Copper homeostasis is essential for cellular function, requiring precise regulation to meet metabolic needs while preventing toxicity. ATP7B, a P‑type ATPase copper transporter, plays a central role by regulating copper delivery to biosynthetic pathways and controlling intracellular copper levels. Its activity and localization are modulated by tissue‑specific expression, copper‑dependent trafficking, and phosphorylation within a serine‑rich domain. Additional interacting proteins may further influence copper balance. Together, these mechanisms highlight the tightly coordinated regulation required to maintain copper homeostasis in human cells.
