| pubmed-article:8978708 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8978708 | lifeskim:mentions | umls-concept:C0087111 | lld:lifeskim |
| pubmed-article:8978708 | lifeskim:mentions | umls-concept:C0006772 | lld:lifeskim |
| pubmed-article:8978708 | lifeskim:mentions | umls-concept:C0815000 | lld:lifeskim |
| pubmed-article:8978708 | lifeskim:mentions | umls-concept:C1280500 | lld:lifeskim |
| pubmed-article:8978708 | lifeskim:mentions | umls-concept:C0031586 | lld:lifeskim |
| pubmed-article:8978708 | lifeskim:mentions | umls-concept:C0549178 | lld:lifeskim |
| pubmed-article:8978708 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:8978708 | pubmed:dateCreated | 1997-1-27 | lld:pubmed |
| pubmed-article:8978708 | pubmed:abstractText | Stimulation of muscarinic receptors by carbachol and activation of protein kinase C elicits the translocation of calmodulin (CaM) from membranes to cytosol in the human neuroblastoma cell line SK-N-SH. Our previous studies have suggested a role for protein kinase C in the regulation of CaM redistribution. To explore further the role of protein kinase C in carbachol-induced calmodulin translocation, we treated cells for 17 h with 12-O-tetradecanoylphorbol 13-acetate (TPA) to down-regulate protein kinase C isozymes or 72 h to differentiate the cells. Treatment of SK-N-SH cells for 17 h with 70 nM TPA nearly abolished the effect of carbachol on CaM redistribution. After 72 h of TPA, however, the cells appeared differentiated, and the ability of carbachol to increase cytosolic CaM levels was restored. In untreated control cells, the carbachol-mediated increase in cytosolic CaM content was mimicked by TPA and blocked by pretreatment with the selective protein kinase C inhibitor Ro 31-8220 at 10 microM. In the 72-h TPA-treated cells, however, the ability of TPA to increase cytosolic CaM levels was significantly reduced, and the action of carbachol was no longer blocked by Ro 31-8220. The effect of prolonged TPA treatment on select protein kinase C isozymes was examined by immunoblotting. Treatment of cells for either 17 or 72 h abolished the alpha-isozyme in the cytosol and reduced (17 h) or abolished (72 h) the content in the membranes. In both 17- and 72-h TPA-treated cells, the epsilon-isozyme was nearly abolished in the cytosol and slightly reduced in the membranes. Some protein kinase C activity may have been maintained during TPA treatment because the basal level of phosphorylation of the protein kinase C substrate myristoylated alanine-rich C kinase substrate was enhanced in cells treated for either 17 or 72 h with TPA. The potential dissociation of carbachol and protein kinase C in eliciting increases in cytosolic CaM content was a function of prolonged TPA treatment and not differentiation per se because carbachol-mediated increases in cytosolic CaM levels were inhibited by Ro 31-8220 in retinoic acid-differentiated SK-N-SH cells. This study demonstrates that continuous TPA treatment, although initially down-regulating the protein kinase C-mediated effect of carbachol on CaM redistribution, uncouples carbachol and protein kinase C at longer times. | lld:pubmed |
| pubmed-article:8978708 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8978708 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8978708 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8978708 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8978708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8978708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8978708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8978708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8978708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8978708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8978708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8978708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8978708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8978708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8978708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8978708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8978708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8978708 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8978708 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8978708 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:8978708 | pubmed:issn | 0022-3042 | lld:pubmed |
| pubmed-article:8978708 | pubmed:author | pubmed-author:GnegyM EME | lld:pubmed |
| pubmed-article:8978708 | pubmed:author | pubmed-author:GoldsmithA... | lld:pubmed |
| pubmed-article:8978708 | pubmed:author | pubmed-author:Shariat-Madar... | lld:pubmed |
| pubmed-article:8978708 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8978708 | pubmed:volume | 68 | lld:pubmed |
| pubmed-article:8978708 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8978708 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8978708 | pubmed:pagination | 40-6 | lld:pubmed |
| pubmed-article:8978708 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:8978708 | pubmed:meshHeading | pubmed-meshheading:8978708-... | lld:pubmed |
| pubmed-article:8978708 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:8978708 | pubmed:articleTitle | Effect of continuous phorbol ester treatment on muscarinic receptor-mediated calmodulin redistribution in SK-N-SH neuroblastoma cells. | lld:pubmed |
| pubmed-article:8978708 | pubmed:affiliation | Department of Pharmacology, University of Michigan Medical School, Ann Arbor 48109-0632, USA. | lld:pubmed |
| pubmed-article:8978708 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:8978708 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
