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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.
The differences in cortical NMDAR expression and post-synaptic density protein 95 (show DLG4 Proteins) 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.
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.
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.
In a model of depressive disorder, the oxidation of NR1 by NOX1 (show NOX1 Proteins)-derived reactive oxygen species was demonstrated in prefrontal cortex.
the present study demonstrates that nNOS-derived NO signaling modulated by spinal Sig-1R activation increases Nox2 activity and concomitant ROS production, which leads to a ROS-induced increase in PKC-dependent pGluN1 expression in the spinal cord dorsal horn and the development of pain hypersensitivity
NMDAR1 plays a pivotal role in hemin-induced NLRP3 (show NLRP3 Proteins)-mediated inflammatory damage through synergistic activation.
Nbea targets glutamate and GABA receptors to the synapse via distinct molecular pathways by interacting with specific effector proteins.
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