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. 2017 Jan 3;114(3):E416–E425. doi: 10.1073/pnas.1612383114

Fig. 5.

Fig. 5.

(A) Dofetilide (1 µmol/L)-sensitive (IKr) tail currents obtained by digital subtraction in a noninfected hiPSC-derived cardiomyocytes. (B) IKr density in a hiPSC-derived cardiomyocyte infected or not with either WT or p.R311C Tbx20. Solid lines represent the fit of a Boltzmann equation. (C) Superimposed APs recorded at 1 Hz in three hiPSC-derived cardiomyocytes infected or not with either WT or p.R311C Tbx20. (Top) The APD90 of each experimental group. (D) APD90 at different stimulation frequencies in cells infected with Tbx20 WT or p.R311C. (E) Simulated IKr traces (Top) and APs (Bottom) obtained at 0.1 Hz by using the Grandi–Bers mathematical model of human ventricular endocardial cells by introducing the modifications produced by heterozygous p.T152HfsX180 hERG alone or in combination with p.R311C Tbx20 on the IKr. (F) Percentage of APD90 prolongation in APs simulated at different frequencies in epicardial and endocardial cells. In B–D, points/bars represent mean ± SEM of ≥7 experiments in each group. *P < 0.05 vs. Tbx20(-); #P < 0.05 vs. Tbx20 WT.