Copper is essential for many copper-dependent processes, including mitochondrial oxidative phosphorylation, free-radical detoxification, pigmentation, neurotransmitter synthesis, and iron metabolism. The identification of proteins for high affinity copper uptake and export has greatly expanded our understanding of cellular copper homeostasis. Copper export in human cells is mediated by the ATP7A and ATP7B P-type ATPases, which are, respectively, affected in the genetic disorders of copper metabolism, Menkes disease and Wilson disease. A different class of transporter known as the SLC31 or Ctr family of proteins mediates cellular copper uptake. These high-affinity copper transporters exist in all eukaryotes and their discovery has provided new insights into how cells acquire and regulate this essential nutrient. The following is a brief overview of the SLC31 copper transporter family with a focus on the human hCtr1 protein.