Fig. 1. KIF1A and KIF5A are involved in the unconventional trafficking of ∆F508-CFTR but not in the conventional trafficking of WT-CFTR.
Effects of KIF1A and KIF5A gene silencing on the unconventional trafficking of ∆F508-CFTR (A) and conventional trafficking of WT-CFTR (C). Cell surface biotinylation assay was conducted using HEK293 cells transfected with control (scrambled) siRNA or target siRNAs (50 nM each, 48 h) together with plasmids encoding ∆F508/WT-CFTR (24 h). ER-to-Golgi transport was inhibited by ARF1Q71L-HA overexpression in some cells. Surface-proteins versus cell lysates were quantified respectively (B, D). (E) Efficacy of each target gene knockdown. Bar graph data are presented as the mean ± SEM. Data were analyzed using one-way ANOVA, followed by Tukey’s multiple comparison test. b, band B (core-glycosylated) CFTR; c, band C (complex-glycosylated) CFTR; CFTR, cystic fibrosis transmembrane conductance regulator; WT, wild-type; ER, endoplasmic reticulum; ns, not significant. **p < 0.01.
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