Abstract
A growing body of research suggests that fructose 1,6-bisphosphatase (FBPase) might be involved in regulation of cell mortality/survival. However, the precise role of FBPase in the process remains unknown. Here, we show for the first time that in HL-1 cardiomyocytes, inhibition of glycogen synthase kinase-3 results in translocation of FBPase to mitochondria. In vitro experiments demonstrate that FBPase reduces the rate of calcium-induced mitochondrial swelling, affects ATP synthesis and interacts with mitochondrial proteins involved in regulation of volume and energy homeostasis. We suggest that FBPase might be engaged in a regulation of cell survival by influencing mitochondrial function.
Copyright © 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adenosine Triphosphate / biosynthesis
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Animals
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Binding, Competitive
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Calcium / metabolism*
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Cell Line
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Enzyme Inhibitors / pharmacology
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Fructose-Bisphosphatase / metabolism*
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Glycogen Synthase Kinase 3 / antagonists & inhibitors*
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Glycogen Synthase Kinase 3 / genetics
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Glycogen Synthase Kinase 3 / metabolism
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Glycogen Synthase Kinase 3 beta
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Indoles / pharmacology
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Maleimides / pharmacology
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Mice
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Mitochondria, Heart / metabolism*
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Mitochondrial Proteins / metabolism
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Mitochondrial Swelling / physiology
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Myocardium / enzymology
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Myocytes, Cardiac / drug effects
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Myocytes, Cardiac / metabolism*
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Protein Transport
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Recombinant Proteins / genetics
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Recombinant Proteins / metabolism
Substances
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Enzyme Inhibitors
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Indoles
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Maleimides
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Mitochondrial Proteins
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Recombinant Proteins
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SB 216763
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Adenosine Triphosphate
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Glycogen Synthase Kinase 3 beta
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Glycogen Synthase Kinase 3
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Fructose-Bisphosphatase
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Calcium