No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
The phenotypic spectrum in grin2a mutations ranged from normal or near-normal development with mild epilepsy and speech delay/apraxia to severe developmental and epileptic encephalopathy, often within the epilepsy-aphasia spectrum.
The findings of this study do not support the hypothesis of an interaction between the GRIN2A-rs4998386 polymorphism and caffeine intake in determining Parkinson disease risk.
The results of this study provide preliminary evidence relevant to genetic continuity between schizophrenia and schizotypy for effects of the NMDA receptor gene GRIN2A.
Three single nucleotide polymorphisms (SNPs) (rs1448258, rs194355, and rs168866) of GRIN2A were genotyped. The distribution of GRIN2A polymorphisms of our participants are shown as follows: rs1448258 CC 516:943, CT 38:75; rs194355 AA 209:381, AG 258:470, GG 78:163; and rs168866 CC 9:17, CT 117:252, TT 425:756. There were no significant discrepancies between cases and controls.
GRIN2A rare deleterious and loss of function variants are specifically associated with typical and atypical Rolandic epilepsy.
GRIN2A mutation is associated with epilepsy-aphasia spectrum disorders but with a relatively low rate.
Lifetime mood disorder emerged as a more significant factor for suicidal ideation in systemic lupus erythematosus compared with NR2A gene polymorphism main and interaction effects.
The results of this study GRIN2A mutation is a genetic cause in less than 11% patients with Landau-Kleffner syndrome or atypical benign partial epilepsy.
Mutations P79R, C231Y, G483R and M705V caused a significant reduction in glutamate and glycine agonist potency, whilst D731N was non-responsive. These mutants, along with E714K, also showed significantly decreased total protein levels and trafficking to the cell surface, whilst C436R was not trafficked at all.
This review showed that GRIN2A associate with Obsessive-compulsive disorder.
This study demonstrates that GRIN2A mutations in melanoma cause heterogenous effects but some may be oncogenic.
data indicate that children with epilepsy due to pathogenic GRIN2A mutations present with different clinical phenotypes and a spectrum of seizure types in the context of a pharmacoresistant epilepsy.
2-methoxyestradiol impacts on glycine/serine-mediated metabolic reprogramming in osteosarcoma cells by its interaction with GRIN1/GluN2A receptors.
a de novo missense mutation in the GRIN2A gene in a patient with childhood focal epilepsy and acquired epileptic aphasia. The mutant decreases NMDAR activation suggesting NMDAR hypofunction may contribute to the epilepsy pathogenesis.
genetic association studies in population in China: Data suggest that one SNP in GRIN2A (rs2650429; but not rs6497540 or rs9302415) is associated with lead-induced neurotoxicity; in this case-control study, cases were lead-exposed workers from battery plants. Lead-exposed individuals have lower serum GRIN2A levels compared with controls; lead decreases GRIN2A expression levels in HEK293 cell.
Two adjacent phenylalanines in the NMDA receptor GluN2A subunit M3 domain interactively regulate alcohol sensitivity and ion channel gating.
The GRIN2A genotype was not associated with the rate of clinical progression of PD in the placebo group.
most rare variants in GluN2A were associated with epilepsy, whereas GluN2B variants were associated with intellectual disability with or without seizures
the gain-of-function M817V mutation causes overactivation of NMDAR and drives neuronal hyperexcitability.
To determine genetic variability within the N-methyl-D-aspartate receptor 2A sub-unit (GRIN2A) gene promoter and its association with concussion recovery time.
GluN2A- and GluN2B-NMDAR nanoscale organizations are differentially regulated and seem to involve distinct signaling complexes during synaptic adaptation.
Triheteromeric GluN1/GluN2A/GluN2C receptors are co-expressed in cerebellar granule cells and are the predominant NMADRs.
UV exposure to the skin decreased doublecortin-positive immature neurons and synaptic proteins, including N-methyl-D-aspartate receptor 2 A and postsynaptic density protein-95, in the hippocampus. Moreover, we observed that UV irradiation to the skin down-regulated brain-derived neurotrophic factor expression and ERK signaling in the hippocampus, which are known to modulate neurogenesis and synaptic plasticity.
Results suggest that spatial learning is more sensitive to the amino acid composition of GluN2A and GluN2B amino-terminal domains/transmembrane domains and long-term memory is more strongly influenced by intracellular signaling sequences in the GluN2 carboxy-terminal domains.
Immune challenge in GluN2A knockout mice resulted in unchanged PSA-NCAM levels and proBDNF increase in both brain structures as well as in increase in BDNF levels in hippocampus. Absence of GluN2A resulted in increased levels of all NCAM isoforms in prefrontal cortex upon lipopolysaccharide which was followed with a decrease in GluN1 and GluN2B subunits. GluN2 A subunit is critical in neuroinflammation-related depression.
The microstructural alterations were detected in the neocortex, the corpus callosum, the hippocampus, and the thalamus of Grin2a KO mice.
Src is implicated in hepatic ischemia reperfusion-induced hippocampus injury and long-term cognitive impairment in young mice via NMDA receptor subunit 2A activation.
Differences in N-methyl D-aspartate receptor subtype 2A (GluN2A ) do not underlie the selective potentiation by positive allosteric modulator, GNE-8324. Rather, a higher ambient glutamate level in the synaptic cleft of excitatory synapses on inhibitory neurons is a key factor that selectively enhances N-methyl-D-aspartate receptor (NMDAR)-mediated synaptic responses in inhibitory but not excitatory neurons.
GluN2A knockout mice did not exhibit increases in ethanol drinking or alterations in Ro 25-6981 mediated alteration of decay kinetics of NMDAR-mediated synaptic transmission following chronic intermittent ethanol vapor exposure.
The nucleus-accumbens-specific knockdown of RGS4 significantly increased the behaviors associated with morphine and did so by phosphorylation of the GluR1 (Ser831) and NR2A (Tyr1325) glutamate receptors in the NAc.
Study indicates that a lack of GluN2A-containing NMDARs alters the fine control of redox status, leading to a delayed maturation of perineuronal nets, and conferring vulnerability for long-term oxidative stress, microglial activation, and parvalbumin interneurons network dysfunction.
this study reveals an unexpected role of glycine in eliciting a non-ionotropic activity of GluN2ARs to confer neuroprotection via Akt activation.
Results show the coupling of GluN subunit 2A with interacting proteins, particularly postsynaptic density-95 (PSD95) is modulated by CIN.
activity-based anorexia resilience, quantified as suppression of hyperactivity, correlated strongly with reserve pools of NR2A-NMDA receptors in spine cytoplasm
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.
Drebrin A can be found co-clustering with NR2B-containing NMDARs at the plasma membrane, while NR2A-containing NMDARs co-traffic into the spine cytoplasm but do not co-cluster at the plasma membrane.
This study demonstrated that Increasing the GluN2A/GluN2B Ratio in Neurons of the Mouse Basal and Lateral Amygdala Inhibits the Modification of an Existing Fear Memory Trace.
Grin2aPKC mice exhibit reduced anxiety in the open field test, light dark emergence test, and elevated plus maze. Overall, these results suggest that at least one of those PKC-mediated phosphorylation sites regulates NMDAR-mediated signaling that modulates anxiety.
These data suggest that chronic early postnatal SSS influences spatial learning and memory ability, levels of hippocampal NR2B, and NR2A/NR2B ratios in adult males.
Rph3A interacts with GluN2A and PSD-95 forming a complex that regulates NMDARs stabilization at postsynaptic membranes.
N-methyl-D-aspartate (NMDA) receptors are a class of ionotropic glutamate-gated ion channels. These receptors have been shown to be involved in long-term potentiation, an activity-dependent increase in the efficiency of synaptic transmission thought to underlie certain kinds of memory and learning. NMDA receptor channels are heteromers composed of the key receptor subunit NMDAR1 (GRIN1) and 1 or more of the 4 NMDAR2 subunits: NMDAR2A (GRIN2A), NMDAR2B (GRIN2B), NMDAR2C (GRIN2C) and NMDAR2D (GRIN2D). Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
N-methyl-D-aspartate receptor subunit NR2A
, glutamate receptor, ionotropic, N-methyl D-aspartate 2A
, glutamate [NMDA] receptor subunit epsilon-1-like
, N-methyl D-aspartate receptor subtype 2A
, N-methyl-D-aspartate receptor channel, subunit epsilon-1
, N-methyl-D-aspartate receptor subunit 2A
, NMDA receptor subtype 2A
, glutamate [NMDA] receptor subunit epsilon-1
, glutamate receptor ionotropic, NMDA 2A
, glutamate [NMDA] receptor subunit epsilon 1
, glutamate receptor, ionotropic, N-methyl-D-aspartate subunit 2A