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Study provides evidence that rs11146020, rs138961287, and rs117783907 in the promoter region of the GRIN1 gene are associated with schizophrenia in a northern Chinese Han population.
The results of this study expand the phenotypic spectrum associated with GRIN1 mutations and highlight the important role of N-methyl-d-aspartate receptor signalling in the pathogenesis of polymicrogyria.
This study provides evidence that GRIN1 IS candidate genes for Dravet and Dravet-like phenotypes.
Glycans potentiate the effect of GluN1 and GluN2B receptors.
In this study, we report a success of the WES approach to the identification of a genetic cause of a challenging case, undiagnosed on clinical grounds. We identified the causative missense mutation (p.Met727Val) in exon 16 of the GRIN1 gene. As the p.Met727Val mutation shown by WES is in the same GluN1 domain, we infer that the pathogenic variant impact on NMDAR is likely similar to that induced by p.Glu662Lys mutation.
one base difference in the GRIN1M promoter sequence (G --> C) results in the inability of the sequence to form a parallel G-quadruplex.
Data suggest GRINL1A (GCOM1)-NMDA receptor-internexin-alpha (INA) 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 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 receptors.
tPA 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.
The differences in cortical NMDAR expression and post-synaptic density protein 95 are present in psychiatric disorders and suicide completion and may contribute to different responses to ketamine.
GRIN1 (rs4880213) was significantly associated with depression and disruptive behavior in adolescents.
Knockdown of PKD1 did not affect NMDAR internalization but prevented the phosphorylation and inhibition of remaining surface NMDARs and NMDAR-mediated synaptic functions.
Study found GluN receptor subunit-specific changes in mixed subcortical ischemic vascular dementia(SIVD)/Alzheimer's disease(AD) (decreased GluN1) and SIVD (increased GluN2A and 2B), likely reflecting interaction of ischemic neurovascular and AD processes
Xray crystal structure and mechanism of NMDA receptor channel block by MK-801 and memantine
An NMDA receptor-dependent mechanism for subcellular segregation of sensory inputs in the tadpole optic tectum has been reported.
analysis of conformational changes at the agonist binding domain of the N-methyl-D-aspartic acid receptor
Establishment of late-phase long-term potentiation (L-LTP) in vivo requires NMDAR activation in the postsynaptic tectal cells within a critical time window after LTP induction.
PIP2 supports the open state of NMDA receptors via the adaptor protein alpha-actinin. PIP2 and alpha-actinin act like a two-component hinge keeping the channel gate in its open state.
Attenuation of thalamic inputs through knockdown of NMDA receptors (NMDARs) in 5HT3aR and reelin interneurons results in expansion of whisker responses, aberrant barrel map formation, and deficits in whisker-dependent behavior.
Triheteromeric GluN1/GluN2A/GluN2C receptors are co-expressed and are the predominant NMDARs in cerebellar granule cells.
Toxoplasma gondii infection induces elevation of NMDAR Autoantibodies and behavioral changes.
WAVE-1 restoration improves maze exploration performance of GluN1 knockdown mice
Pyramidal cell-selective GluN1 knockout leads to inappropriate attribution of salience for irrelevant stimuli as characterized by abnormalities in both behavior and brain circuitry functions in a mouse model of schizophrenia.
Genetic deletion of the GluN1 subunit, which is required for assembly of functional NMDARs, leads to a strong reduction of GABAergic synaptic transmission.
Increased PKC activity and altered GSK3B/NMDAR function drive behavior cycling in HINT1-deficient mice.
Data show that NMDA receptor Grin1(Rgsc174/+) heterozygous missense mutation mice retained increased basal activity and exploring behaviour under a group-housed environment.
Data (including data from in vitro studies using tissues from transgenic mice) suggest that vitamin D3 suppresses NMDA-receptor- (Grin1)-mediated and kainate-receptor- (Grik1)-mediated excitation of GnRH- (gonadotrophin-releasing hormone)-secreting neurons of pre-optic area of hypothalamus. These studies were conducted with brain slices from male and female mice in pre-pubertal period.
mGluR5 was significantly more mobile at synapses in hippocampal Fmr1 KO neurons, causing an increased synaptic surface co-clustering of mGluR5 and NMDAR.
We demonstrate that neocortical neurons that have only one copy of Sip1 (heterozygous, Sip1(fI/wt)), are more sensitive to both NMDA- and AMPA- receptors agonists as compared to wild type neurons (Sip1(wt/wt)).
Study shows that social isolation to a series of schizophrenia-related deficits and that potential interactions among histidine triad nucleotide binding protein 1, NMDA receptor 1, and dopamine receptor 2 may underlie the behavioral deficits induced by social isolation.
Loss of NMDA receptors caused irregularity in activity of noradrenergic neurons, affected exploratory behavior, attention and impulsivity.
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, GluN2B and GluN1 but not the levels of synaptophysin 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 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 phosphorylation.
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.
N-methyl-D-aspartate receptor channel, subunit zeta-1
, N-methyl-D-aspartate receptor subunit NR1
, glutamate [NMDA] receptor subunit zeta 1
, glutamate [NMDA] receptor subunit zeta-1
, glutamate receptor ionotropic, NMDA 1
, N-methyl-D-aspartate receptor
, NMDA glutamate receptor
, glutamate receptor, ionotropic, N-methyl D-aspartate 1
, N-methyl-D-aspartate glutamate receptor
, NMDA R1 receptor C1 cassette
, neurotransmitter receptor
, NMDA-type glutamate receptor 1
, NMDA-type glutamate receptor subunit 1
, N-methyl-D-aspartate receptor 1
, Glutamate [NMDA] receptor subunit zeta-1
, glutamate receptor subunit zeta 1
, N-methyl-D-aspartate receptor type 1
, NMDA receptor glycine-binding subunit NR1.1
, glutamate receptor, ionotropic, N-methyl D-aspartate 1a
, round spermatid basic protein 1