Lipid transporter that specifically mediates export of sphingosine-1-phosphate (sphing-4-enine 1-phosphate, S1P) and sphinganine-1-phosphate in the lymph, thereby playing a role in lymphocyte trafficking (PubMed:22664872, PubMed:23103166, PubMed:22406534, PubMed:23180825, PubMed:34260944). S1P is a bioactive signaling molecule that regulates many physiological processes important for the development and for the immune system (PubMed:22664872, PubMed:23103166, PubMed:22406534, PubMed:23180825, PubMed:34260944). Regulates levels of S1P and the S1P gradient that exists between the high circulating concentrations of S1P and low tissue levels that control lymphocyte trafficking (PubMed:22664872, PubMed:22406534, PubMed:23180825, PubMed:34260944). Required for the egress of T-cells from lymph nodes during an immune response by mediating S1P secretion, which generates a gradient that enables activated T-cells to access lymph (PubMed:22406534, PubMed:34260944). Also required for the egress of immature B-cells from the bone marrow (PubMed:22406534). In contrast, it does not mediate S1P release from red blood cells (PubMed:23103166, PubMed:22406534). Involved in auditory function: S1P release in the inner ear is required for maintenance of the endocochlear potential in the cochlea (PubMed:25356849). In addition to export, also able to mediate S1P import (PubMed:33785361). sphing-4-enine 1-phosphate(in) = sphing-4-enine 1-phosphate(out) sphinganine 1-phosphate(in) = sphinganine 1-phosphate(out) Expression is high in the lungs and liver, low in the lymph nodes, spleen and bone marrow, and very low but detectable in the thymus (PubMed:22664872). Not expressed in red blood cells (PubMed:23103166). Also expressed in the inner ear: expressed in the cochlea, both in the lateral wall and organ of Corti (PubMed:25356849). Deficient mice are viable, do not exhibit cardiac defects or embryonic lethality, and are generally normal and fertile (PubMed:22664872, PubMed:22406534). Deficient mice have decreased levels of sphingosine 1-phosphate (S1P) and dihydro-S1P in blood, accompanied by increases in very long chain ceramide species, and have defective lymphocyte trafficking (PubMed:22664872, PubMed:22406534, PubMed:23180825). S1P levels are increased in lymph from deficient mice as well as in specific tissues, including lymph nodes, and interstitial fluid (PubMed:23180825). Moreover, these mice have aberrant lymphatic sinus that appeared collapsed, with reduced numbers of lymphocytes (PubMed:23180825). Mice display marked accumulation of mature T-cells in thymus and decreased numbers of peripheral T-cells in blood and secondary lymphoid organs (PubMed:22406534, PubMed:34260944). Mature recirculating B-cells are reduced in frequency in the bone marrow as well as in blood and secondary lymphoid organs (PubMed:22406534). Mice do not show defects in S1P release from blood cells (PubMed:22406534). Knockout mice are protected against experimental autoimmune encephalomyelitis (PubMed:34260944). Mutants also show a profound hearing impairment, characterized by a progressive degeneration of sensory hair cells in the organ of Corti (PubMed:25356849, PubMed:30973865). Hearing loss is caused by a decline in the endocochlear potential (PubMed:25356849). Conditional deletion in the cochlea causes early onset progressive hearing loss (PubMed:25356849). In contrast, hearing impairment is not observed in mice with targeted deletion in red blood cells, platelets, lymphatic or vascular endothelial cells (PubMed:25356849). Belongs to the major facilitator superfamily. Spinster (TC 2.A.1.49) family. Extended N-terminus.