Latrotoxin stimulates secretion in permeabilized cells by regulating an intracellular Ca2+ - and ATP-dependent event: a role for protein kinase C
| Autor: | M A, Bittner, R W, Holz |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
Cell Membrane Permeability
Time Factors Dose-Response Relationship Drug Chromaffin Cells Magnesium Chloride Spider Venoms Inositol 1 4 5-Trisphosphate Cell Line Calcium Chloride Adenosine Triphosphate Spectrometry Fluorescence Concanavalin A Animals Humans Calcium Cattle Electrophoresis Polyacrylamide Gel Trypsin Cells Cultured Protein Kinase C Signal Transduction |
| Zdroj: | The Journal of biological chemistry. 275(33) |
| ISSN: | 0021-9258 |
| Popis: | alpha-Latrotoxin, a component of black widow spider venom, stimulates transmitter release from nerve terminals and intact chromaffin cells and enhances secretion from permeabilized chromaffin cells already maximally stimulated by Ca(2+). In this study we demonstrate that chromaffin cells contain a protein antigenically similar to the cloned Ca(2+)-independent receptor for alpha-latrotoxin. Although this receptor has homology to the secretin family of G-protein-linked receptors, pertussis toxin has no effect on the ability of alpha-latrotoxin to enhance secretion, suggesting that neither G(i) nor G(o) is involved in the response. Furthermore, in the absence of Ca(2+), alpha-latrotoxin does not stimulate polyphosphoinositide-specific phospholipase C. alpha-Latrotoxin specifically enhances ATP-dependent secretion in permeabilized cells. An in situ assay for protein kinase C reveals that alpha-latrotoxin augments the activation of protein kinase C by Ca(2+), and use of protein kinase inhibitors demonstrates that this activation is important for the toxin's enhancing effect. This enhancement of secretion requires Ca(2+) concentrations above 3 microm and is not supported by Ba(2+) or nonhydrolyzable guanine nucleotides, which do not stimulate protein kinase C. We conclude that alpha-latrotoxin stimulates secretion in permeabilized cells by regulating a Ca(2+)- and ATP-dependent event involving protein kinase C. |
| Databáze: | OpenAIRE |
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