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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 (zeige GRIN1 ELISA Kits)/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 (zeige GRIN1 ELISA Kits) activation suggesting NMDAR (zeige GRIN1 ELISA Kits) 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 (zeige GRIN2B ELISA Kits) variants were associated with intellectual disability with or without seizures
the gain-of-function M817V mutation causes overactivation of NMDAR (zeige GRIN1 ELISA Kits) 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.
Knockdown of PKD1 (zeige PKD1 ELISA Kits) did not affect NMDAR (zeige GRIN1 ELISA Kits) internalization but prevented the phosphorylation and inhibition of remaining surface NMDARs and NMDAR (zeige GRIN1 ELISA Kits)-mediated synaptic functions.
Sepsis selectively decreased the protein and mRNA levels of GluN2A, GluN2B (zeige GRIN2B ELISA Kits) and GluN1 (zeige GRIN1 ELISA Kits) but not the levels of synaptophysin (zeige SYP ELISA Kits) or the neuronal number in the hippocampus of septic mice.
Drebrin A (zeige DBN1 ELISA Kits) can be found co-clustering with NR2B (zeige GRIN2B ELISA Kits)-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 (zeige GRIN2B ELISA Kits) 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 (zeige PKC ELISA Kits)-mediated phosphorylation sites regulates NMDAR (zeige GRIN1 ELISA Kits)-mediated signaling that modulates anxiety.
These data suggest that chronic early postnatal SSS influences spatial learning and memory ability, levels of hippocampal NR2B (zeige GRIN2B ELISA Kits), and NR2A/NR2B (zeige GRIN2B ELISA Kits) ratios in adult males.
Rph3A (zeige RPH3A ELISA Kits) interacts with GluN2A and PSD-95 (zeige DLG4 ELISA Kits) forming a complex that regulates NMDARs stabilization at postsynaptic membranes.
Egr-1 (zeige EGR1 ELISA Kits) is involved in NMDAR (zeige GRIN1 ELISA Kits)-mediated PSD-95 (zeige DLG4 ELISA Kits) down-regulation and AMPAR endocytosis, a process important in the expression of long term depression
Study demonstrated that GluN2A carboxy-terminal domain is responsible for the impaired long-term olfactory and social memory observed in the GluN2A overexpression mice
Results establish the GluN2A subunit as a significant contributor to both bidirectional synaptic plasticity and spatial pattern separation in the dentate gyrus
Best1 (zeige BEST1 ELISA Kits)-mediated astrocytic glutamate (zeige GRIN1 ELISA Kits) activates the synaptic N-methyl-D-aspartate receptor (zeige GRIN1 ELISA Kits) (NMDAR (zeige GRIN1 ELISA Kits)) and modulates NMDAR (zeige GRIN1 ELISA Kits)-dependent synaptic plasticity.
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