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MinK-dependent internalization of the IKs potassium channel

Item Type:Article
Title:MinK-dependent internalization of the IKs potassium channel
Creators Name:Xu, X. and Kanda, V.A. and Choi, E. and Panaghie, G. and Roepke, T.K. and Gaeta, S.A. and Christini, D.J. and Lerner, D.J. and Abbott, G.W.
Abstract:KCNQ1-MinK potassium channel complexes (4alpha:2beta stoichiometry) generate IKs, the slowly activating human cardiac ventricular repolarization current. The MinK ancillary subunit slows KCNQ1 activation, eliminates its inactivation, and increases its unitary conductance. However, KCNQ1 transcripts outnumber MinK transcripts five to one in human ventricles, suggesting KCNQ1 also forms other heteromeric or even homomeric channels there. Mechanisms governing which channel types prevail have not previously been reported, despite their significance: normal cardiac rhythm requires tight control of IKs density and kinetics, and inherited mutations in KCNQ1 and MinK can cause ventricular fibrillation and sudden death. Here, we describe a novel mechanism for this control.
Keywords:KCNE1, MinK-Related Peptide, Ventricular Repolarization, Voltage-Gated Potassium Channel, Animals, Guinea Pigs
Source:Cardiovascular Research
Publisher:Oxford University Press
Page Range:430-438
Date:1 June 2009
Official Publication:https://doi.org/10.1093/cvr/cvp047
PubMed:View item in PubMed

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