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. 2016 Jan 25;63(6):1842–1859. doi: 10.1002/hep.28398

Figure 4.

Figure 4

Impact of p38 and JNK inhibitors on localization of ER‐retained ATP7B mutants. (A) HeLa cells were transfected with different ATP7B mutants (indicated in each panel), then treated for 24 hours with either p38 or JNK inhibitor and exposed to 100 μM CuSO4 for 2 hours. Cells were then fixed, labeled for TGN46, and visualized under a confocal microscope. All mutants exhibited clear ER patterns in cells that were not treated with inhibitors. Incubation with either p38 or JNK inhibitor allowed R778L, D765N, and L776V mutants of ATP7B to be transported to the Golgi, post‐Golgi vesicles (arrows), and PM. In contrast, inhibitors did not recover either L1083F or A874V mutants of ATP7B from the ER (two bottom rows). (B) Cells were treated as in (A). The percentage of cells (average ± standard deviation, n = 10 fields) with ATP7B signal in the ER was calculated for each mutant. p38 and JNK inhibitors reduced the percentage of cells that exhibited R778L, D765N, and L776V in the ER. Scale bar = 5 μm (A). Abbreviation: inh, inhibitor.