Department of Biochemistry and Redox Biology Center Seminar Series

"Molecular Mechanisms of Copper Transport"

Copper is an essential trace element for growth and development because copper acts as an indispensable cofactor for an array of enzymes, and mutations of genes involved in copper transport result in severe, even lethal, neurodegenerative diseases. Since copper is potentially toxic, appropriate copper levels are tightly regulated by a sophisticated network of copper transporters, chaperones and acceptors, which orchestrate the uptake, distribution, storage and release of this essential metal. The principal copper transporters include the plasma-membrane high-affinity copper importer, CTR1, and the copper-exporting ATPases ATP7A and ATP7B, in which mutations cause Menkes and Wilson's diseases, respectively. Here we discuss our recent progress in elucidating the molecular mechanisms of copper transport in these transporters and aim to develop a comprehensive molecular understanding of cellular copper transport, thus establishing a foundation for designing novel therapeutics for the treatment of copper metabolism diseases.