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. 2020 Dec 29;296:100227. doi: 10.1074/jbc.RA120.014288

Figure 1.

Figure 1

The Nav1.7/I848T mutation changes the voltage dependence for activation but not for inactivation. A, schematic representation of Nav1.7 with the location of the I848T mutation, which leads to inherited erythromelalgia. The voltage protocol of activation (top) with two representative traces for the Nav1.7/WT (middle, black) and I848T mutant (bottom, red). B, the I848T mutant produces significantly less current than Nav1.7/WT (p = 0.04 Mann–Whitney test, median diff. −122.7 pA/pF, 95.11% confidence interval 3.79–248.8 pA/pF). C, current–voltage relationship shown for WT and I848T mutant. D, the I848T mutant leads to a hyperpolarized shift of −9.77 ± 1.53 mV in the voltage dependence of activation of Nav1.7. E, values of half-maximal voltage dependence of activation (V1/2) for WT and I848T mutant (p < 0.0001, t = 6.61, df = 59, unpaired t test, mean diff. −9.73 ± 1.45 mV, 95% confidence interval −12.67 to −6.86 mV). F, there is no difference in the voltage dependence of steady-state fast inactivation for the I848T mutant. The applied voltage protocol is shown in the inset. See Table 1 for all values. All data are presented as mean ± SD.