Abstract
Gating of the delayed rectifier K+ channel KvLQT1 is drastically slowed by the association with the small membrane protein minK and it is thought that the KvLQT1/minK complex underlies the slow delayed rectifier K+ current of cardiac cells. There is controversy about the effects of the association between KvLQT1 and minK on the single-channel conductance. Here, nonstationary fluctuation analysis was applied to inward K+ tail currents recorded with a high-time resolution (5 kHz bandwidth) from macropatches of homomeric KvLQT1 and heteromeric KvLQT1/minK channels expressed in Xenopus oocytes to estimate their single-channel conductance. It was found that heteromers have a threefold larger conductance (5.8 pS) compared to homomeric channels (1.8 pS) in symmetrical high-K+ solutions. The larger conductance of heteromers explains in part their larger macroscopic conductance in heterologous expression systems. The molecular mechanism underlying the conductance increase remains to be identified.
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Received: 1 September 1998 / Received after revision 9 October 1998 / Accepted: 12 October 1998
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Pusch, M. Increase of the single-channel conductance of KvLQT1 potassium channels induced by the association with minK. Pflügers Arch 437, 172–174 (1998). https://doi.org/10.1007/s004240050765
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DOI: https://doi.org/10.1007/s004240050765