ATP7B
- Retromer retrieves the Wilson disease protein ATP7B from endolysosomes in a copper-dependent manner
Summary: The Wilson disease protein ATP7B utilizes lysosomal exocytosis to export excess copper in hepatocytes. The retromer complex retrieves ATP7B from endolysosomes and recycles it back to the trans-Golgi network.
- COMMD1 and PtdIns(4,5)P2 interaction maintain ATP7B copper transporter trafficking fidelity in HepG2 cells
Summary: Quantitative analysis of 3D protein colocalization defines the cellular function of COMMD1 in maintenance of ATP7B copper transporter trafficking fidelity and the importance of PtdIns(4,5)P2 in this action.
- Basolateral sorting and transcytosis define the Cu+-regulated translocation of ATP7B to the bile canaliculus
Highlighted Article: Excess Cu+ induces the transport of ATP7B from the TGN to the membrane of the bile canaliculus through basolateral sorting and transcytosis for biliary Cu+ excretion without lysosomal involvement.
- Myosin Vb mediates Cu+ export in polarized hepatocytes
Summary: Myosin Vb regulates Cu+-induced recycling of ATP7B at the apical membrane in polarized hepatocytes.