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Data suggest GRINL1A (GCOM1 (show GRINL1A Proteins))-NMDA receptor-internexin-alpha (INA (show INA Proteins)) interaction pathway may be relevant to neuroprotection.
These results indicate these individuals may have suffered neurodevelopmental deficits as a result of the decreased presence of GluN1-G620R/GluN2B (show GRIN2B Proteins) complexes on the neuronal surface during embryonic brain development and reduced current responses of GluN1-G620R-containing NMDARs after birth.
Mice with GRIN1 disrupted in the intralaminar thalamic nuclei exhibited various schizophrenia-like phenotypes, including deficits in working memory, long-term spatial memory, and attention, as well as impulsivity, impaired prepulse inhibition, hyperlocomotion and hyperarousal.
2-methoxyestradiol impacts on glycine/serine-mediated metabolic reprogramming in osteosarcoma cells by its interaction with GRIN1/GluN2A (show GRIN2A Proteins) receptors.
tPA (show PLAT Proteins) is a ligand of the N-terminal domain of the obligatory GluN1 subunit of NMDAR acting as a modulator of their dynamic distribution at the neuronal surface and subsequent signaling.
Two novel Grin1 mutations were identified in 2 cases of severe early infantile encephalopathy. Se688Tyr mutation results in disruption of NMDA ligand binding and the p.Gly827Arg mutation results in disrupted gating of the ion channel.
A homozygous missense variant of GRIN1 was identified in two consanguineous sibs affected with severe intellectual disability and autistic features.
NMDA receptor-dependent signaling is involved in melanosome transfer, which is associated with calcium influx, cytoskeleton protein redistribution, dendrites and filopodia formation
Findings show that N-methyl-d-aspartic acid receptor subunit GluN1 is expressed on oligodendrocytes and myelin in humans.
De novo GRIN1 mutations are associated with severe intellectual disability with cortical visual impairment as well as oculomotor and movement disorders being discriminating phenotypic features. Loss of NMDA receptor function appears to be the underlying disease mechanism. The identification of both heterozygous and homozygous mutations blurs the borders of dominant and recessive inheritance of GRIN1-associated disorders.
Establishment of late-phase long-term potentiation (L-LTP (show SCP2 Proteins)) in vivo requires NMDAR activation in the postsynaptic tectal cells within a critical time window after LTP (show SCP2 Proteins) induction.
PIP2 supports the open state of NMDA receptors via the adaptor protein alpha-actinin (show ACTN1 Proteins). PIP2 and alpha-actinin (show ACTN1 Proteins) act like a two-component hinge keeping the channel gate in its open state.
Study shows that social isolation to a series of schizophrenia-related deficits and that potential interactions among histidine triad nucleotide binding protein 1 (show HINT1 Proteins), NMDA receptor 1, and dopamine receptor 2 (show DRD2 Proteins) may underlie the behavioral deficits induced by social isolation.
We found that the inducible deletion of the NMDA receptors prior to behavioral assays impaired, not only object and social recognition memory tests, but also resulted in profound deficits in social motivation. Mice with ablated NR1 subunits in the forebrain demonstrated significant decreases in sociability compared to their wild type counterparts.
Isoflurane relieves zymosan-induced neutrophil inflammatory lung response by targeting NMDA glutamate receptor and Toll-like receptor 2 signaling pathway.
Sepsis selectively decreased the protein and mRNA levels of GluN2A (show GRIN2A Proteins), GluN2B (show GRIN2B Proteins) and GluN1 but not the levels of synaptophysin (show SYP Proteins) or the neuronal number in the hippocampus of septic mice.
The present study provides additional support for roles for GRIN1 in the etiology of depression following early adversity.
NMDARs are critical for developmental programs involved in appropriate expression of short-term plasticity, AMPA (show GRIA3 Proteins) receptor (AMPAR) function and dendrite patterning.
Study showed that NR1(D1CreERT2) mice lack the ability to associate contextual cues with the rewarding effects of drugs of abuse, with minor or no deficits in other reward-conditioned behaviors or learning in general.
tau overexpression mediates the excitatory toxicity induced by E-NMDAR activation through inhibiting ERK (show EPHB2 Proteins) phosphorylation.
GluN1 deletions in D1- and A2A-expressing cell types reveal distinct modes of behavioral regulation. The data supports the hypothesis that cell type-specific NMDAR signaling regulates separable behavioral outcomes related to locomotion, despair, and relapse.
In diabetic mice, knockdown of NR1 using lentivirus carrying NR1-shRNA ameliorated the pathological features associated with diabetic kidney disease. NR1 knockdown decreased the cell shape remodelling, cell collapse, bovine serum albumin (show ALB Proteins) permeability, and migration induced by high glucose.
The protein encoded by this gene is a critical subunit of N-methyl-D-aspartate receptors, members of the glutamate receptor channel superfamily which are heteromeric protein complexes with multiple subunits arranged to form a ligand-gated ion channel. These subunits play a key role in the plasticity of synapses, which is believed to underlie memory and learning. Cell-specific factors are thought to control expression of different isoforms, possibly contributing to the functional diversity of the subunits. Alternatively spliced transcript variants have been described.
glutamate receptor, ionotropic, N-methyl D-aspartate 1
, NMDA-type glutamate receptor 1
, NMDA-type glutamate receptor subunit 1
, N-methyl-D-aspartate receptor 1
, glutamate [NMDA] receptor subunit zeta-1
, N-methyl-D-aspartate receptor channel, subunit zeta-1
, N-methyl-D-aspartate receptor subunit NR1
, glutamate [NMDA] receptor subunit zeta 1
, glutamate receptor ionotropic, NMDA 1
, N-methyl-D-aspartate glutamate receptor
, NMDA R1 receptor C1 cassette
, neurotransmitter receptor
, Glutamate [NMDA] receptor subunit zeta-1
, glutamate receptor subunit zeta 1
, N-methyl-D-aspartate receptor
, NMDA glutamate receptor
, N-methyl-D-aspartate receptor type 1
, NADPH-dependent diflavin oxidoreductase 1