anti-Glycine Transporter 1 (GLYT1) Antibodies

Human Glycine Transporter 1 (GLYT1) interaction partners

1. 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), namely respiratory distress and hypotonia.

2. This study demonstrates that lack of GLYT1 leads to a distinct human neurological syndrome hallmarked by mildly elevated cerebrospinal fluid glycine and normal serum glycine.

3. Study found that temporal lobe epilepsy is associated with increased levels of GlyT1

4. Following biopterin administration, glycine transporter type I occupancy correlates with biopterin plasma concentration.

5. The increased sensitivity of human GlyT1c to sanguinarine is abolished by the mutation of only cysteine 475.

6. 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.

7. Synaptic and extrasynaptic concentrations of glycine are regulated by its type-1 glycine transporter, which is primarily expressed in astroglial and glutamatergic cell membranes.

8. metabolic functions of GLYT1 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]

9. The mechanism of allosteric interaction of cytoplasmic and extracellular Cl- in the glial glycine transporter (hGlyTlb).

10. Genetic variation of the glycine transporter 1 gene may contribute to individual vulnerability to methamphetamine dependence and psychosis.

11. Single nucleotide polymorphism or haplotype of the gene produce risks for susceptibility to drug dependence.

12. SLC6A9 gene is associated with schizophrenia.

13. the results suggest that GLYT1 and membrane rafts are co-localized in the membrane, and that this influences the rate of glycine transport.

14. association between SLC6A9 SNPs and essential hypertension in a Japanese population, suggesting that SLC6A9 is a susceptibility locus for essential hypertension.

Mouse (Murine) Glycine Transporter 1 (GLYT1) interaction partners

1. GlyT1 and not GlyT2 is essential for the replenishment of the presynaptic glycine pool in retinal AII amacrine cells and is a major determinant of the glycinergic phenotype of this cell population.

2. the expression of inhibitory neurotransmitter transporters GlyT1, GAT-1, and GAT-3 in inferior colliculus and hippocampus astrocytes, was examined.

3. 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), namely respiratory distress and hypotonia.

4. pharmacologic or genetic abolishment of GlyT1 activity in mice leads to mildly elevated glycine in the CSF but not in blood

5. 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

6. Results suggest that the excessive GAT-1 and GlyT-1/2 heterotransporter-mediated Glu release, in the spinal cord of SOD1(G93A) mice, is due to the heterotransporter over-expression at the nerve terminal membrane, promoted by the excessive Glu exocytosis

7. the possible involvement of calmodulin or calmodulin-like interactions in the regulation of GlyT1 C-mediated transporter trafficking

8. Disruption of GlyT1 in forebrain neurons does not increase the risk of forming spurious and potentially maladaptive fear associations.

9. 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.

10. This study demonistrated that the GlyT1-/+ subjects quickly reached a plateau response to AMPH, which remained stable during drug withdrawal

11. These alterations in the activities and expression profiles of the GlyTs suggest that the contributions of GlyT1 and GlyT2 to the regulation of extracellular glycine concentrations at glycinergic synapses changes during development.

12. This study demonistrated that forebrain neuronal glycine transporter 1 deficine not cause working memory disorders.

13. HMGN3a/b binding leads to increased H3K14 (Lys(14) of histone H3) acetylation and stimulates Glyt1a expression

14. These results demonstrate in mice that depending on the regional and/or cell-type specificity, deletion of the GlyT1 gene could yield divergent effects on prepulse inhibition.

15. mice with Glyt1 disruption in forebrain demonstrated enhanced adversive Pavlovian conditioning, which was modified with age. Also increase in the number of immature neurons in the hippocampus of the mutants

16. This study demonistrated that Adenoviral-mediated Cre expression effectively suppresses GlyT1 binding in the thalamic area of GlyT1 conditional knock-out mice.

17. We show that immunoreactivity against the last 12 amino acids of GlyT1C-terminal region exhibits robust calcium dependent decline

18. glial GlyT1 is critical for the regulation of glycine levels at inhibitory synapses only during early postnatal life

19. study examined the role of GlyT1, the high-affinity glycine transporter, in the retina with an emphasis on the role of glycine as a coagonist of N-methyl-D-aspartic acid (NMDA) receptor

20. GLYT1, a glycine transporter of the neurotransmitter transporter gene family, functions as the organic osmolyte transporter that mediates the osmotically regulated accumulation of glycine and regulates cell volume in early embryos.

Zebrafish Glycine Transporter 1 (GLYT1) interaction partners

1. A missense mutation in the slc6a9 gene that encodes a glycine transporter (GlyT1) was identified as the cause of the sho phenotype,attributable to elevated extracellular glycine within the CNS.

2. glycine tolerance and reduced glycine receptor expression in GlyT1 mutants reflect compensatory mechanisms for functional recovery from excess nervous system inhibition