Key result
KCNE2 expression in transiently transfected COS cells accelerated the deactivation kinetics of KCNQ2 and the KCNQ2-KCNQ3 complex.
KCNE2, a known modulator of the HERG potassium channel in the heart, also associates with and modulates the deactivation kinetics of KCNQ2/KCNQ3 potassium channels in the brain.
May inform neonatal convulsion mechanisms; leaves open any clinical role for KCNE2-KCNQ interactions.
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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Tinel et al. (2000) studied this question. KCNE2 expression was evaluated on Deactivation kinetics of KCNQ2 and KCNQ2-KCNQ3 complex. KCNE2 expression in transiently transfected COS cells accelerated the deactivation kinetics of KCNQ2 and the KCNQ2-KCNQ3 complex.
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