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

FEBS Letters

Lazdunski, Michel¹  Barhanin, Jacques¹  Diochot, Sylvie¹  Lauritzen, Inger¹  Tinel, Norbert¹  Borsotto, Marc¹ 

[1] Institut de Pharmacologie Moléculaire et Cellulaire, CNRS-UPR 411, 660 route des Lucioles, Sophia Antipolis, 06560 Valbonne, France

关键词: Potassium channel;    Epilepsy;    Regulatory protein;    Immunoprecipitation;    In situ hybridization;    PCR;    polymerase chain reaction;    BFNC;    benign familial neonatal convulsions;   

DOI  :  10.1016/S0014-5793(00)01918-9

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown