disease:Defects in SLC16A1 are the cause of familial hyperinsulinemic hypoglycemia type 7 (HHF7) [MIM:610021]; also known as exercise-induced hyperinsulinemic hypoglycemia. HHF7 is a dominantly inherited hypoglycemic disorder characterized by inappropriate insulin secretion during anaerobic exercise or on pyruvate load.,disease:Defects in SLC16A1 are the cause of symptomatic deficiency in lactate transport (SDLT) [MIM:245340]; also known as erythrocyte lactate transporter defect. Deficiency of lactate transporter may result in an acidic intracellular environment created by muscle activity with consequent degeneration of muscle and release of myoglobin and creatine kinase. This defect might compromise extreme performance in otherwise healthy individuals.,function:Proton-linked monocarboxylate transporter. Catalyzes the rapid transport across the plasma membrane of many monocarboxylates such as lactate, pyruvate, branched-chain oxo acids derived from leucine, valine and isoleucine, and the ketone bodies acetoacetate, beta-hydroxybutyrate and acetate.,similarity:Belongs to the major facilitator superfamily. Monocarboxylate porter (TC 2.A.1.13) family.,tissue specificity:Widely expressed in normal and in cancer cells.,
Cell membrane ; Multi-pass membrane protein .
Detected in heart and in blood lymphocytes and monocytes (at protein level). Widely expressed.