Figure 8: Loss of cysteine mutation from patient with cardiac arrhythmia affects biophysical properties of Nav1.5. | Nature Communications

Figure 8: Loss of cysteine mutation from patient with cardiac arrhythmia affects biophysical properties of Nav1.5.

From: Cardiac sodium channel palmitoylation regulates channel availability and myocyte excitability with implications for arrhythmia generation

Figure 8

All data are shown as mean±s.e.m. (a) Long-QT3 mutation (C981F, red) that can potentially abolish the endogenous palmitoylation in wild-type Nav1.5. (b) Comparison of voltage dependence of activation and steady-state inactivation of wild-type Nav1.5 (black) and C981F mutant channels (red). n=10. (c) Normalized current of wild-type Nav1.5 channel (black) and Nav1.5-C981F (red). Current traces were averaged data from 9 measurements. (d) Nav1.5-C981F channel activation and steady-state inactivation with (green) and without (black) 2-Br-palmitate(2BP) treatment. n=10. (e) Nav1.5-C981A voltage dependence of activation and steady-state inactivation with (green) and without (black) 2-Br-palmitate treatment. The dotted line indicates the wild-type Nav1.5 steady-state inactivation. n=7. (f,g) 2-Br-palmitate treatment (green) affect Nav1.5-AAA (f) and Nav1.5-C1178A (g) voltage dependence of activation and steady-state inactivation. n=10.

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