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The SLC6A1 gene encodes a gamma-aminobutyric acid (GABA) transporter, which removes GABA from the synaptic cleft (Hirunsatit et al., 2009.
Results demonstrated that GAT-1-/- mice have phenotypes of hyperactivity, impaired sustained attention and learning deficiency, and the performance of GAT-1-/- mice is similar to ADHD symptoms.
Results suggest that the excessive GAT-1 and GlyT-1 (show GLYT1 ELISA Kits)/2 heterotransporter-mediated Glu (show GCG ELISA Kits) release, in the spinal cord of SOD1 (show SOD1 ELISA Kits)(G93A) mice, is due to the heterotransporter over-expression at the nerve terminal membrane, promoted by the excessive Glu (show GCG ELISA Kits) exocytosis
Results demonstrate that high-affinity activation by GABA of GAT1 transporters provokes release of [3H]GABA from nerve terminals by different mechanisms
these data show that during paclitaxel-induced neuropathic pain there is significant increase in GAT-1 expression in the ACC. GAT-1 is the main transporter of GABA from the synapse
Development of GABA-removal system and its relationship to development of GABAergic networks studied by examination of changes in GAT-1 and GAT-3 expression and localization in embryonic and postnatal mouse spinal cord
GAT1 plays a critical role in the regulation of rapid eye movement (REM (show REM1 ELISA Kits)) sleep and homeostasis of non-REM (show REM1 ELISA Kits) sleep.
results suggest that GAT1 ko mouse is a new animal model for ADHD studying and GAT1 may be a new target to treat ADHD
We failed to provide proof-of-concept evidence that lower PV and GAT1 expression in schizophrenia are a consequence of lower GAD67 (show GAD1 ELISA Kits) expression
Results suggest that a moderate reduction in GAT1 activity causes the enhancement of learning and memory in mice.
the terminal sialic acid of N-linked oligosaccharides of GAT1 plays a crucial role in the gamma aminobutyric acid transport process
the "extra" residue in transmembrane domain 10 of the GABA transporter GAT-1 provides extra bulk, probably in the form of a pi-helix, which is required for stringent gating and tight coupling of ion and substrate fluxes in the GABA transporter family.
Results show that SLC6A1 minor genotypes/alleles were protective against risk for alcoholism in 3 ethnically diverse cohorts.
Genome-wide significant associations were highly biological plausible, including associations within GABA transporter 1, SLC6A1 (solute carrier family 6, member 1), and exonic hits in LOC100129340 (mitofusin-1 (show MFN1 ELISA Kits)-like
targeted resequencing of 644 individuals with epileptic encephalopathies led to the identification of six SLC6A1 mutations in seven individuals, all of whom have epilepsy with myoclonic-atonic seizures (MAE).
3p25.3 microdeletion of GABA transporters SLC6A1 and SLC6A11 results in intellectual disability, epilepsy and stereotypic behavior.
Cysteine mutagenesis of GAT-1 pointed to conformationally sensitive proximity of extracellular loops 2 and 4 in this protein.
The aromatic and charge pairs of the thin extracellular gate of the GABA transporter GAT-1 are differently impacted by mutation.
a functional interaction of the external and internal gates of GAT-1 is essential for transport
TM10 of GAT-1 lines an accessibility pathway from the extracellular space into the binding pocket and plays a role in the opening and closing of the extracellular transporter gate.
GABA Transporter Mutagenesis Database (GATMD), a web-accessible, relational database of manually annotated biochemical, functional and pharmacological data reported on GAT1.
The SLC6A1 gene encodes a gamma-aminobutyric acid (GABA) transporter, which removes GABA from the synaptic cleft (Hirunsatit et al., 2009
gamma-aminobutyric acid (GABA-A) transporter 1
, sodium- and chloride-dependent GABA transporter 1
, solute carrier family 6 member 1
, GABA transporter GAT-1 homolog
, GABA transporter protein
, solute carrier family 6 (neurotransmitter transporter, GABA), member 1
, GABA transporter 1