Since the cloning of the first γ-aminobutyric acid (GABA) transporter (GAT1; SLC6A1) from rat brain in 1990 (Guastella et al., 1990), more than fifty published studies have provided structure-function information on investigator-designed rat and mouse GAT1 mutants. To date, more than 200 of 599 GAT1 residues have been subjected to mutagenesis experiments by substitution with different amino acids, and the resulting transporter functional properties have significantly advanced our understanding of the mechanism of Na+- and Cl--coupled GABA transport by this important member of the neurotransmitter:sodium symporter family. Moreover, many studies have addressed the functional consequences of amino acid deletion or insertion at various positions along the primary sequence.
The enormity of this growing body of structure-function information has prompted us to develop GABA Transporter Mutagenesis Database (GATMD), a web-accessible, relational database of manually annotated biochemical, functional, and pharmacological data reported on GAT1 - the most intensely studied GABA transporter isoform.
As of the last update of GATMD, 54 GAT1 mutagenesis papers have yielded 3,567 experimental records, which collectively contain a total of ~110,000 annotated parameters.
GATMD was supported in part by a grant from the U.S. National Institute of General Medical Sciences (SC1GM086344).
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