G Protein-Activated Inwardly Rectifying Potassium Channels as Potential Therapeutic Targets
Toru Kobayashi, Kazutaka Ikeda
Abstract
Toru Kobayashi, Kazutaka Ikeda
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.
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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.
Key concepts: G protein-coupled inwardly-rectifying potassium channel, Potassium channel, Knockout mouse, Inward-rectifier potassium ion channel, Gene knockin, G protein, Cell biology, Chemistry