Skip to main content
. 2022 May 2;10:871877. doi: 10.3389/fcell.2022.871877

FIGURE 1.

FIGURE 1

Cu homeostasis in liver (A) and Cu-handling proteins in liver cells (B). (A) Cu enters liver via portal circulation and transported into liver cells primarily by the high affinity uptake protein, CTR1. Cytosolic Cu chaperones shuttle Cu to specific intracellular targets; CCS transports Cu to SOD1, ATOX1 - to the Cu-transporting ATPase ATP7B. ATP7B transports Cu into the trans-Golgi network (TGN) for incorporation into ceruloplasmin (CP) and to the apical membrane for excretion. Inactivation of ATP7B causes Cu overload, which manifests clinically as WD (ATP7B-ATPase Cu(I) transporting beta polypeptide; CTR1-high affinity Cu uptake protein 1; MT-Metallothionein; GSH-Glutathione, ATOX1-antioxidant protein 1; SOD1-Superoxide dismutase; CCS-Cu Chaperone for SOD, COX17-Cytochrome C oxidase) (Lutsenko 2016; Członkowska et al., 2018). (B) Expression of ATP7B, CP and CTR in liver cells. The figure is generated using Liver Cell Atlas (https://www.livercellatlas.org/), which aggregates single cells sequencing data for human and animal livers.