Linked Life Data

3058689

Source:http://linkedlifedata.com/resource/pubmed/id/3058689

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pubmed-article:3058689pubmed:abstractTextIn bovine adrenal chromaffin cells nicotinic stimulation or a depolarizing concentration of K+ caused a rapid, transient translocation to membranes of as much as 14% of the total cellular protein kinase C activity. The quantitative relationship between membrane-bound protein kinase C and Ca2+-dependent secretion was determined in cells rendered leaky by digitonin treatment. Intact cells were incubated with various concentrations of 12-O-tetradecanoylphorbol-13-acetate (TPA) to activate and cause translocation of protein kinase C to membrane before permeabilization in the presence of Ca2+. For the same amount of membrane-bound protein kinase C, a similar degree of enhancement of Ca2+-dependent secretion occurred in cells incubated for 1 or 30 min with TPA. Translocation of as little as 2-3% of the cellular protein kinase C to the membrane enhanced Ca2+-dependent secretion by 25-30%. Muscarinic agonists caused a 5% increase in membrane-bound protein kinase C at 2 s which rapidly reversed. Nicotinic and muscarinic receptor-mediated increases in membrane-bound protein kinase C were additive at 10 s and synergistic at 3 min. Muscarinic stimulation enhanced nicotinic receptor-dependent secretion. Prior incubation with TPA caused a similar enhancement of nicotinic-mediated secretion. The data indicate that protein kinase C which is translocated within seconds of stimulation of the cells with a nicotinic agonist or elevated K+ probably enhances the secretory response immediately or soon after exocytosis begins. In addition, the muscarinic receptor-mediated enhancement of nicotinic receptor-stimulated secretion may be due to newly activated protein kinase C.lld:pubmed
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pubmed-article:3058689pubmed:articleTitleCa2+ influx causes rapid translocation of protein kinase C to membranes. Studies of the effects of secretagogues in adrenal chromaffin cells.lld:pubmed
pubmed-article:3058689pubmed:affiliationDepartment of Pharmacology, University of Michigan, Ann Arbor 48109-0626.lld:pubmed
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pubmed-article:3058689pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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