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transporter for glycine which is dependent on external Na+ and Cl- and may be involved in inhibitory glycinergic transmission [RGD, Feb 2006].. Additionally we are shipping Glycine Transporter 1 Antibodies (33) and Glycine Transporter 1 Kits (5) and many more products for this protein.
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Whole-exome sequencing revealed a novel homozygous missense variant in exon 9 of SLC6A9 NM_201649.3: c.1219 A>G (p.Ser407Gly) that segregates with the disease within the family. In murine model, knockout of Slc6a9 is associated with equivalent phenotype of non-ketotic hyperglycinemia (NKH (show AMT Proteins)), namely respiratory distress and hypotonia.
This study demonstrates that lack of GLYT1 le (show MGAT1 Proteins)ads to a distinct human neurological syndrome hallmarked by m (show CSF2 Proteins)ildly elevated cerebrospinal fluid glycine and normal serum glycine.
Study found that temporal lobe epilepsy is asso (show MGAT1 Proteins)ciated with increased levels of GlyT1
Human positron-emission tomography studies determine the test-retest reproducibility of [11C]GSK931145, a ligand which readily enters the brain, displaying a heterogeneous uptake which corresponds well with the known distribution of GlyT-1 (show MGAT1 Proteins).
metabolic functions of GLYT1 (show MGAT1 Proteins) in intestine: metabolism/regulation of glycine/glutathione; role in response to physiological stress (e.g., oxidative stress); possible role in pathophysiology/therapy of inflammatory bowel diseases [REVIEW]
Genetic variation of the glycine transporter 1 gene may contribute to individual vulnerability to methamphetamine dependence and psychosis.
SLC6A9 gene is associated with schizophrenia.
the results suggest that GLYT1 (show MGAT1 Proteins) and membrane rafts are co-localized in the membrane, and that this influences the rate of glycine transport.
association between SLC6A9 SNPs and essential hypertension in a Japanese population, suggesting that SLC6A9 is a susceptibility locus for essential hypertension.
the expression of inhibitory neurotransmitter transporters GlyT1, GAT-1, and GAT-3 in inferior colliculus and hippocampus astrocytes, was examined.
Whole-exome sequencing revealed a novel homozygous missense variant in exon 9 of SLC6A9 NM_201649.3: c.1219 A>G (p.Ser407Gly) that segregates with the disease within the family. In murine model, knockout of Slc6a9 is associated with equivalent phenotype of non-ketotic hyperglycinemia (NKH (show GCSH Proteins)), namely respiratory distress and hypotonia.
pharmacologic or genetic abolishment of GlyT1 activity in mice leads to mildly elevated glycine in the CSF (show CSF2 Proteins) but not in blood
Study demonstrated a biphasic response of GlyT1 expression during epileptogenesis with initial downregulation of GlyT1 after epileptogenesis-precipitating seizures followed by sustained pathological overexpression of GlyT1 in chronic epilepsy
Results suggest that the excessive GAT-1 and GlyT-1/2 heterotransporter-mediated Glu (show GCG Proteins) release, in the spinal cord of SOD1 (show SOD1 Proteins)(G93A) mice, is due to the heterotransporter over-expression at the nerve terminal membrane, promoted by the excessive Glu (show GCG Proteins) exocytosis
the possible involvement of calmodulin or calmodulin-like (show KRIT1 Proteins) interactions in the regulation of GlyT1 C-mediated transporter trafficking
Disruption of GlyT1 in forebrain neurons does not increase the risk of forming spurious and potentially maladaptive fear associations.
The demonstrated increased sensitivity to the effect of CS-US temporal discontiguity further highlights the importance of GlyT1-dependent mechanisms in the regulation of associative learning.
This study demonistrated that the GlyT1-/+ subjects quickly reached a plateau response to AMPH (show AMPH Proteins), which remained stable during drug withdrawal
These alterations in the activities and expression profiles of the GlyTs suggest that the contributions of GlyT1 and GlyT2 (show SLC6A5 Proteins) to the regulation of extracellular glycine concentrations at glycinergic synapses changes during development.
A missense mutation in the slc6a9 gene that encodes a glycine transporter (GlyT1) was identified as the cause of the sho (show SPRN Proteins) phenotype,attributable to elevated extracellular glycine within the CNS.
glycine tolerance and reduced glycine receptor (show GLRB Proteins) expression in GlyT1 mutants reflect compensatory mechanisms for functional recovery from excess nervous system inhibition
transporter for glycine which is dependent on external Na+ and Cl- and may be involved in inhibitory glycinergic transmission
, sodium- and chloride-dependent glycine transporter 1
, solute carrier family 6 member 9
, glycine transporter 1
, glycine transporter variant 1a
, Sodium- and chloride-dependent glycine transporter 1