Fig. 3. FYCO1 and SKIP, acting as adaptor proteins, are involved in the unconventional trafficking of ∆F508-CFTR.
Effects of SKIP, ARL8b, and FYCO1 gene silencing on the unconventional trafficking of ∆F508-CFTR. (A) Cell surface biotinylation assay was conducted using HEK293 cells transfected with control (scrambled) siRNA or target siRNAs (100 nM each, 48 h) together with plasmids encoding ∆F508-CFTR (24 h). ER-to-Golgi transport was inhibited by ARF1Q71L-HA overexpression in some cells. (B) ∆F508-CFTR in lysate were quantified respectively. (C) Surface-proteins versus cell lysates were quantified respectively. (D) Efficacy of each target genes knockdown. Bar graph data are presented as the mean ± SEM. Data were analyzed using one-way ANOVA, followed by Tukey’s multiple comparison test. CFTR, cystic fibrosis transmembrane conductance regulator; ER, endoplasmic reticulum. *p < 0.05, **p < 0.01.
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