Abstract
G protein-activated inwardly rectifying K(+) (GIRK; Kir3) channels regulate the neuronal activity and heart rate. Molecular cloning of the GIRK channel genes has led to remarkable progress in our understanding of the molecular structure, distribution and functional modulation of these channels. Furthermore, the roles of GIRK channels in vivo have been shown by studies using GIRK knockout mice and weaver mutant mice, which have a missense mutation in the GIRK2 gene. We also review the possible roles of GIRK channels in the pathophysiology of various disorders, and discuss the therapeutic potential of GIRK channel modulation.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Analgesics / pharmacology
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Animals
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Anti-Arrhythmia Agents / pharmacology
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Anticonvulsants / pharmacology
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Antidepressive Agents / pharmacology
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Anxiety / metabolism
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Arrhythmias, Cardiac / metabolism
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Diabetes Mellitus / metabolism
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Epilepsy / metabolism
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G Protein-Coupled Inwardly-Rectifying Potassium Channels / drug effects*
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G Protein-Coupled Inwardly-Rectifying Potassium Channels / metabolism*
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Humans
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Hyperkinesis / metabolism
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Hypoglycemic Agents / pharmacology
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Ion Channel Gating / drug effects*
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Ischemia / metabolism
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Mice
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Pain / metabolism
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Potassium Channel Blockers / pharmacology*
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Potassium Channel Blockers / therapeutic use
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Substance-Related Disorders / metabolism
Substances
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Analgesics
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Anti-Arrhythmia Agents
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Anticonvulsants
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Antidepressive Agents
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G Protein-Coupled Inwardly-Rectifying Potassium Channels
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Hypoglycemic Agents
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Potassium Channel Blockers