pubmed-article:7832755 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:7832755 | lifeskim:mentions | umls-concept:C0007600 | lld:lifeskim |
pubmed-article:7832755 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:7832755 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:7832755 | lifeskim:mentions | umls-concept:C0016030 | lld:lifeskim |
pubmed-article:7832755 | lifeskim:mentions | umls-concept:C0026473 | lld:lifeskim |
pubmed-article:7832755 | lifeskim:mentions | umls-concept:C0017636 | lld:lifeskim |
pubmed-article:7832755 | lifeskim:mentions | umls-concept:C0220781 | lld:lifeskim |
pubmed-article:7832755 | lifeskim:mentions | umls-concept:C0009505 | lld:lifeskim |
pubmed-article:7832755 | lifeskim:mentions | umls-concept:C0033453 | lld:lifeskim |
pubmed-article:7832755 | lifeskim:mentions | umls-concept:C1883254 | lld:lifeskim |
pubmed-article:7832755 | lifeskim:mentions | umls-concept:C1155437 | lld:lifeskim |
pubmed-article:7832755 | pubmed:dateCreated | 1995-2-23 | lld:pubmed |
pubmed-article:7832755 | pubmed:abstractText | The synthesis of C2 and factor B, the key components of complement system, is performed by various kinds of cells and is also up-regulated by interferon-gamma (IFN-gamma). By using human fibroblasts, human glioblastoma cell line A172 and monocytes, we investigated the signal-transduction mechanism for IFN-gamma-induced synthesis of C2 and factor B. The C2 and factor B synthesis induced by IFN-gamma in all three cell types was inhibited by a protein kinase C (PKC) inhibitor, 1-(5-isoquinolinyl-sulphonyl)-2-methylpiperazine (H-7). The depletion of PKC in these cell types after treatment with phorbol 12-myristate 13-acetate (PMA) resulted in inhibition of IFN-gamma-induced C2 production. In addition, IFN-gamma treatment elicited a decrease in cytoplasmic PKC in A172 cells, indicating that PKC is activated by IFN-gamma. These results suggest that PKC is crucial for IFN-gamma-induced C2 and factor B synthesis. Northern-blot analysis showed that the effects at H-7 were at least partly mediated by modulation of C2 and factor B mRNA abundance in A172 cells. Since treatment of fibroblasts and A172 cells with IFN-gamma had no effect on intracellular Ca2+ concentration, and since neither EGTA nor nifedipine inhibited C2 or factor B synthesis induced by IFN-gamma, we concluded that intracellular Ca2+ mobilization was not involved in the effect of IFN-gamma. In addition, genistein, herbimycin A and N-(6-aminohexyl)-5-chloro-1-naphthalene-sulphonamide (W-7) had no inhibitory effect on IFN-gamma-mediated action in any of the three cell types, which suggests that IFN-gamma acts independently of tyrosine kinases and calmodulin-dependent protein kinases. | lld:pubmed |
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pubmed-article:7832755 | pubmed:language | eng | lld:pubmed |
pubmed-article:7832755 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7832755 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:7832755 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7832755 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:7832755 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:7832755 | pubmed:month | Jan | lld:pubmed |
pubmed-article:7832755 | pubmed:issn | 0264-6021 | lld:pubmed |
pubmed-article:7832755 | pubmed:author | pubmed-author:WatanabeII | lld:pubmed |
pubmed-article:7832755 | pubmed:author | pubmed-author:FujitaSS | lld:pubmed |
pubmed-article:7832755 | pubmed:author | pubmed-author:HoriuchiTT | lld:pubmed |
pubmed-article:7832755 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:7832755 | pubmed:day | 15 | lld:pubmed |
pubmed-article:7832755 | pubmed:volume | 305 ( Pt 2) | lld:pubmed |
pubmed-article:7832755 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:7832755 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:7832755 | pubmed:pagination | 425-31 | lld:pubmed |
pubmed-article:7832755 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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