Abstract
A dynamic positive feedback mechanism, known as 'facilitation', augments L-type calcium-ion currents (ICa) in response to increased intracellular Ca2+ concentrations. The Ca2+-binding protein calmodulin (CaM) has been implicated in facilitation, but the single-channel signature and the signalling events underlying Ca2+/CaM-dependent facilitation are unknown. Here we show that the Ca2+/CaM-dependent protein kinase II (CaMK) is necessary and possibly sufficient for ICa facilitation. CaMK induces a channel-gating mode that is characterized by frequent, long openings of L-type Ca2+ channels. We conclude that CaMK-mediated phosphorylation is an essential signalling event in triggering Ca2+/CaM-dependent ICa facilitation.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
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Retracted Publication
MeSH terms
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Animals
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Barium / pharmacology
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Calcium / metabolism
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Calcium / pharmacology
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Calcium Channels, L-Type / metabolism*
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Calcium-Calmodulin-Dependent Protein Kinase Type 2
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Calcium-Calmodulin-Dependent Protein Kinases / antagonists & inhibitors
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Calcium-Calmodulin-Dependent Protein Kinases / genetics
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Calcium-Calmodulin-Dependent Protein Kinases / metabolism*
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Calmodulin / metabolism
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Calmodulin / pharmacology
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Cell Membrane / enzymology
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Cells, Cultured
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Enzyme Activation / drug effects
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Enzyme Inhibitors / pharmacology
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Feedback
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Ion Channel Gating / drug effects
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Mice
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Myocardium / cytology
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Myocardium / enzymology*
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Patch-Clamp Techniques
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Peptides / pharmacology
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Phosphorylation / drug effects
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Signal Transduction / drug effects
Substances
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Calcium Channels, L-Type
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Calmodulin
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Enzyme Inhibitors
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Peptides
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Barium
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Calcium-Calmodulin-Dependent Protein Kinase Type 2
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Calcium-Calmodulin-Dependent Protein Kinases
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Calcium