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. 2020 Apr 23;72(1):213–229. doi: 10.1002/hep.31002

Figure 6.

Figure 6

The role of rab8 and rab11a binding sites in the disrupting effect of motorless myoVb on canalicular protein localization. (A) Schematic depiction of the amino acid sequences of myoVb mutants. (B) Quantification of the percentage of HepG2 cells showing intracellular accumulation of ABCC2 on expression of myoVb tail domain mutants. (C) HepG2 cells expressing myc‐myoVb/Δ1‐1460 showed intracellular ABCC2 accumulation (white arrows). Myc labeling showed myc‐myoVb/Δ1‐1460 localized diffusely in the cytoplasm. (D) Labeling of ABCC2, F‐actin, and myc in HepG2 expressing myc‐myoVb/Δ1‐1195‐Q1300L and untreated control. White arrows indicate intracellular ABCC2 accumulation. (E) In HepG2 cells expressing myc‐myoVb/Δ1‐1460‐Y1714E ABCC2 localized at the BC with F‐actin (yellow arrowheads). Labeling for myc confirmed expression of the construct. (F) Quantification of the percentage of cells with intracellular multidrug resistance protein (MDR) 1‐GFP accumulations (depicted in Fig. 8G), on expression of myc‐myoVb/Δ1‐1460 or its Y1714E mutant variant. (G) HepG2 cells expressing myc‐myoVb/Δ1‐1460 showed intracellular accumulation of the coexpressed BC marker MDR1‐GFP (white arrows) but not when the Y1714E mutation was introduced in myc‐myoVb/Δ1‐1460.