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 5
Electrophysiological characteristics of the p.Glu87Gln mutant. (A) Representative traces of sodium current. (B) Current density at –30 mV for Na_V1.5 alone (n = 13), Na_V1.5 coexpressed with WT β1 (n = 17), Na_V1.5 coexpressed with p.Glu87Gln β1 (n = 18), and Na_V1.5 coexpressed with WT β1 plus p.Glu87Gln β1 (n = 15). (C) Voltage dependence of activation and inactivation. Filled circles, open circles, and squares indicate Na_V1.5 alone, Na_V1.5 coexpressed with WT β1, and Na_V1.5 coexpressed with p.Glu87Gln β1, respectively. (D) Recovery from inactivation. Biophysical properties are provided in Table 2.