Regulation of Ins P 3 -mediated Ca 2+ release by CaMKII in Xenopus oocytes
| Autor: | Frédéric Hague, Gérard Brûlé, Fabrices Matifat, Thibault Collin |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
Benzylamines
Cytoplasm endocrine system medicine.medical_specialty Microinjections Calmodulin Phosphodiesterase Inhibitors Physiology Clinical Biochemistry Xenopus Inositol 1 4 5-Trisphosphate Second Messenger Systems Xenopus laevis chemistry.chemical_compound Caffeine Physiology (medical) Internal medicine Ca2+/calmodulin-dependent protein kinase Lysophosphatidic acid medicine Animals Enzyme Inhibitors Inositol phosphate Receptor chemistry.chemical_classification Sulfonamides biology Heparin Anticoagulants biology.organism_classification Molecular medicine Cell biology carbohydrates (lipids) Endocrinology chemistry Calcium-Calmodulin-Dependent Protein Kinases Oocytes biology.protein Calcium Calcium-Calmodulin-Dependent Protein Kinase Type 2 Peptides Intracellular |
| Zdroj: | Pfl�gers Archiv European Journal of Physiology. 441:796-801 |
| ISSN: | 1432-2013 0031-6768 |
| DOI: | 10.1007/s004240000479 |
| Popis: | Inhibition of calmodulin (CaM) sensitizes Ca2+ release mediated by D-myo-inositol (1,4,5)-trisphosphate (InsP 3) in Xenopus oocytes, which results in spontaneous Ca2+-dependent Cl– current oscillations or in a shift of the concentration threshold for lysophosphatidic acid (LPA) by a tenfold factor. The oscillatory currents appear at a low initial Ca2+ concentration and without any significant increase in the inositol phosphate (InsPs) concentrations. These data led us to rule out the direct involvement of CaM, as well as the implied involvement of InsP 3 3-kinase. The response to intracellular injection of the non-metabolizable InsP 3 analog 3-deoxy-3-fluoro InsP 3 (InsP 3-F) is obviously affected by previous treatment with CaM inhibitory peptide. Furthermore, these effects have been consistently obtained with specific CaMKII inhibitors such as KN-93 and AIP. CaM plays a key role in the Ca2+-dependent inactivation of type I InsP 3 receptors. The experiments presented hereby allow us to postulate that CaM could also exert its inhibitory effect through CaMKII in a way that does not involve InsP 3 metabolism regulation. It is concluded that CaMKII could participate in Ca2+-evoked inhibition of InsP 3-mediated Ca2+ release by inhibiting the InsP 3 receptor. |
| Databáze: | OpenAIRE |
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