Mouse Glutamate [NMDA] receptor subunit epsilon-2(GRIN2B) ELISA kit

Component of NMDA receptor complexes that function as heterotetrameric, ligand-gated ion channels with high calcium permeability and voltage-dependent sensitivity to magnesium. Channel activation requires binding of the neurotransmitter glutamate to the epsilon subunit, glycine binding to the zeta subunit, plus membrane depolarization to eliminate channel inhibition by Mg(2+). Sensitivity to glutamate and channel kinetics depend on the subunit composition. In concert with DAPK1 at extrasynaptic sites, acts as a central mediator for stroke damage. Its phosphorylation at Ser-1303 by DAPK1 enhances synaptic NMDA receptor channel activity inducing injurious Ca2+ influx through them, resulting in an irreversible neuronal death. Contributes to neural pattern formation in the developing brain. Plays a role in long-term depression (LTD) of hippocampus membrane currents and in synaptic plasticity.

1. chronic KOR activation increased phosphorylation of NR2B subunit of NMDA at tyrosine 1472 (pNR2B NMDA) in the hippocampus, but not in the cortex. PMID: 27634008
2. NR4A1 knockdown partly decreased surface NR2B by promoting NR2B internalization. PMID: 27876882
3. Study generated the Cdkl5 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 KO mice. These data indicate that CDKL5 plays an important role in controlling postsynaptic localization of the GluN2B-SAP102 complex in the hippocampus. PMID: 28688852
4. APP intracellular domain increase in mature neurons, as reported in Alzheimer's disease, alters synaptic NMDAR composition to an immature-like GluN2B-rich profile. This disrupts synaptic signal integration, via over-activation of SK channels, and synapse plasticity. PMID: 28682239
5. 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. PMID: 28174113
6. Negative regulation of REST on NR2B in spinal cord takes part in the exacerbation of bone cancer pain. PMID: 27732941
7. results demonstrated that phosphorylation level of S1284 in GluN2B was regulated by acute stress PMID: 28359951
8. 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 receptor pathway PMID: 27422716
9. GluN2B gene deletion mice consumed significantly less alcohol, than non-mutant controls. PMID: 28109345
10. Neonatal hypoxic-ischemia reshaped the postsynaptic GluN2B interactome by recruiting new proteins, including multiple kinases, into the complexes PMID: 28993251
11. PGRN decrease, resulting from pathogenic mutations, might compromise the trophism of cortical neurons by affecting GluN2B-contaning NMDA receptors PMID: 28899992
12. HumanTau(AT) causes excitotoxicity mediated by NR2B-containing NMDA receptors due to enhanced extracellular glutamate. PMID: 26931569
13. These in vivo changes reflect changes in glutamate transporter protein in HD mice and human HD post-mortem tissue. Furthermore, NAC was able to rescue changes in key glutamate receptor proteins related to excitotoxicity in HD, including NMDAR2B. PMID: 27179791
14. Data show that hydroxyproline HyP(10) plays a critical role in maintaining the structural integrity of conantokins conRl-B, which can be correlated with its glutamate receptor, ionotropic, N-methyl D-aspartate 2B (GluN2B) subunit-selective inhibition. PMID: 27981829
15. These results highlight the requirement for stringent pharmacogenetic approaches to separate specific on-target effects from nonspecific off-target effects. Importantly, they also demonstrate that the CaMKII/GluN2B interaction is required not only for normal long-term potentiation induction but also for the maintenance of synaptic strength. PMID: 27246855
16. rs2284411 not associated with the need for neonatal resuscitation PMID: 27059438
17. GluN2B-dependent calcium signaling and excitatory postsynaptic current, long-term depression, and spatial reversal learning are enhanced in the hippocampus of AC6(-/-) mice without altering the gross anatomy of the brain PMID: 26932446
18. Unpredictable chronic mild stress mice exhibited elevated nucleus accumbens (NAC) shell levels of Glun2B. GluN2b levels were also lower within the NAC core. PMID: 25916683
19. Results identify crucial determinants in the C-terminal domain of GluN2B subunits in promoting neuronal death in ischemic conditions. PMID: 26581639
20. The results suggest that NR2B vulnerability represents a target for environmental toxicants in the brain. PMID: 26901155
21. Results show that monomeric Abeta1-42 application induces an increase of the Ca2+-response and of the membrane expression of the extrasynaptic subunit of the NMDA receptor GluN2B in PC12 cells, while the opposite effects were observed in cultured neurons PMID: 26401567
22. Results demonstrate that up-regulation of NR2B expression facilitates acquisition of auditory cued fear memory and enhances long-term potentiation at thalamus-lateral amygdala synapses PMID: 26118841
23. Loss of GluN2B in principal neurons of the forebrain results in reduced punished food reward-seeking. PMID: 26223494
24. Study demonstrated that the GluN2B carboxy-terminal domain is necessary for enhanced social recognition memory in GluN2B transgenic overexpression mice PMID: 26179233
25. Visual plasticity in adult mice was dramatically enhanced following magnesium treatment, which was concurrent with an increase in the expression of NR2 subunits of N-methyl-D-aspartate receptors. PMID: 26282667
26. Results support the role of N-methyl-D-aspartate receptor, and GluN2B, on modulation of striatal function necessary for efficient choice behavior and suggest that NMDAR on interneurons may play a critical role in associative learning. PMID: 25968910
27. Study suggests that NMDA receptor NR2B subunits contribute to epilepsy-associated pathological and biochemical events, including hippocampal astrocytosis, oxidative stress and neuron loss, and these events might be correlated with BDNF up-regulation PMID: 25896886
28. Study provides further evidence of antidepressant-like activity of GluN2B antagonism and offers novel insight into the glutamate receptor subunits, interacting molecules and brain regions mediating these effects PMID: 25800971
29. results revealed that the phosphorylation change of GluN2B at Tyr-1070 accompanied the Tyr-1472 phosphorylation and Fyn associated with GluN2B in synaptic plasticity induced by both chemical and contextual fear learning. PMID: 26229100
30. Corticohippocampal loss of GluN2B selectively impaired an initial reversal in a stimulus specific manner and impaired the ability of mutant mice to form an attentional set. PMID: 25798630
31. GluN2B accumulates in endoplasmic reticulum-enriched synaptic fractions in AIDA-1 knock-out mice. PMID: 26085624
32. study suggested that a chronic increase of NMDARs activation by NR2B overexpression in the forebrain may enhance the protein serine/threonine phosphorylation levels of MAPK/ERK-CREB and thereby regulated their signaling pathway PMID: 25128602
33. GluN1 amino-terminal domain adopts a more open conformation when coassembled with GluN2A than with GluN2B. PMID: 25829490
34. findings indicated that CaMKII-mediated KIF17/NR2B trafficking may contribute to bone cancer pain, and inhibition of CaMKII may be a useful alternative or adjunct therapy for relieving cancer pain PMID: 24836181
35. Chronic neuropathic pain was found to be modulated via regulation of NR2B. PMID: 25568101
36. Upregulation of NR2B phosphorylation at Y1472 after neonatal hypoxia-ischemia is involved in superoxide-mediated oxidative stress and contributes to brain injury. PMID: 25158771
37. The expression of the GluN2B subunit was increased in hippocampus following enhanced synaptic transmission by simvastatin. PMID: 24687455
38. GluN2B-containing NMDARs keep the hippocampal circuit activity under control by promoting the maturation of excitatory synapses in interneurons. PMID: 25429143
39. Gentiopicroside downregulates GluN2B receptors, but not GluN2A receptors, in the amygdala of rats with reserpine-induced pain. PMID: 24584520
40. GluN2B expressed at glutamatergic synapses on glutamatergic projection neurons facilitates refinement of ascending pathway synapses directly PMID: 25164652
41. Neural activity of newborn neurons is regulated by their own NR2B-containing NMDA glutamate receptors. PMID: 23904361
42. Knockdown of GluN2B in the bed nucleus of stria terminalis decreased the latency to consume food in novelty-induced hypophagia, a surrogate marker of affective state. PMID: 24301649
43. Disrupting NR2B-Cdk5 interaction via a small interfering peptide (siP) increases NR2B surface levels, facilitates synaptic transmission, and improves memory formation in vivo. PMID: 24607229
44. the PS1/gamma-secretase system regulates release of glutamate, tyrosine phosphorylation, and surface expression of GluN2B-containing NMDARs. PMID: 24025330
45. elevated intraocular pressure-induced increase in expression of NR2B subunits of NMDARs may be involved in retinal ganglion cell degeneration of DBA/2J mice. PMID: 24175101
46. the increase in the amount of NMDARs required phosphorylation of the NMDAR subunit GluN2B at Tyr(1472) by a pathway involving adenylyl cyclase subtype 1 (AC1), protein kinase A (PKA), and Src family kinases. PMID: 23674822
47. GluN2B- and GluN2D-containing NMDA receptors play a critical role in N-methyl-D-aspartate-induced excitotoxic retinal cell death. PMID: 23902942
48. Inhibition of NR2B-containing NMDARs abolished Abeta-induced hTau phosphorylation and toxicity by preventing GSK-3beta activation but did not affect dendritic spine loss. PMID: 23618906
49. An increased association of GluN2B-containing NMDA receptors with synaptic scaffolding proteins in aged animals may have contributed to the age-related memory declines. PMID: 23884936
50. Corticostriatal or striatal deletion of Grin2b or dorsal-striatum-restricted GluN2B antagonism impaired choice learning. Cortical Grin2b deletion or orbitofrontal GluN2B antagonism impaired shifting. PMID: 23831965

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Cell membrane; Multi-pass membrane protein. Cell junction, synapse, postsynaptic cell membrane; Multi-pass membrane protein. Late endosome. Lysosome. Cytoplasm, cytoskeleton.

Glutamate-gated ion channel (TC 1.A.10.1) family, NR2B/GRIN2B subfamily

Detected in brain (at protein level). Detected throughout the brain, and in brain stem trigeminal nucleus. Detected in forebrain.

KEGG: mmu:14812

STRING: 10090.ENSMUSP00000062284

UniGene: Mm.436649