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The disease is caused by a mutation in the ATP7B gene, which codes for a protein that facilitates the incorporation of copper into proteins (such as ceruloplasmin) and also the transportation of copper into vesicles that allow it to be secreted in bile.1 The critical effect of a mutation in ATP7B is diminished copper secretion into bile, which leads to excess copper accumulation in the hepatocyte

14, 223238 (Springer, 1996)

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Cell viability relative to untreated controls was quantified using a standard Cell Counting Kit-8 (CCK-8) assay (YEASEN, Shanghai, China)