| pubmed-article:10750590 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10750590 | lifeskim:mentions | umls-concept:C0018787 | lld:lifeskim |
| pubmed-article:10750590 | lifeskim:mentions | umls-concept:C0243192 | lld:lifeskim |
| pubmed-article:10750590 | lifeskim:mentions | umls-concept:C0682972 | lld:lifeskim |
| pubmed-article:10750590 | lifeskim:mentions | umls-concept:C0333959 | lld:lifeskim |
| pubmed-article:10750590 | lifeskim:mentions | umls-concept:C1155502 | lld:lifeskim |
| pubmed-article:10750590 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:10750590 | pubmed:issue | 12A | lld:pubmed |
| pubmed-article:10750590 | pubmed:dateCreated | 2000-4-19 | lld:pubmed |
| pubmed-article:10750590 | pubmed:abstractText | Cardiac myocyte hypertrophy involves changes in cell structure and alterations in protein expression regulated at both the transcriptional and translational levels. Hypertrophic G protein-coupled receptor (GPCR) agonists such as endothelin-(ET-1) and phenylephrine stimulate a number of protein kinase cascades in the heart. Mitogen-activated protein kinase (MAPK) cascades stimulated include the extracellularly regulated kinase cascade, the stress-activated protein kinase/c-Jun N-terminal kinase cascade, and the p38 MAPK cascade. All 3 pathways have been implicated in hypertrophy, but recent ex vivo evidence also suggests that there may be additional effects on cell survival. ET-1 and phenylephrine also stimulate the protein kinase B pathway, and this may be involved in the regulation of protein synthesis by these agonists. Thus, protein kinase-mediated signaling may be important in the regulation of the development of myocyte hypertrophy. | lld:pubmed |
| pubmed-article:10750590 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10750590 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10750590 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:10750590 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10750590 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:10750590 | pubmed:issn | 0002-9149 | lld:pubmed |
| pubmed-article:10750590 | pubmed:author | pubmed-author:SugdenP HPH | lld:pubmed |
| pubmed-article:10750590 | pubmed:author | pubmed-author:ClerkAA | lld:pubmed |
| pubmed-article:10750590 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10750590 | pubmed:day | 17 | lld:pubmed |
| pubmed-article:10750590 | pubmed:volume | 83 | lld:pubmed |
| pubmed-article:10750590 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10750590 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10750590 | pubmed:pagination | 64H-69H | lld:pubmed |
| pubmed-article:10750590 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:10750590 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10750590 | pubmed:articleTitle | Activation of protein kinase cascades in the heart by hypertrophic G protein-coupled receptor agonists. | lld:pubmed |
| pubmed-article:10750590 | pubmed:affiliation | Division of Biomedical Sciences, Imperial College School of Medicine, London, United Kingdom. | lld:pubmed |
| pubmed-article:10750590 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10750590 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:10750590 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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