Sodium channel β1 subunit mutations associated with Brugada syndrome and cardiac conduction disease in humans
J. Clin. Invest. Hiroshi Watanabe, et al. 118:2260 doi:10.1172/JCI33891 [Go to this article.]

Figure 4
Electrophysiological characteristics of the p. Trp179X β1B mutant. (A) Representative traces of sodium current demonstrating an increase in sodium current with WT but not mutant subunit. (B) Sodium current density at –30 mV for Na_V1.5 alone (n = 29), Na_V1.5 coexpressed with WT β1B (n = 28), Na_V1.5 coexpressed with p.Trp179X β1B (n = 18), Na_V1.5 coexpressed with WT β1B plus p.Trp179X β1B (1 μg for each; n = 14), and Na_V1.5 coexpressed with WT β1B plus p.Trp179X β1B (0.5 μg for each; n = 10). (C) Voltage dependence of activation and inactivation. Filled circles, open circles, and squares indicate Na_V1.5 alone, Na_V1.5 coexpressed with WT β1B, and Na_V1.5 coexpressed with p.Trp179X β1B, respectively. The pulse protocol used to study the voltage dependence of inactivation is shown in the inset. (D) Recovery from inactivation. Biophysical properties are provided in Table 1.