M-type KCNQ2-KCNQ3 potassium channels are modulated by the KCNE2 subunit

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Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes
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Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes

Published on: March 12, 2013

N Tinel1, S Diochot, I Lauritzen

  • 1Institut de Pharmacologie Moléculaire et Cellulaire, CNRS-UPR 411, Valbonne, France.

FEBS Letters
|October 18, 2000
PubMed

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.

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