| pubmed-article:7545165 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7545165 | lifeskim:mentions | umls-concept:C0015576 | lld:lifeskim |
| pubmed-article:7545165 | lifeskim:mentions | umls-concept:C0680022 | lld:lifeskim |
| pubmed-article:7545165 | lifeskim:mentions | umls-concept:C0034818 | lld:lifeskim |
| pubmed-article:7545165 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:7545165 | lifeskim:mentions | umls-concept:C0256371 | lld:lifeskim |
| pubmed-article:7545165 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:7545165 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:7545165 | pubmed:issue | 37 | lld:pubmed |
| pubmed-article:7545165 | pubmed:dateCreated | 1995-10-12 | lld:pubmed |
| pubmed-article:7545165 | pubmed:abstractText | Stimulation of the activity of protein kinase C by pretreatment of cells with phorbol esters was tested for its ability to inhibit signaling by four members of the insulin receptor family, including the human insulin and insulin-like growth factor-I receptors, the human insulin receptor-related receptor, and the Drosophila insulin receptor. Activation of overexpressed protein kinase C alpha resulted in a subsequent inhibition of the ligand-stimulated increase in antiphosphotyrosine-precipitable phosphatidylinositol 3-kinase mediated by the kinase domains of all four receptors. This inhibition varied from 97% for the insulin receptor-related receptor to 65% for the Drosophila insulin receptor. In addition, the activation of protein kinase C alpha inhibited the in situ ligand-stimulated increase in tyrosine phosphorylation of the GTPase-activating protein-associated p60 protein as well as Shc mediated by these receptors. The mechanism for this inhibition was further studied in the case of the insulin-like growth factor-I receptor. Although the in situ phosphorylation of insulin-receptor substrate-1 and p60 by this receptor was inhibited by prior stimulation of protein kinase C alpha, the in vitro tyrosine phosphorylation of these two substrates by this receptor was not decreased by prior stimulation of the protein kinase C alpha in the cells that served as a source of the substrates. Finally, the insulin-like growth factor-I-stimulated increase in cell proliferation was found to be inhibited by prior activation of protein kinase C alpha.(ABSTRACT TRUNCATED AT 250 WORDS) | lld:pubmed |
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| pubmed-article:7545165 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:7545165 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7545165 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7545165 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:7545165 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:7545165 | pubmed:author | pubmed-author:LisHH | lld:pubmed |
| pubmed-article:7545165 | pubmed:author | pubmed-author:RothR ARA | lld:pubmed |
| pubmed-article:7545165 | pubmed:author | pubmed-author:RATHF WFW | lld:pubmed |
| pubmed-article:7545165 | pubmed:author | pubmed-author:HosomiYY | lld:pubmed |
| pubmed-article:7545165 | pubmed:author | pubmed-author:DanielsenA... | lld:pubmed |
| pubmed-article:7545165 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7545165 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:7545165 | pubmed:volume | 270 | lld:pubmed |
| pubmed-article:7545165 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7545165 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7545165 | pubmed:pagination | 21600-5 | lld:pubmed |
| pubmed-article:7545165 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:7545165 | pubmed:year | 1995 | lld:pubmed |
| pubmed-article:7545165 | pubmed:articleTitle | Activation of protein kinase C alpha inhibits signaling by members of the insulin receptor family. | lld:pubmed |
| pubmed-article:7545165 | pubmed:affiliation | Department of Molecular Pharmacology, Stanford University School of Medicine, California 94305, USA. | lld:pubmed |
| pubmed-article:7545165 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7545165 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:7545165 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:7545165 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:42549 | entrezgene:pubmed | pubmed-article:7545165 | lld:entrezgene |
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