Fig. 1
From: An epilepsy-causing mutation leads to co-translational misfolding of the Kv7.2 channel
Functional consequences of the W344R mutation. a Representative current traces evoked in cells expressing the indicated subunits. Inset: voltage protocol. b Representation of the current density (pA/pF) from each group at + 20 mV from tail currents. Kv7.2 wild type homomers (WT, white) and heteromers (WT/W344R, gray) had 57.0 ± 11.74 pA/pF and 49.0 ± 8.51 pA/pF, respectively. Kv7.2 mutant (W344R) and Kv7.2-W344R/Kv7.3 heteromers produced negligible current. Number of cells is indicated in brackets. c Current-voltage relationship from tail currents measured at − 30 mV of Kv7.2 WT homomers (V1/2 = − 35.3 ± 0.43 mV, k = 10.5; n = 12) and WT/W344R heteromers (V1/2 = − 30.8 ± 0.64 mV, k = 11.01; n = 14). ***p < 0.001. d Top: Representative immunoblot revealed with anti-Kv7.2 antibody before (left) and after (right) immunoprecipitating with anti-Myc antibody from cells expressing the indicated Myc-tagged Kv7.2 subunits (~ 125 kDa) and CFP-tagged Kv7.2 (~ 135 kDa). Bottom: Relative densitometry of the two bands. IP, immunoprecipitation; IB, immunobloting. n = 3