E1676 Sheynin et al. that both the missense and in-frame deletion pore mutations hamper the surface expression of Nav1.7, and may explain the reason for the loss of pain phenotype seen in these patients. Figure 2. (a) Immunostaining of PC12 cells expressing the Nav1.7 sodium channel. From left to right the staining is as follows: anti-Nav1.7, anti-pan cadherin, merged image (with DAPI in blue). The WT Nav1.7 shows a faint but distinct ‘rim’ which colocalizes with the plasma membrane marker pan cadherin. Both the missense (Nav1.7-R896Q) and the in-frame deletion (Nav1.7-ΔR1370-L1374) typically do not show this rim effect. For each transfection experiment a representative cell is shown, with the Z slice chosen as the one with the most plasma membrane staining according to the anti-pan cadherin marker. Untransfected cells showed some golgi-localized staining, but never staining at the plasma membrane. (b) For each Nav1.7 construct, at least 300 cells were assessed for plasma membrane staining of Nav1.7. There were significantly more transfected cells with Nav1.7 staining at the plasma membrane for the WT transfections compared to each of the mutants (* indicates statistically significant result).