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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
|
pubmed:dateCreated |
1997-2-14
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pubmed:abstractText |
Mitogen-activated protein (MAP) kinases are proline-directed serine/threonine kinases that are activated by dual phosphorylation on threonine and tyrosine residues in response to a wide array of extracellular stimuli. Three distinct groups of MAP kinases have been identified in mammalian cells [extracellular-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38]. These MAP kinases are mediators of signal transduction from the cell surface to the nucleus. One nuclear target of these MAP kinase signaling pathways is the transcription factor AP-1. MAP kinases regulate AP-1 transcriptional activity by multiple mechanisms. Here we review recent progress towards understanding AP-1 regulation by the ERK, JNK, and p38 MAP kinase signal transduction pathways.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Oct
|
pubmed:issn |
0946-2716
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pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
74
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
|
pubmed:pagination |
589-607
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pubmed:dateRevised |
2011-7-8
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pubmed:meshHeading | |
pubmed:year |
1996
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pubmed:articleTitle |
Transcription factor AP-1 regulation by mitogen-activated protein kinase signal transduction pathways.
|
pubmed:affiliation |
Howard Hughes Medical Institute, University of Massachusetts Medical School, Worcester 01605, USA.
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pubmed:publicationType |
Journal Article,
Review
|