Browse our anti-GLRA1 (GLRA1) Antibodies

Human Glycine Receptor, alpha 1 (GLRA1) interaction partners

1. Results support the notion that the efficacies of ligands for the alpha1 GlyR are determined by conformational changes that occur within and near the ligand-binding domain: disruption of the D97-R119 interaction may be an important element in receptor activation and that agonists may break this putative intersubunit bond in order to destabilize the initial shut state and facilitate transitions towards the open state.

2. The E103K startle mutation reduces the sensitivity of glycine receptor alpha 1 to both glycine and sarcosine and impairs channel gating.

3. gain-of-function GLRA1 mutations also cause hyperekplexia, although the mechanism is unknown. Here we identify two new gain-of-function mutations (I43F and W170S) and characterize these along with known gain-of-function mutations (Q226E, V280M, and R414H) to identify how they cause hyperekplexia.

4. GLRA1 and GLRB mutations are responsible for abnormal startled reactions in humans. (Review)

5. in two sisters with hyperekplexia a compound heterozygosis of 2 novel mutations of GLRA1 gene was found - heterozygous for a C-to-G base transition resulting in a phenylalanine to leucine amino acid change in position 235 and for a T-to-C base transition resulting in a cysteine to arginine amino acid change in position 237

6. the TM3-4 loop length is critical for glycine receptor alpha1 desensitization and a direct neighborhood of both basic stretches changes receptor properties from non-desensitizing to desensitizing.

7. Self-declared ethnicity can predict gene-screening outcomes. Cultural practices influence the inheritance patterns and a Caucasian founder is postulated for R271 mutations.

8. Mutations in the GLRA1 were identified in 16 Japanese patients with hyperekplexia.

9. Data indicate that alpha1Q-26'E-containing glycine receptors have longer active periods and lower conductances.

10. The first X-ray structure of the TMD of the alpha1GlyR solved here using GLIC as a scaffold paves the way for mechanistic investigation and design of allosteric modulators of a human receptor.

11. In GlyRA1 mutants, a portion of them can be transported to the plasma membrane but don't form funtional channels; a possible cause for hyperekplexia.

12. Comparison of glycine-mediated conformational changes in the extracellular M2-M3 domain finds significantly different structures between GlyR alpha3 and GlyR alpha1 isoforms.

13. Conformation and function of the human GLRA1 chloride channel.

14. Analysis of hyperekplexia mutations identifies transmembrane domain rearrangements that mediate glycine receptor activation.

15. p.E375X truncated subunits are incorporated into functional hGlyRs together with unmutated alpha1 or alpha1 plus beta subunits.

16. Normal-mode analysis shows that a glycine alpha-1 receptor suspended in a fully hydrated lipid bilayer continues to demonstrate an iris-like channel gating motion as a low-frequency, high-amplitude natural harmonic vibration consistent with channel gating.

17. Glycine receptor alpha1 subunit specific-autoantibody study aids identification of autoimmune brainstem/spinal cord hyperexcitability disorders and may extend to the glycinergic visual system.

18. Ethanol mediated potentiation of GlyR is in part by Gbetagamma activation.

19. TM3-4 loop subdomains are important for functional reconstitution of glycine receptors by independent domains

20. A 12-amino-acid segment incorporating the 271 residue on the glycine receptor alpha1271Q/L subunit was replaced by the homologous segment from the glycine receptor beta subunit (alpha1(Ch) 271Q/L). The function of the alpha1(Ch) 271Q/L glycine receptor was examined.

Zebrafish Glycine Receptor, alpha 1 (GLRA1) interaction partners

1. cryo-microscopy structures of the zebrafish alpha1 GlyR with strychnine, glycine, or glycine and ivermectin (glycine/ivermectin)

2. A new alphaZ1 subunit likely arising from the alphaZ1 gene by an alternative splice process is cloned and characterized; mRNA expression of embryonic and adult alphaZ1 and its spliced product, alphaZ1L, is restricted to the central nervous system.

Mouse (Murine) Glycine Receptor, alpha 1 (GLRA1) interaction partners

1. These findings suggest that spinal alpha1 GlyR is a potential target for cannabinoid analgesia in chronic inflammatory pain.

2. The results of this study suggested that the Glra1 activation can regulate receptor diffusion and cluster size at inhibitory synapses in mature stage, providing not only new insights into the postsynaptic mechanism of shifting inhibitory neurotransmission but also the inhibitory synaptic plasticity in mature nervous system

3. Glra1 receptor Beta8-Beta9 loop is an essential regulator of conformational rearrangements in ion channel opening and closing.

4. Absence of GlyRalpha1 input unmasked a serial and a direct feedforward GABAAergic modulation in PV5 RGCs, reflecting a complex interaction between glycinergic and GABAAergic inhibition.

5. Results suggest an important function of alpha1 GlyR on sedative effects of ethanol and confirms the role of KK385-386 residues in these effects

6. Meanwhile, neonatal incision significantly decreased the density of tonic GlyR-mediated current only in the presumed glutamatergic population during adulthood.

7. Histamine is an inverse agonist at strychnine sensitive glycine receptors.

8. Mutation of a zinc-binding residue in the glycine receptor alpha1 changes ethanol sensitivity in vitro and alcohol consumption in Glra1(D80A) knock-in mice.

9. TM3-4 loop subdomains are important for functional reconstitution of glycine receptors by independent domains

10. The distinct developmental regulation of GlyRalpha1 in the murine cochlea advocates a contribution of these chloride channels to efferent olivocochlear innervation.

11. Mutations in the GlyR alpha-1 subunit, M287L and Q266I, resulted in a small but general impairment of glycine action, that is most evident in the glycine-induced maximal currents.

12. Mutations in the GlyR alpha-1 subunit, M287L and Q266I, decreased specific behavioral actions of ethanol and altered other nonethanol behaviors, demonstrating the importance of GlyR function in diverse neuronal systems.

13. these data suggest most glycine receptors and glycinergic synapses in the superficial dorsal horn contain alpha1 subunits and few are composed exclusively of alpha3 subunits.

14. The values of breathing frequency, tidal volume, and minute ventilation in newborn Glra1-deficient oscillator mice decrease rapidly during postnatal development.

15. The new Glra1 mutation appears to affect glycine's inhibitory neurotransmission in the central nervous system (CNS) of the nmf11 homozygotes, which suffer from a severe startle disease-related phenotype and die by postnatal day 21.

16. Thus, the hyperekplexia phenotype of Glra1(D80A) mice is due to the loss of Zn(2+) potentiation of alpha1 subunit containing GlyRs, indicating that synaptic Zn(2+) is essential for proper in vivo functioning of glycinergic neurotransmission.

17. These results show that insulin has a novel regulatory action on the potency of glycine for ionotropic glycine receptors.

18. Our results suggest crosstalk between postsynaptic and presynaptic elements, leading to the developmental regulation of the presynaptic terminal neurotransmitter content according to the level of postsynaptic GlyR aggregation.