Abstract
KCNQ2 and KCNQ3 subunits belong to the six transmembrane domain K+ channel family and loss of function mutations are associated with benign familial neonatal convulsions. KCNE2 (MirP1) is a single transmembrane domain subunit first described to be a modulator of the HERG potassium channel in the heart. Here, we show that KCNE2 is present in brain, in areas which also express KCNQ2 and KCNQ3 channels. We demonstrate that KCNE2 associates with KCNQ2 and/or KCNQ3 subunits. In transiently transfected COS cells, KCNE2 expression produces an acceleration of deactivation kinetics of KCNQ2 and of the KCNQ2-KCNQ3 complex. Effects of two previously identified arrhythmogenic mutations of KCNE2 have also been analyzed.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Amino Acid Sequence
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Animals
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Brain / metabolism
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Brain / pathology
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COS Cells
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Electrophysiology
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Humans
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In Situ Hybridization / methods
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KCNQ2 Potassium Channel
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KCNQ3 Potassium Channel
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Molecular Sequence Data
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Potassium Channels / genetics
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Potassium Channels / metabolism*
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Potassium Channels / physiology
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Potassium Channels, Voltage-Gated*
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Precipitin Tests
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Rats
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Sequence Analysis, Protein
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Sequence Homology, Amino Acid
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Tissue Distribution
Substances
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KCNQ2 Potassium Channel
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KCNQ2 protein, human
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KCNQ3 Potassium Channel
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KCNQ3 protein, human
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Kcnq2 protein, rat
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Kcnq3 protein, rat
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Potassium Channels
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Potassium Channels, Voltage-Gated
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potassium channel protein I(sk)