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.
Keywords: GIRK channel, Kir channel, pharmacological modulation, therapeutic target, GIRK knockout mice, weaver mutant mice
Current Pharmaceutical Design
Title: G Protein-Activated Inwardly Rectifying Potassium Channels as Potential Therapeutic Targets
Volume: 12 Issue: 34
Author(s): Toru Kobayashi and Kazutaka Ikeda
Affiliation:
Keywords: GIRK channel, Kir channel, pharmacological modulation, therapeutic target, GIRK knockout mice, weaver mutant mice
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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Cite this article as:
Kobayashi Toru and Ikeda Kazutaka, G Protein-Activated Inwardly Rectifying Potassium Channels as Potential Therapeutic Targets, Current Pharmaceutical Design 2006; 12 (34) . https://dx.doi.org/10.2174/138161206779010468
DOI https://dx.doi.org/10.2174/138161206779010468 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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