GRIN2B
Purified Mouse Monoclonal Antibody
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application ![]()
| WB, IHC, ICC, E |
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Primary Accession | Q13224 |
Reactivity | Human |
Host | Mouse |
Clonality | Monoclonal |
Clone Names | 6E9A8 |
Isotype | Mouse IgG1 |
Calculated MW | 166.4kDa |
Immunogen | Purified recombinant fragment of human GRIN2B (AA: extra 27-163) expressed in E. Coli. |
Formulation | Purified antibody in PBS with 0.05% sodium azide |
Gene ID | 2904 |
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Other Names | MRD6; NR2B; hNR3; EIEE27; GluN2B; NMDAR2B |
Dilution | E~~ 1/10000 WB~~ 1/500 - 1/2000 ICC~~ 1/100 - 1/500 |
Storage | Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | GRIN2B is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | GRIN2B {ECO:0000303|Ref.3, ECO:0000312|HGNC:HGNC:4586} |
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Function | Component of N-methyl-D-aspartate (NMDA) receptors (NMDARs) that function as heterotetrameric, ligand-gated cation channels with high calcium permeability and voltage-dependent block by Mg(2+) (PubMed:24272827, PubMed:24863970, PubMed:26875626, PubMed:26919761, PubMed:27839871, PubMed:28095420, PubMed:28126851, PubMed:38538865, PubMed:8768735). Participates in synaptic plasticity for learning and memory formation by contributing to the long-term depression (LTD) of hippocampus membrane currents (By similarity). Channel activation requires binding of the neurotransmitter L-glutamate to the GluN2 subunit, glycine or D-serine binding to the GluN1 subunit, plus membrane depolarization to eliminate channel inhibition by Mg(2+) (PubMed:24272827, PubMed:24863970, PubMed:26875626, PubMed:26919761, PubMed:27839871, PubMed:28095420, PubMed:28126851, PubMed:38538865, PubMed:8768735). NMDARs mediate simultaneously the potasium efflux and the influx of calcium and sodium (By similarity). Each GluN2 subunit confers differential attributes to channel properties, including activation, deactivation and desensitization kinetics, pH sensitivity, Ca2(+) permeability, and binding to allosteric modulators (PubMed:26875626, PubMed:28095420, PubMed:28126851, PubMed:38538865, PubMed:8768735). 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 (By similarity). |
Cellular Location | Cell membrane; Multi-pass membrane protein. Postsynaptic cell membrane {ECO:0000250|UniProtKB:Q00960}; Multi-pass membrane protein. Cell projection, dendrite. Late endosome {ECO:0000250|UniProtKB:Q01097}. Lysosome {ECO:0000250|UniProtKB:Q01097}. Cytoplasm, cytoskeleton {ECO:0000250|UniProtKB:Q01097}. Note=Co-localizes with the motor protein KIF17 along microtubules. {ECO:0000250|UniProtKB:Q01097} |
Tissue Location | Primarily found in the fronto-parieto-temporal cortex and hippocampus pyramidal cells, lower expression in the basal ganglia. |

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Provided below are standard protocols that you may find useful for product applications.
References
1.J Neural Transm (Vienna). 2014 May;121(5):533-42. 2.Psychopharmacology (Berl). 2014 Feb;231(4):685-93.

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