| pubmed-article:8833904 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8833904 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:8833904 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:8833904 | lifeskim:mentions | umls-concept:C0221464 | lld:lifeskim |
| pubmed-article:8833904 | lifeskim:mentions | umls-concept:C0752312 | lld:lifeskim |
| pubmed-article:8833904 | lifeskim:mentions | umls-concept:C1658578 | lld:lifeskim |
| pubmed-article:8833904 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:8833904 | pubmed:dateCreated | 1996-11-19 | lld:pubmed |
| pubmed-article:8833904 | pubmed:abstractText | Smooth muscle cell proliferation and migration is important in arteriosclerosis. In this process, cytokines and growth factors are upregulated and bind to their respective receptors, which in turn stimulate mitogen-activated protein (MAP) kinases. MAP kinases then relay signals to the nucleus that activate quiescent smooth muscle cells. Phosphatases downregulate MAP kinases. We investigated the role of a dual-specificity tyrosine phosphatase, MAP kinase phosphatase-1 (MKP-1), in smooth muscle cell proliferation. MKP-1 expression was high in arterial tissue by Northern analysis, and MKP-1 message was detected mainly in the arterial smooth muscle layer by in situ hybridization. After balloon injury of the rat carotid artery, expression of MKP-1 decreased greatly, whereas that of MAP kinases, especially p44 MAP kinase, increased. The time course of the reduction in MKP-1 message correlated with increased tyrosine phosphorylation and elevated p44 MAP kinase enzymatic activity. In rat arterial smooth muscle cells overexpressing MKP-1, growth was arrested in the G1 phase and entry into the S phase was blocked. A reduction in MKP-1 expression may contribute in part to proliferation of smooth muscle cells after vascular injury, possibly through a decrease in dephosphorylation of p44 MAP kinase. | lld:pubmed |
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| pubmed-article:8833904 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8833904 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8833904 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:8833904 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8833904 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:8833904 | pubmed:issn | 0021-9738 | lld:pubmed |
| pubmed-article:8833904 | pubmed:author | pubmed-author:KINGD WDWJr | lld:pubmed |
| pubmed-article:8833904 | pubmed:author | pubmed-author:MAS | lld:pubmed |
| pubmed-article:8833904 | pubmed:author | pubmed-author:HaberEE | lld:pubmed |
| pubmed-article:8833904 | pubmed:author | pubmed-author:KUON MNM | lld:pubmed |
| pubmed-article:8833904 | pubmed:author | pubmed-author:WangHH | lld:pubmed |
| pubmed-article:8833904 | pubmed:author | pubmed-author:LeeW SWS | lld:pubmed |
| pubmed-article:8833904 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8833904 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:8833904 | pubmed:volume | 98 | lld:pubmed |
| pubmed-article:8833904 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8833904 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8833904 | pubmed:pagination | 1560-7 | lld:pubmed |
| pubmed-article:8833904 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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