Copper ion transmembrane transporter involved in the export of copper out of the cells. It is involved in copper homeostasis in the liver, where it ensures the efflux of copper from hepatocytes into the bile in response to copper overload. ATP + Cu(+)(in) + H2O = ADP + Cu(+)(out) + H(+) + phosphate Monomer. Interacts with COMMD1/MURR1 (PubMed:12968035, PubMed:17919502). Interacts with DCTN4, in a copper-dependent manner (PubMed:16554302). Interacts with ATOX1 (PubMed:18558714, PubMed:17919502). Interacts (via C-terminus) with ZBTB16/PLZF (PubMed:16676348). Predominantly found in the trans-Golgi network (TGN). Localized in the trans-Golgi network under low copper conditions, redistributes to cytoplasmic vesicles when cells are exposed to elevated copper levels, and then recycles back to the trans-Golgi network when copper is removed (PubMed:10942420). Most abundant in liver and kidney and also found in brain. Isoform 2 is expressed in brain but not in liver. The cleaved form WND/140 kDa is found in liver cell lines and other tissues. Each HMA domain can bind a copper ion, they are tightly packed and closely interact with each other. Wild-type ATP7B can usually be loaded with an average 5.5 copper atoms per molecule. Isoform 1 may be proteolytically cleaved at the N-terminus to produce the WND/140 kDa form. The disease is caused by variants affecting the gene represented in this entry. May arise by a -1 programmed ribosomal frameshift at codon 233. A nucleotide 'slippery sequence' followed by an mRNA pseudoknot are found downstream of the frameshift site and direct frameshifting of a gene fragment with about 10% efficiency. Belongs to the cation transport ATPase (P-type) (TC 3.A.3) family. Type IB subfamily.