:8887554 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:8887554 | lifeskim:mentions | umls-concept:C1314939 | lld:lifeskim |
| pubmed-article:8887554 | pubmed:issue | 17 | lld:pubmed |
| pubmed-article:8887554 | pubmed:dateCreated | 1997-1-2 | lld:pubmed |
| pubmed-article:8887554 | pubmed:abstractText | Fibroblast growth factor (FGF) activates a protein kinase cascade in SK-N-MC cells that regulates gene expression at a cyclic-AMP response element (CRE) by stimulating the transcriptional activity of CREB. The activation of CREB is prevented by a dominant negative mutant of Ras and triggered via the same site (Ser133) that becomes phosphorylated in response to cyclic AMP and Ca2+. However, the effect of FGF is not mediated by cyclic AMP-dependent protein kinase, TPA-sensitive isoforms of protein kinase-C, p70S6K or p90rsk (all of which phosphorylate CREB at Ser133 in vitro). Instead, we identify the FGF-stimulated CREB kinase as MAP kinase-activated protein (MAPKAP) kinase-2, an enzyme that lies immediately downstream of p38 MAP kinase, in a pathway that is also stimulated by cellular stresses. We show that MAPKAP kinase-2 phosphorylates CREB at Ser133 in vitro, that the FGF- or stress-induced activation of MAPKAP kinase-2 and phosphorylation of CREB and ATF-1 are prevented by similar concentrations of the specific p38 MAP kinase inhibitor SB 203580, and that MAPKAP kinase-2 is the only detectable SB 203580-sensitive CREB kinase in SK-N-MC cell extracts. We also show that transfection of RK/p38 MAP kinase in SK-N-MC cells, but not transfection of p44 MAP kinase, activates Gal4-CREB-dependent transcription via Ser133. These findings identify a new growth factor and stress-activated signaling pathway that regulates gene expression at the CRE. | lld:pubmed |
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| pubmed-article:8887554 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8887554 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8887554 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8887554 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:8887554 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:8887554 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8887554 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8887554 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:8887554 | pubmed:issn | 0261-4189 | lld:pubmed |
