Figure 4: The subunit compound dependent distinct Na+ current of WT and E1784 SCN5A in tsA-201 cells.
From: Embryonic type Na+ channel β-subunit, SCN3B masks the disease phenotype of Brugada syndrome
(A) Quantitative RT-PCR analyses for SCN1B, SCN2B, SCN3B, SCN4B and ANK2B in adult human heart (mixed sample from three men aged 30–39 years), embryonic heart (mixed human sample from 34 male and female embryos at 12–31 weeks gestation), control-iPSC-derived-cardiomyocytes and LQTS3/BrS-iPSC-derived cardiomyocytes. (B) Current–voltage relationships for peak current during the test depolarization pulse in tsA-201 cells with either WT SCN5A or the SCN5A E1784K mutation alone (n = 15 and 11, respectively) or with the SCN1B (n = 17 for both), SCN2B (n = 20 and 17, respectively), or SCN3B (n = 17 for both) genes. (C) Voltage dependency of activation and inactivation curves in tsA-201 cells with either WT SCN5A or the SCN5A E1784K mutation alone (n = 11 and 15, respectively) or with the SCN1B (n = 17 for both), SCN2B (n = 18 and 17, respectively) or SCN3B (n = 17 for both) genes. (D) Fractional recovery from inactivation of tsA-201 cells with either WT SCN5A or the SCN5A E1784K mutation alone (n = 15 and 11, respectively) or with the SCN1B (n = 21 and 19, respectively), SCN2B (n = 19 and 17, respectively) or SCN3B (n = 19 and 17, respectively) genes. Where appropriate, data are given as the mean ± SEM.
