GABA transporter type 2
protein-coding gene in the species Homo sapiens
GABA transporter 2 (GAT2; SLC6A13) also known as sodium- and chloride-dependent GABA transporter 2 is one of four GABA transporters, GAT1 (SLC6A1), GAT2 (SLC6A13), GAT3 (SLC6A11) and BGT1 (SLC6A12). Note that GAT2 is different from BGT1 despite the fact that the latter transporter is sometimes referred at as (mouse) GAT-2.
All these transporters are highly hydrophobic proteins with 12 transmembrane segments, extracellular glycosylation sites, and intracellular consensus sites for phosphorylation, and there is over 50% amino acid homology between each of them. Each binds GABA with varying affinities with BGT1 having the lowest affinity and GAT3 the highest. GAT2 (SLC6A13) is predominantly expressed in hepatocytes in the liver, but is also found in proximal tubules in the kidney as well as in the leptomeninges and in some blood vessels in the brain.
Biological function
Brain
Deletion of the GAT2 gene in mice does not appear to have any dramatic effects on brain function in a normal situation. The only difference noted so far is a slight elevation of brain Taurine levels. This was an unexpected finding, but is in agreement with the notion that GAT2 permits efflux of GABA and taurine from the brain to circulating blood through the blood brain barrier. GAT1 and GAT3 have higher concentrations in the brain and have higher affinity to GABA. This makes them more likely than GAT2 to influence the activity of neurotransmitter GABA in the brain.
Liver
GAT2 is expressed in hepatocytes and is well positioned to take up GABA entering the liver from the intestine (via the portal vein), but it is not known if this is an important function.
The public source identifies “GABA transporter type 2” as protein-coding gene in the species Homo sapiens. This brief keeps that definition visible, then builds a research path around GABA, transporter and type.
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This entry incorporates text from “GABA transporter type 2” on English Wikipedia. Contributors are listed in the page history. Text is available under the Creative Commons Attribution-ShareAlike 4.0 License. Selected authority identifiers and statements are retrieved from Wikidata under CC0; their references and qualifiers remain part of the verification path.