Heme transporter that exports cytoplasmic heme. It can also export coproporphyrin and protoporphyrin IX, which are both intermediate products in the heme biosynthetic pathway. Does not export bilirubin. Heme export depends on the presence of HPX and is required to maintain intracellular free heme balance, protecting cells from heme toxicity. Heme export provides protection from heme or ferrous iron toxicities in liver, brain, sensory neurons and during erythtopoiesis, a process in which heme synthesis intensifies. Causes susceptibility to FeLV-C in vitro. Heme transporter that promotes heme efflux from the mitochondrion to the cytoplasm. Essential for erythroid differentiation. Interacts with HPX. N-Glycosylated. Lack definitive erythropoiesis, have craniofacial and limb deformities, and die in midgestation. Mice with FLVCR1 that is deleted neonatally develop a severe macrocytic anemia with proerythroblast maturation arrest. Mice lacking the plasma membrane isoform (Flvcr1a) but expressing Flvcr1b had normal erythropoiesis, but exhibited hemorrhages, edema, and skeletal abnormalities. Has a probable mitochondrial transit peptide at positions 1-38. Belongs to the major facilitator superfamily. Feline leukemia virus subgroup C receptor (TC 2.A.1.28.1) family.