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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].. De plus, nous expédions Glycine Transporter 1 Anticorps (33) et Glycine Transporter 1 Kits (5) et beaucoup plus de produits pour cette protéine.
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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 (Montrer AMT Protéines)), namely respiratory distress and hypotonia.
This study demonstrates that lack of GLYT1 le (Montrer MGAT1 Protéines)ads to a distinct human neurological syndrome hallmarked by m (Montrer CSF2 Protéines)ildly elevated cerebrospinal fluid glycine and normal serum glycine.
Study found that temporal lobe epilepsy is asso (Montrer MGAT1 Protéines)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 (Montrer MGAT1 Protéines).
metabolic functions of GLYT1 (Montrer MGAT1 Protéines) 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 (Montrer MGAT1 Protéines) 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.
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 (Montrer GCSH Protéines)), namely respiratory distress and hypotonia.
pharmacologic or genetic abolishment of GlyT1 activity in mice leads to mildly elevated glycine in the CSF (Montrer CSF2 Protéines) 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 (Montrer GCG Protéines) release, in the spinal cord of SOD1 (Montrer SOD1 Protéines)(G93A) mice, is due to the heterotransporter over-expression at the nerve terminal membrane, promoted by the excessive Glu (Montrer GCG Protéines) exocytosis
the possible involvement of calmodulin or calmodulin-like (Montrer KRIT1 Protéines) 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 (Montrer AMPH Protéines), 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 (Montrer SLC6A5 Protéines) to the regulation of extracellular glycine concentrations at glycinergic synapses changes during development.
This study demonistrated that forebrain neuronal glycine transporter 1 deficine not cause working memory disorders.
A missense mutation in the slc6a9 gene that encodes a glycine transporter (GlyT1) was identified as the cause of the sho (Montrer SPRN Protéines) phenotype,attributable to elevated extracellular glycine within the CNS.
glycine tolerance and reduced glycine receptor (Montrer GLRB Protéines) 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