GABA Transporter 1 / GAT 1 Recombinant Rabbit Monoclonal Antibody [JE34-61] (HA721496)

UNIPROT #

P30531

PROTEIN NAME

GABA Transporter 1 / GAT 1

SYNONYMS

GABATHG antibody;GABATR antibody;GABT 1 antibody;GABT1 antibody;GAT-1 antibody;GAT1 antibody;SC6A1_HUMAN antibody;Slc6a1 antibody;Sodium and chloride dependent GABA transporter 1 antibody;Sodium- and chloride-dependent GABA transporter 1 antibody;Solute carrier family 6 (neurotransmitter transporter GABA) member 1 antibody;Solute carrier family 6 member 1 antibody

SUBCELLULAR LOCATION

Cell membrane, Presynapse.

FUNCTION

GABA transporter 1 (GAT1) also known as sodium- and chloride-dependent GABA transporter 1 is a protein that in humans is encoded by the SLC6A1 gene and belongs to the solute carrier 6 (SLC6) family of transporters. It mediates gamma-aminobutyric acid's translocation from the extracellular to intracellular spaces within brain tissue and the central nervous system as a whole. GAT1 is a gamma-aminobutyric acid (GABA) transporter, which removes GABA from the synaptic cleft by shuttling it to presynaptic neurons (where GABA can be recycled) and astrocytes (where GABA can be broken down). GABA Transporter 1 uses energy from the dissipation of a Na+ gradient, aided by the presence of a Cl− gradient, to translocate GABA across CNS neuronal membranes. The stoichiometry for GABA Transporter 1 is 2 Na+: 1 Cl−: 1 GABA. The presence of a Cl−/Cl− exchange is also proposed because the Cl− transported across the membrane does not affect the net charge. GABA is also the primary inhibitory neurotransmitter in the cerebral cortex and has the highest level of expression within it. The GABA affinity (Km) of the mouse isoform of GAT1 is 8 μM. In the brain of a mature mammal, glutamate is converted to GABA by the enzyme glutamate decarboxylase (GAD) along with the addition of vitamin B6. GABA is then packed and released into the post-synaptic terminals of neurons after synthesis. GABA can also be used to form succinate, which is involved in the citric acid cycle. Vesicle uptake has been shown to prioritize newly synthesized GABA over preformed GABA, though the reasoning behind this mechanism is currently not completely understood. The regulation of the modular functioning of GATs is highly dependent on a multitude of second messengers and synaptic proteins.