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

Figure 7. p.D1690N and p.G1748D are endoplasmic reticulum and Golgi trafficking–defective channels, respectively.

Figure 7

(A and B) Maximum Nav1.5 current (INav1.5) density generated by p.D1690N and p.G1748D channels in CHO cells incubated at 37°C (black circles) or 25°C (white circles) (A) or in the presence (white circles) or absence (black circles) of 4-phenylbutyrate (B). (C) Maximum INav1.5 density generated by WT or mutated Nav1.5 channels cotransfected (white circles) or not (black circles) with MOG1. *P < 0.05 vs. p.D1690N without treatment. Each bar represents mean ± SEM of n cells from at least 3 different batches, and each dot represents 1 experiment. Unpaired t test and multilevel mixed-effects model were used for comparisons. (D and E) Colocalization of Nav1.5 p.D1690N-GFP channels and the endoplasmic reticulum (ER) marker calnexin in 2 different COS cells representative of 3 different dishes. In D, inset images are included to make low-contrast highlighted regions visible. (F and G) Colocalization between Nav1.5 p.G1748D-GFP channels and the Golgi marker mCherry-Golgi in 2 different COS cells representative of 3 different dishes. Cell contours are delineated in gray for enhanced visualization. Scale bars: 25 μm.