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SLC6A5 encodes a sodium- and chloride-dependent glycine neurotransmitter transporter. Additionally we are shipping SLC6A5 Antibodies (17) and SLC6A5 Proteins (7) and many more products for this protein.
that the deletion of VIAAT (show SLC32A1 ELISA Kits) in GlyT2-Cre expressing neurons also strongly affects GABAergic transmission
Results suggest that the excessive GAT-1 (show SLC6A1 ELISA Kits) 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
Report that in the presence of a GlyT2 mechanism-based toxicity, reversible inhibitors might allow a tolerable balance between efficacy and toxicity.
These alterations in the activities and expression profiles of the GlyTs suggest that the contributions of GlyT1 (show GLYT1 ELISA Kits) and GlyT2 to the regulation of extracellular glycine concentrations at glycinergic synapses changes during development.
Data show that the GlyT2 protein is undetectable in homozygous mutants, indicating a null allele.
In the first postnatal week, loss of the glycine transporter 2 is neither compensated by glycine de-novo synthesis nor by up-regulation of the GABAergic transmission in GlyT2(-/-) mice.
These data indicate that the C-terminal PDZ (show INADL ELISA Kits)-ligand motif of GlyT2 plays an important role in transporter trafficking to and/or stabilization at synaptic sites.
Glyt2-mediated release of glycine from axon terminals involves exocytosis triggered by intraterminal mitochondrial Ca2 (show CA2 ELISA Kits)+ ions.
our results demonstrate the central role played by GlyT2 in determining inhibitory phenotype and therefore in the physiology and pathology of inhibitory circuits.
analysis of the human SLC6A5 (show SLC6A2 ELISA Kits) gene mutation associated with hyperekplexia
Constitutive endocytosis and turnover of the neuronal glycine transporter GlyT2 is dependent on ubiquitination of a C-terminal lysine cluster.
A novel dominant hyperekplexia mutation Y705C alters trafficking and biochemical properties of the presynaptic glycine transporter GlyT2.
This study firmly establishes the combination of missense, nonsense, frameshift, and splice site mutations in the GlyT2 gene as the second major cause of startle disease.
A transgenic cell line is studied in which green fluorescent protein (GFP) is expressed under the control of the promoter for the glycine transporter GlyT2 during zebrafish development.
Inspiratory-modulated neurons with pacemaker properties are present in the preBotzinger complex of newborn transgenic mice and express the glycine tranporter (GlyT)2 protein.
SLC6A5 (show SLC6A2 ELISA Kits) mutations result in defective subcellular GlyT2 localization, decreased glycine uptake or both, with selected mutations affecting predicted glycine and Na+ binding sites.
results are consistent with GLYT2 being a disease gene in human hyperekplexia
SLC6A5 (show SLC6A2 ELISA Kits) gene is associated with schizophrenia.
This gene encodes a sodium- and chloride-dependent glycine neurotransmitter transporter. This integral membrane glycoprotein is responsible for the clearance of extracellular glycine during glycine-mediated neurotransmission. This protein is found in glycinergic axons and maintains a high presynaptic pool of neurotransmitter at glycinergic synapses. Mutations in this gene cause hyperekplexia\; a heterogenous neurological disorder characterized by exaggerated startle responses and neonatal apnea.
solute carrier family 6 (neurotransmitter transporter, glycine), member 5
, sodium- and chloride-dependent glycine transporter 2-like
, glycine transporter 2
, sodium- and chloride-dependent glycine transporter 2
, solute carrier family 6 member 5