Major iron transporter that plays a key role in balancing cellular and systemic iron levels. Transports iron from intestinal, splenic, and hepatic cells into the blood to provide iron to other tissues (PubMed:30213870). Controls therefore dietary iron uptake, iron recycling by macrophages, and release of iron stores in hepatocytes (PubMed:16054062). When iron is in excess hepcidin/HAMP levels increase, resulting in a degradation of ferroportin/SLC40A1 limiting the iron efflux to plasma (By similarity). Fe(2+)(in) = Fe(2+)(out) During elevated serum iron levels, liver-derived hepcidin/HAMP negatively regulates cell surface ferroportin/SLC40A1 by inducing its ubiquitination, internalization, and degradation. Indeed, hepcidin/HAMP affinity towards ferroportin/SLC40A1 increases by 80-fold in the presence of iron. Identified in a complex with STOM. Interacts with HAMP; this interaction promotes SLC40A1 rapid ubiquitination. Localized to the basolateral membrane of polarized epithelial cells. High expression in spleen, liver, kidney, heart and duodenum. Polyubiquitinated by RNF217; leading to proteasomal degradation (PubMed:33895792). Ubiquitination is necessary for its internalization by hepcidin/HAMP (By similarity). Deletion mice die prenatallys. These mice cannot transfer iron from the extraembryonic visceral endoderm into the embryo proper, leading to a defect in embryonic growth and consequent death (PubMed:16054062). Erythroid-specific deletion reduces serum iron but increased tissue iron contents (PubMed:30213870). Belongs to the ferroportin (FP) (TC 2.A.100) family. SLC40A subfamily.