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This study demonstrated that a significant decrease in the protein level of GluA1 in major depression disorder.
The findings do not support the association of GRIA1 SNPs with schizophrenia in the Chinese Han population.
Our data of this study confirmed the association of GRIA1 (rs2195450) to female migraine susceptibility in the Chinese Han population.
Polymorphisms in GRIA1 gene are a risk factor for asparaginase hypersensitivity during the treatment of childhood acute lymphoblastic leukemia
The level of phosphorylated GluA1 at S831 and S845, two major sites implicated in AMPAR regulation, is almost negligible. Results impel us to reconsider the mechanisms underlying synaptic plasticity.
This study failed to replicate previously reported association between GRIA1 rs548294 and migraine without aura (show AURKA Proteins), either as single marker or when analyzed in haplotype combination with rs2195450.
the levels were comparable for complexes containing GluR2 (show GRIA2 Proteins), GluR3 (show GRIA3 Proteins) and GluR4 (show GRIA4 Proteins) as well as 5-HT1A (show HTR1A Proteins). Moreover, the levels of complexes containing muscarinic AChR M1, NR1 (show GRIN1 Proteins) and GluR1 were significantly increased in male patients with AD.
The N-terminal domain modulates alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA (show GRIA3 Proteins)) receptor desensitization.
insight into the structure and function of the C-terminal domain of GluA1, which controls AMPA (show GRIA3 Proteins) receptor function and trafficking during synaptic plasticity in the central nervous system.
Inhibition of CREB (show CREB1 Proteins) function is associated with a specific reduction of AMPA (show GRIA3 Proteins) receptor subunit GluA1.
Presynaptic (CA3 (show CA3 Proteins) pyramidal cell), but not postsynaptic (CA1 (show CA1 Proteins) pyramidal cell), deletion of N-methyl-d-aspartate (NMDA)-type glutamate (show GRIN1 Proteins) receptors eliminated the ketamine-induced enhancement of excitatory synaptic transmission in hippocampal slices and the antidepressant actions of ketamine
In the present study, by combining a 64-channel multielectrode system and a novel analysis and visualization method, we observed the accurate spatial localization and dynamic temporal changes of network fEPSP signals and LTP responses within the ACC circuit and found that PKA phosphorylation, but not PKC phosphorylation, of the GluA1 is required for LTP in the ACC.
Data suggest that phosphorylation of Shp2/Ptpn11 (show PTPN11 Proteins) at Tyr542 and its translocation to postsynaptic compartment are integral processes in synaptic scaling/homeostasis; Shp2 (show PTPN11 Proteins) phosphatase activity is critical to regulation of Ser (show SIGLEC1 Proteins)(P)845 GluA1 and surface expression of GluA1 during synaptic scaling. (Shp2/Ptpn11 (show PTPN11 Proteins) = protein tyrosine phosphatase non-receptor type 11 (show PTPN11 Proteins); GluA1 = glutamate receptor ionotropic Ampa1 [alpha 1])
Gria1 expression in Purkinje cells is not required for cerebellar motor learning.
Three epilepsy-associated missense mutations reduce neural precursor cell expressed developmentally down-regulated gene 4 (show NEDD4 Proteins)-2 (Nedd4-2 (show NEDD4L Proteins))-mediated AMPA (show GRIA3 Proteins) receptor GluA1 ubiquitination.
Chronic stress-elicited depressive behavior may be due to hypertrophy of basolateral amygdala (BLA (show LACTB Proteins)) neuronal dendrites and increased of Glur1-Glur2 (show GRIA2 Proteins) ratio in BLA (show LACTB Proteins) neurons.
Study demonstrated that naltrexone-induced plasticity in excitatory synapses, via the transitory increase of GluA1 insertion at the postsynaptic density and GluA1-S845 phosphorylation, facilitates learning
Although dephosphorylation of Serine 845 is thought to have a key role in long term depression (LTD), results indicate that few GluA1 subunits in hippocampal neurons are phosphorylated at this site. In contrast, approximately 50% of GluA1 subunits are phosphorylated at threonine 840, suggesting that dephosphorylation of this site can contribute to the down-regulation of AMPAR-mediated synaptic transmission in LTD.
Information load regulates AMPA (show GRIA3 Proteins)-R phosphorylation within the hippocampus, and an overload condition associated with impaired memory is paralleled by a lack of AMPA (show GRIA3 Proteins)-R phosphorylation.
The findings of this study suggested that phosphorylation of GluA1 at S831 plays an important role in the development of hypersensitivity after SCL (show TAL1 Proteins).
the intracellularly located CTD of GLUR1 is the origin of TARP-specific functional modulation and not merely a facilitator of trafficking
We also assessed ionotropic glutamate (show GRIN2A Proteins) receptor GLR-1 cell-specifically within AIB and determined that GLR-1 fine-tunes AIB activity to modify locomotion following reversal events. Our research highlights that signal integration underlying the initiation and fine-tuning of backwards locomotion is AIB and NPR (show NPTXR Proteins)-9 dependent, and has demonstrated the suitability of C. elegans for analysis of multisensory integration
We propose a model in which synaptic activity regulates the nuclear localization of CMK-1 to mediate a negative feedback mechanism coupling GLR-1 activity with its own transcription.
Mutants lacking p38 MAPK (show MAPK14 Proteins) components pmk (show PMVK Proteins)-1 or sek-1 (show MAP2K4 Proteins) resemble mutants lacking the hypoxia response component and prolyl hydroxylase egl-9, with impaired subcellular localization of Mint orthologue LIN-10, internalization of glutamate (show GRIN2A Proteins) receptor GLR-1, and depression of GLR-1-mediated behaviors.
KEL-8 is a substrate receptor for Cullin 3 ubiquitin ligases that is required for the proteolysis of GLR-1 receptors and suggest a novel postmitotic role in neurons for Kelch/CUL3 ubiquitin ligases.
WDR-20 and WDR-48 form a complex with USP-46 and stimulate the DUB to deubiquitinate and stabilize GLR-1 in vivo.
glr-1 is required for long-term memory for habituation and memory for context conditioning.
Study indicates kinesin KLP-4 as a novel regulator of anterograde GLR-1 glutamate (show GRIN2A Proteins) receptors trafficking and reveals a cellular control mechanism by which receptor cargo is targeted for degradation in tje absence of its motor.
An auxiliary protein SOL-2, a CUB-domain protein, associates with both the related auxiliary subunit SOL-1 and with the GLR-1 AMPA (show GRIA3 Proteins) receptor.
UEV-1 could regulate a small subset of K63-linked ubiquitination events in nematodes, at least one of which is critical in regulating GLR-1 trafficking
Long-term memory in C. elegans is dependent on glr-1 and likely involves changes in the expression or localization of glutamate (show GRIN2A Proteins) receptors
Glutamate receptors are the predominant excitatory neurotransmitter receptors in the mammalian brain and are activated in a variety of normal neurophysiologic processes. These receptors are heteromeric protein complexes with multiple subunits, each possessing transmembrane regions, and all arranged to form a ligand-gated ion channel. The classification of glutamate receptors is based on their activation by different pharmacologic agonists. This gene belongs to a family of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
, AMPA-selective glutamate receptor 1
, glutamate receptor 1
, glutamate receptor A
, glutamate receptor subunit GluR1
, glutamate receptor, ionotropic, AMPA1 (alpha 1)
, glutamate receptor ionotropic, AMPA 1
, AMPA glutamate receptor
, glutamate receptor, ionotropic, AMPA 1
, GluR1 protein