Journal
CURRENT PHARMACEUTICAL DESIGN
Volume 12, Issue 28, Pages 3631-3644Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/138161206778522065
Keywords
arrhythmia; hERG; I-Kr; I-Kr; KCNE; KCNQ1; Kv1.5; MinK; MiR1
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Funding
- NHLBI NIH HHS [R01 HL079275] Funding Source: Medline
- NIDCD NIH HHS [R03 DC07060] Funding Source: Medline
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL079275] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS [R03DC007060] Funding Source: NIH RePORTER
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Potassium channels form highly K+ ion-selective pores in the plasma membrane of excitable cells. Voltage-gated potassium (Kv) channels open in response to membrane depolarization to allow rapid diffusion of K+ ions out of the cell, thus repolarizing the cell to restore a negative resting membrane potential. Inherited mutations in Kv channel genes produce abnormal cellular repolarization and cause diseases of excitable tissues. Small molecule interactions with Kv channels can cause similar pathologies. During the last decade of research into Kv channels and associated diseases termed 'channelopathies' - we have begun to understand Kv channel function and dysfunction at the molecular level. In this review, the molecular mechanisms of Kv channelopathies are discussed, with particular emphasis on the overlap between inherited and acquired disease, and the drive towards novel channel-targeted therapies.
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