Depolarizing stimuli reduce Ca2+/calmodulin-dependent protein kinase II activity in islets of Langerhans

Harris, T. E., Persaud, S. J., Squires, Paul E. and Jones, P. M. (2000) Depolarizing stimuli reduce Ca2+/calmodulin-dependent protein kinase II activity in islets of Langerhans. Biochemical and Biophysical Research Communications, 270 (3). pp. 1119-1123. ISSN 0006-291X

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Elevations in intracellular Ca2+ (Ca2+(i)) initiate insulin secretion from pancreatic β-cells, but the secretory responses become rapidly desensitised to maintained elevations in Ca2+(i). We have investigated the mechanisms underlying the Ca2+ desensitization of insulin secretion using electrically permeabilized rat islets of Langerhans. Measurements of Ca2+/calmodulin-dependent protein kinase II (CaMK II) enzyme activity and immunoreactivity in permeabilized islets demonstrated Ca2+-induced reductions in enzyme activity which could not be attributed to reductions in CaMK II immunoreactive protein. Measurements in intact islets demonstrated that the Ca2+-induced reduction of CaMK II activity was also operative in intact cells, suggesting that this mechanism may have pathophysiological implications for β-cell function. (C) 2000 Academic Press.

Keywords:calcium ion, insulin, protein kinase (calcium,calmodulin) II, animal cell, article, calcium cell level, cell function, cell membrane depolarization, controlled study, enzyme activity, insulin release, nonhuman, pancreas islet, pancreas islet beta cell, pathophysiology, priority journal, rat, Animals, Ca(2+)-Calmodulin Dependent Protein Kinase, Calcium, Cell Membrane Permeability, Electrophysiology, Glucose, Islets of Langerhans, Membrane Potentials, Potassium Chloride, Rats, Tolbutamide, Animalia
Subjects:C Biological Sciences > C990 Biological Sciences not elsewhere classified
Divisions:College of Science > School of Life Sciences
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ID Code:14350
Deposited On:18 Jun 2014 14:09

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