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. 2018 Sep 20;3(18):e96291. doi: 10.1172/jci.insight.96291

Figure 1. Heterozygous deletion of the SCN5A gene in mice concomitantly decreased the inward rectifier current, and Kir2.1 overexpression rescued the sodium current.

Figure 1

(A) Inward rectifier current (IK1) traces recorded in ventricular cardiomyocytes (CMs) from WT, Kcnj2OE+/–, and Kcnj2OE+/–-Scn5a+/– mice. (B) Mean current density-voltage curves for IK1 recorded in ventricular CMs from 3 WT (black circles), 4 Scn5a+/– (white circles), 3 Kcnj2OE+/– (black squares), and 3 Kcnj2OE+/–-Scn5a+/– (white squares) mice. (C) Sodium current (INa) traces recorded in ventricular CMs from WT, Scn5a+/-, and Kcnj2OE+/–-Scn5a+/– mice. (D) Mean current density-voltage curves for INa recorded in ventricular CMs from 3 WT (black circles), 3 Scn5a+/–, and 3 Kcnj2OE+/–-Scn5a+/– mice. Each point represents the mean ± SEM of n cells. One-way ANOVA followed by Newman-Keuls and multilevel mixed-effects model were used for comparisons. *P < 0.05 vs. WT; #P < 0.05 vs. Kcnj2OE+/–-Scn5a+/–.