Sodium- and chloride-dependent GABA transporter 2 (GAT2)

Sodium- and chloride-dependent GABA transporter 2 (GAT2; SLC6A13) is a neurotransmitter transporter responsible for the sodium- and chloride-dependent reuptake of GABA, as well as the transport of beta-alanine and taurine. While four major GABA transporters exist—GAT1, GAT2, GAT3, and BGT1—GAT2 is primarily expressed in the liver (hepatocytes), kidney (proximal tubules), brain leptomeninges, and selectively in some blood vessels. In the brain, its deletion does not cause major phenotypes under normal conditions, but it may enable GABA and taurine efflux across the blood–brain barrier. In the liver, it functions as the major taurine transporter and participates in GABA uptake from the portal circulation. GAT2 shows homology with other SLC6 family members and is a hydrophobic membrane protein with 12 transmembrane domains and several regulatory sites. Although pharmacological targeting is possible, no clinically approved drugs specifically and selectively inhibit GAT2, and its unique physiological roles mean targeting may have hepatic, renal, and neurological consequences[1][2][3][4][7].

Other names

SLC6A13GAT2Solute carrier family 6 member 13gamma-aminobutyric acid transporter 2

Inhibition of GAT2 blocks reuptake of GABA, increasing extracellular GABA concentrations - Inhibition may modulate taurine and beta-alanine transport