The role of calmodulin on Ca2+-dependent K+ transport regulation in the human red cell |
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| Affiliation: | 1. Gene Center/Department of Biochemistry, Ludwig-Maximilians Universität München, Munich 81377, Germany;2. Institute for Diabetes and Obesity, Helmholtz Zentrum München, Neuherberg 85764, Germany;3. Department of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA;4. Instituto de Biología y Genética Molecular (IBGM), University of Valladolid and Consejo Superior de Investigaciones Científicas (CSIC), Valladolid 47003, Spain;5. Chair for Proteomics and Bioanalytics, Technical University Munich, Freising 85354, Germany;6. Center for Integrated Protein Science Munich, Freising 85354, Germany;7. Biomedical Center, Department of Physiological Chemistry, Ludwig-Maximilians Universität München, Martinsried 81377, Germany;8. Department of Cell and Developmental Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA;1. Department of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA;2. Mitocare Center, Department of Pathology, Anatomy and Cell Biology, Thomas Jefferson University, Philadelphia, PA 19107, USA;1. Research Center of Bioenergy and Bioremediation, College of Resources and Environment, Southwest University, Beibei, Chongqing 400715, China;2. Academy of Agricultural Sciences, Southwest University, Beibei, Chongqing 400715, China |
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| Abstract: | Several lipophilic calmodulin antagonists (phenotiazines, butyrophenones and diphenylbutylpiperidines) inhibited Ca2+-induced loss of KCl from human red cells. However, the Ki values for this effect did not bear good correlation with the Ki values reported for well-known calmodulin-dependent systems. In addition, the inhibition was strongly dependent on the haematocrit and valinomycin-induced KCl fluxes were also affected. Added calmodulin did not have any effect on Ca2+-dependent 86Rb uptake by inside-out vesicles derived from red cell membranes whereas stimulation of Ca2+-dependent ATPase was apparent. Lipophilic anticalmodulins at high doses had all kinds of effects on 86Rb uptake by inside-out vesicles: increase, decrease or no change of the fraction of activated vesicles reached at submaximal Ca2+ concentrations, with or without modification of the relative rate of 86Rb uptake. The hydrophylic compound 48/80 decreased the fraction of activated vesicles reached at submaximal Ca2+ concentrations without affecting the relative rate of 86Rb uptake, but this effect took place only at concentrations 10-fold higher than the reported Ki for calmodulin-dependent systems. These results suggest that Ca2+-dependent K+ channels of red cells are not regulated by calmodulin. |
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