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The role of hexokinase as a possible modulator of Ca2+ movements in isolated rat brain mitochondria
Authors:E Panfili  G Sandri
Affiliation:1. Department of Internal Medicine (Cardiology), University of Texas Southwestern Medical Center, Dallas, TX 75390-8573, USA;2. Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390-8573, USA;3. Advanced Center for Chronic Diseases (ACCDiS), Center for Exercise, Metabolism and Cancer Studies (CEMC), Universidad de Chile, Chile;4. Instituto de Investigación en Ciencias Odontológicas (ICOD), Facultad de Odontología, Universidad de Chile, Chile;5. Instituto de Ciencias Biomédicas, Facultad Medicina, Universidad de Chile, Chile;6. Departamento de Bioquímica y Biología Molecular, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Santiago, Chile;7. Departamento de Fisiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago 7820436, Chile;8. Department of Internal Medicine, Yale University, New Haven, CT, USA;9. Department of Molecular Cell Biology, Katholieke Universiteit Leuven, Leuven 3000, Belgium;10. Department of Advanced Biomedical Sciences, Federico II University, Via Pansini 5, 80131 Naples, Italy
Abstract:The present study shows that in brain mitochondria the active calcium uptake and the sodium-dependent calcium efflux are modulated by the porin-bound enzyme hexokinase. The release of the enzyme, promoted by glucose-6-phosphate (G-6-P), under conditions which do not affect mitochondrial functions, is accompanied by a decrease of the rates of fluxes of the cation. This phenomenon is discussed and correlated with the formation of microcompartments between the inner and outer mitochondrial membranes, where the hexokinase-porin complex may constitute a regulating gate system for calcium.
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