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Functional conversion between A-type and delayed rectifier K+ channels by membrane lipids.

Dominik Oliver·Cheng-Chang Lien·Malle Soom·Thomas Baukrowitz·Peter Jonas·Bernd Fakler
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Abstract

Voltage-gated potassium (Kv) channels control action potential repolarization, interspike membrane potential, and action potential frequency in excitable cells. It is thought that the combinatorial association between distinct alpha and beta subunits determines whether Kv channels function as non-inactivating delayed rectifiers or as rapidly inactivating A-type channels. We show that membrane lipids can convert A-type channels into delayed rectifiers and vice versa. Phosphoinositides remove N-type inactivation from A-type channels by immobilizing the inactivation domains. Conversely, arachidonic acid and its amide anandamide endow delayed rectifiers with rapid voltage-dependent inactivation. The bidirectional control of Kv channel gating by lipids may provide a mechanism for the dynamic regulation of electrical signaling in the nervous system.

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AnimalsArachidonic AcidsBrainCationsCell MembraneDelayed Rectifier Potassium ChannelsEicosanoic AcidsEndocannabinoidsInterneuronsIon Channel GatingKineticsMembrane LipidsOocytesPatch-Clamp TechniquesPermeabilityPhosphatidylinositol 4,5-DiphosphatePolylysinePolyunsaturated AlkamidesPotassium ChannelsPotassium Channels, Voltage-GatedProtein Structure, TertiaryProtein SubunitsRecombinant ProteinsSignal TransductionXenopusJournal Article

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Dominik Oliver, Cheng-Chang Lien, Malle Soom, Thomas Baukrowitz, Peter Jonas, Bernd Fakler. 2004-03-18. Functional conversion between A-type and delayed rectifier K+ channels by membrane lipids.. https://doi.org/10.1126/science.1094113

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