Figure 4
From: Calcineurin Controls Voltage-Dependent-Inactivation (VDI) of the Normal and Timothy Cardiac Channels
A mutation within CaN binding motif of TS α11.2/G406R subunit increases VDI of the Timothy channel.
(a) Schematic illustration and location (b) of the Timothy α11.2G406R subunit and the His1926A and His1927A mutations within the CaN binding motif of the human α11.2 subunit (c) Normalized ICa (left) and IBa (right) records from representative oocytes expressing Cav1.2/G406R and Cav1.2/G406R/HH/AA (d) The voltage-dependence of inactivation of Cav1.2G406R and Cav1.2G406R/HH/AA in Ca2+ (left) and Ba2+ (right). Values are displayed as mean ± S.E.M (n = 10−12). Peak currents for ICa α11.2/G406R, −493 ± 74 nA (n = 13); α11.2/G406R/HH/AA, −338 ± 52 nA (n = 14) For IBa, α11.2/G406R, −377 ± 61 nA (n = 13); α11.2G406R/HH/AA −518 ± 23 nA (n = 10).
