Copper transport

Copper transport refers to the highly regulated system of proteins responsible for the uptake, intracellular distribution, and efflux of copper ions to maintain cellular homeostasis (PubMed, 2008; PMC, 2011). The primary components of this system include the high-affinity copper transporter 1 (CTR1/SLC31A1) for cellular uptake, and the copper-transporting ATPases, ATP7A and ATP7B, which facilitate copper export and delivery to the secretory pathway (UniProt; PMC, 2011). Within the cell, copper is shuttled by specific chaperones such as ATOX1, CCS, and COX17 to various organelles and enzymes, ensuring that free copper levels remain extremely low to prevent oxidative damage (PMC, 2011). Dysregulation of this system is central to genetic disorders such as Wilson disease (caused by ATP7B deficiency) and Menkes disease (caused by ATP7A deficiency), and it plays a significant role in cancer, particularly in the resistance to platinum-based chemotherapies like cisplatin, which utilize these transporters for cellular entry and exit (PMC, 2009; PMC, 2011). Therapeutic strategies targeting copper transport include the use of chelators to remove excess copper, ionophores to increase intracellular copper for "cuproptosis" induction, and modulators to overcome chemotherapy resistance (PubMed, 2022; PMC, 2021).

Other names

Copper homeostasisCopper traffickingCopper uptake and effluxCopper metabolism

Copper chelation, copper ionophore activity, transport substrate competition, and induction of metallothionein-mediated sequestration.