Figure 5
Mutation A735V shifts the activation curve of NaV1.5 channels heterologously expressed in HEK293T cells. (a,b) Voltage protocol for sodium channel activation and representative current traces of WT (a) and mutant A735V (b) -NaV1.5 channels heterologously expressed in HEK293T cells. c) Voltage dependence of mean current densities (pA/pF) from HEK293T cells expressing WT or mutant A735V-NaV1.5 channels. Inset: Bar graph on comparison of the maximum current density for WT and mutant A735V NaV1.5 channels. (d,e) Voltage protocol for sodium channel inactivation and representative current traces of WT (d) and mutant A735V (e) NaV1.5 channels heterologously expressed in HEK293T cells. (f) Sodium channel activation (G/Gmax) and inactivation (I/Imax) curves of WT and A735V NaV1.5 channels expressed in HEK293T cells. Solid lines represent fits with Boltzmann functions. (g,h) Scatter plots and mean values (±s.e.m.) of mid-voltages (V0.5) of activation (g) and inactivation (h) for WT and mutant A735V-NaV1.5 channels. (i) Representative western blot analysis for heterologous NaV1.5 channel expression in HEK293T cells, showing similar intensities for WT and mutant A735V-NaV1.5 bands. Untransfected HEK293T cells served as negative control (Neg.). GAPDH is visualized as loading control for comparable concentrations of total protein. (j) Scatter plot and mean values (±s.e.m.) of relative expression levels of NaV1.5/GAPDH (WT: n = 7; A735V: n = 7, Student´s t-test, p = 0.27). - Data volume in (c) and (f–h): WT, n = 25; A735V, n = 18.
