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There was no significant association between selected GRIN2B polymorphisms and personality traits.
No association between GRIN2B rs1805502 polymorphism and OCD, symptom dimensions or treatment response in South Indian patients.
Results showed that NRG1 (show NRG1 Proteins)-ErbB4 (show ERBB4 Proteins) signaling suppressed phosphorylation of GluN2B at position 1472 by Src kinase (show CSK Proteins), and decreased levels of phosphorylation level of GluN2B and Src (show SRC Proteins) were detected in human symptomatic epilepsy tissues.
Results suggest that alterations in the glutamate (show GRIN1 Proteins) and dopamine system (GRIN2B and DRD4 (show DRD4 Proteins)) in attention-deficit/hyperactivity disorder may contribute to abnormalities in local functional connectivity and its dynamic repertoire in the superior parietal area, and these abnormalities would be related to dysfunction in sustained and divided attention.
GRIN2B SNP rs219927 is associated with brain volume in the left posterior cingulate cortex in adolescent alcohol dependence.
The results suggest that the GRIN2B gene may modify the linguistic processes involved in the retrieval of information from the mental lexicon on the basis of semantic traits and, moreover, contribute to the variability of clinical symptoms of impairment of abstract thinking in patients with schizophrenia.
It is this DAPK1 (show DAPK1 Proteins)-NR2B interaction that arbitrates the pathological processes like apoptosis, necrosis, and autophagy of neuronal cells observed in stroke injury, hence we aimed to inhibit this vital interaction to prevent neuronal damage.
Five rare missense mutations in the GRIN2B gene are not associated with schizophrenia or autism spectrum disorder in a Japanese population.
NR4A1 (show NR4A1 Proteins) knockdown partly decreased surface NR2B by promoting NR2B internalization.
This review showed that GRIN2B associate with Obsessive-compulsive disorder.
chronic KOR (show OPRK1 Proteins) activation increased phosphorylation of NR2B subunit of NMDA at tyrosine 1472 (pNR2B NMDA) in the hippocampus, but not in the cortex.
Study generated the Cdkl5 (show CDKL5 Proteins) KO mice, and identified hyperexcitability in response to NMDA and postsynaptic overaccumulation of GluN2B-containing NMDARs in the hippocampus. The GluN2B-selective antagonist ifenprodil abrogated the NMDA-induced hyperexcitability of Cdkl5 (show CDKL5 Proteins) KO mice. These data indicate that CDKL5 (show CDKL5 Proteins) plays an important role in controlling postsynaptic localization of the GluN2B-SAP102 (show DLG3 Proteins) complex in the hippocampus.
APP (show APP Proteins) intracellular domain increase in mature neurons, as reported in Alzheimer's disease, alters synaptic NMDAR (show GRIN1 Proteins) composition to an immature-like GluN2B-rich profile. This disrupts synaptic signal integration, via over-activation of SK channels, and synapse plasticity.
The induction of a conditional forebrain-specific haploinsufficiency of GluN2B in transgenic model mice reverses the pathophysiological changes in hippocampal synaptic plasticity in a mouse model of Alzheimer's disease (AD). These results provide further evidence for the involvement of the glutamatergic system in AD pathology and emphasize the GluN2B subunit as a potential target for AD treatment.
activity-based anorexia resilience, quantified as suppression of hyperactivity, correlated strongly with reserve pools of NR2A (show GRIN2A Proteins)-NMDA receptors in spine cytoplasm
Negative regulation of REST on NR2B in spinal cord takes part in the exacerbation of bone cancer pain.
results demonstrated that phosphorylation level of S1284 in GluN2B was regulated by acute stress
study are the first to demonstrate that phosphorylation of GluN2B subunit at Tyr1472 is important for trigeminal transmission of itch and suggest that the NMDA receptor activation occurs upstream of the receptor of gastrin-releasing peptide (GRP)-GRP (show GRP Proteins) receptor pathway
GluN2B gene deletion mice consumed significantly less alcohol, than non-mutant controls.
N-methyl-D-aspartate (NMDA) receptors are a class of ionotropic glutamate receptors. NMDA receptor channel has 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 three different subunits: NR1 (GRIN1), NR2 (GRIN2A, GRIN2B, GRIN2C, or GRIN2D) and NR3 (GRIN3A or GRIN3B). The NR2 subunit acts as the agonist binding site for glutamate. This receptor is the predominant excitatory neurotransmitter receptor in the mammalian brain.
NMDA type glutamate receptor
, N-methyl D-aspartate receptor subtype 2B
, N-methyl-D-aspartate receptor subunit 2B
, glutamate [NMDA] receptor subunit epsilon-2
, glutamate receptor ionotropic, NMDA 2B
, N-methyl-D-aspartate receptor subunit 3
, glutamate receptor subunit epsilon-2
, glutamate receptor, ionotropic, NMDA2B
, N-methyl-D-aspartate receptor subunit NR2B
, N-methyl D-aspartate receptor 2B