Internal gate mutants of the GABA transporter GAT1 are capable of substrate exchange
Author:
Funder
Rosetrees Trust
Israel Science Foundation
Publisher
Elsevier BV
Subject
Cellular and Molecular Neuroscience,Pharmacology
Reference35 articles.
1. An acidic amino acid transmembrane helix 10 residue conserved in the neurotransmitter:sodium:symporters is essential for the formation of the extracellular gate of the gamma-aminobutyric acid (GABA) transporter GAT-1;Ben-Yona;J. Biol. Chem.,2012
2. Functional defects in the external and internal thin gates of the gamma-aminobutyric acid (GABA) transporter GAT-1 can compensate each other;Ben-Yona;J. Biol. Chem.,2013
3. A glutamine residue conserved in the neurotransmitter:sodium:symporters is essential for the interaction of chloride with the GABA transporter GAT-1;Ben-Yona;J. Biol. Chem.,2011
4. Mutation of arginine 44 of GAT-1, a (Na(+) + Cl(-))-coupled gamma-aminobutyric acid transporter from rat brain, impairs net flux but not exchange;Bennett;J. Biol. Chem.,2000
5. X-ray structures and mechanism of the human serotonin transporter;Coleman;Nature,2016
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1. A comparative review on the well-studied GAT1 and the understudied BGT-1 in the brain;Frontiers in Physiology;2023-04-13
2. Experimental and Bioinformatic Insights into the Effects of Epileptogenic Variants on the Function and Trafficking of the GABA Transporter GAT-1;International Journal of Molecular Sciences;2023-01-04
3. Inhibitory co-transmission from midbrain dopamine neurons relies on presynaptic GABA uptake;Cell Reports;2022-04
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5. Elucidating the Mechanism Behind Sodium-Coupled Neurotransmitter Transporters by Reconstitution;Neurochemical Research;2021-08-04
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