Rabbit Recombinant Monoclonal NMDAR2A antibody. Suitable for WB and reacts with Mouse, Rat, Human samples. Cited in 42 publications.
pH: 7.2 - 7.4
Preservative: 0.01% Sodium azide
Constituents: 59% PBS, 40% Glycerol (glycerin, glycerine), 0.05% BSA
WB | |
---|---|
Human | Tested |
Mouse | Tested |
Rat | Tested |
Species | Dilution info | Notes |
---|---|---|
Species Mouse | Dilution info 1/1000 | Notes We recommend to use 1%SDS Hot lysis prepare method to get desired Western Blot results. For Lysate preparation protocol, please refer to the protocol book in the protocol section and/or here. |
Species Rat | Dilution info 1/1000 | Notes We recommend to use 1%SDS Hot lysis prepare method to get desired Western Blot results. For Lysate preparation protocol, please refer to the protocol book in the protocol section and/or here. |
Species Human | Dilution info 1/1000 | Notes We recommend to use 1%SDS Hot lysis prepare method to get desired Western Blot results. For Lysate preparation protocol, please refer to the protocol book in the protocol section and/or here. |
Select an associated product type
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:20890276, PubMed:23933818, PubMed:23933819, PubMed:23933820, PubMed:24504326, PubMed:26875626, PubMed:26919761, PubMed:28242877, PubMed:36117210, PubMed:38538865, PubMed:8768735). NMDARs participate in synaptic plasticity for learning and memory formation by contributing to the slow phase of excitatory postsynaptic current, long-term synaptic potentiation, and learning (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:23933818, PubMed:23933819, PubMed:23933820, PubMed:24504326, PubMed:26875626, PubMed:26919761, PubMed:27288002, PubMed:28095420, PubMed:28105280, PubMed:28126851, PubMed:28182669, PubMed:29644724, PubMed:38307912, 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:26919761). Participates in the synaptic plasticity regulation through activation by the L-glutamate releaseed by BEST1, into the synaptic cleft, upon F2R/PAR-1 activation in astrocyte (By similarity).
NMDAR2A, GRIN2A, GluN2A, Glutamate [NMDA] receptor subunit epsilon-1, N-methyl D-aspartate receptor subtype 2A, NR2A, hNR2A
Rabbit Recombinant Monoclonal NMDAR2A antibody. Suitable for WB and reacts with Mouse, Rat, Human samples. Cited in 42 publications.
pH: 7.2 - 7.4
Preservative: 0.01% Sodium azide
Constituents: 59% PBS, 40% Glycerol (glycerin, glycerine), 0.05% BSA
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb® patents.
This product is a recombinant monoclonal antibody, which offers several advantages including:
For more information, read more on recombinant antibodies.
NMDAR2A also known as GRIN2A is a subunit of the N-methyl-D-aspartate (NMDA) receptor which belongs to the family of ionotropic glutamate receptors. This receptor functions as a ligand-gated ion channel and requires both glutamate and glycine for activation. NMDAR2A has a molecular mass of about 164 kDa. It plays a significant role in synaptic transmission and plasticity and is mainly expressed in the brain particularly in the cerebral cortex and hippocampus. Its expression is important for normal brain function affecting learning and memory.
NMDAR2A participates in synaptic signaling by forming part of the NMDA receptor complex. As part of this complex NMDAR2A interacts with other receptor subunits such as NR1 and NR2B which together modulate calcium influx into the neuron. This influx is essential for activating downstream signaling pathways that influence synaptic strength. The receptor's activation is tightly regulated which helps to maintain the balance between synaptic excitation and inhibition in the central nervous system.
NMDAR2A serves essential roles in the long-term potentiation (LTP) and synaptic plasticity pathways. LTP is a process that strengthens synaptic connections and is important for memory formation. NMDAR2A interacts with proteins like postsynaptic density protein 95 (PSD-95) within these pathways to mediate downstream signaling events. It is also involved in the MAPK/ERK pathway affecting cellular processes such as gene expression differentiation and survival.
NMDAR2A has been associated with epilepsy and schizophrenia. Mutations or altered expression of NMDAR2A can disrupt normal receptor function and contribute to these conditions. It shows links with other proteins such as NR2B where imbalances between different NMDA receptor subunits may exacerbate disease pathology. Understanding how NMDAR2A functions and misfunctions helps in investigating therapeutic targets for these neurological diseases.
We have tested this species and application combination and it works. It is covered by our product promise.
We have not tested this specific species and application combination in-house, but expect it will work. It is covered by our product promise.
This species and application combination has not been tested, but we predict it will work based on strong homology. However, this combination is not covered by our product promise.
We do not recommend this combination. It is not covered by our product promise.
We are dedicated to supporting your work with high quality reagents and we are here for you every step of the way should you need us.
In the unlikely event of one of our products not working as expected, you are covered by our product promise.
Full details and terms and conditions can be found here:
Terms & Conditions.
We have systematically measured KD (the equilibrium dissociation constant between the antibody and its antigen), of more than 840 recombinant antibodies to assess not only their individual KD values but also to see the average affinity of antibody.
Based on the comparison with published literature values for mouse monoclonal antibodies, Recombinant antibodies appear to be on average 1-2 order of magnitude higher affinity.
Blocking buffer: 5% NFDM/TBST
Dilution buffer: 5% NFDM/TBST
All lanes: Western blot - Anti-NMDAR2A antibody [EPR2465(2)] (ab124913) at 1/1000 dilution
All lanes: Human cerebellum tissue lysate at 10 µg
All lanes: HRP goat anti-rabbit (H+L) at 1/1000 dilution
Predicted band size: 165 kDa
Observed band size: 165 kDa
Blocking buffer: 5% NFDM/TBST
Dilution buffer: 5% NFDM/TBST
All lanes: Western blot - Anti-NMDAR2A antibody [EPR2465(2)] (ab124913) at 1/20000 dilution
All lanes: Human fetal brain tissue lysate at 10 µg
All lanes: HRP goat anti-rabbit (H+L) at 1/1000 dilution
Predicted band size: 165 kDa
Observed band size: 165 kDa
All lanes: Western blot - Anti-NMDAR2A antibody [EPR2465(2)] (ab124913) at 1/1000 dilution
Lane 1: Mouse brain lysate at 10 µg
Lane 2: Rat brain lysate at 10 µg
Lane 3: Human brain lysate at 10 µg
All lanes: HRP labelled goat anti-rabbit at 1/2000 dilution
Predicted band size: 165 kDa
Lanes 1 to 2: 40 seconds
Lanes 3 to 6: 20 seconds
We recommend to use 1%SDS Hot lysis prepare method to get desired Western Blot results.
We are unsure how to define the extra bands.
All lanes: Western blot - Anti-NMDAR2A antibody [EPR2465(2)] (ab124913) at 1/2000 dilution
Lane 1: Human brain lysates prepared in RIPA lysis method at 20 µg
Lane 2: Human brain lysates prepared in 1%SDS Hot lysis method at 20 µg
Lane 3: Mouse brain lysates prepared in RIPA lysis method at 20 µg
Lane 4: Mouse brain lysates prepared in 1%SDS Hot lysis method at 20 µg
Lane 5: Rat brain lysates prepared in RIPA lysis method at 20 µg
Lane 6: Rat brain lysates prepared in 1%SDS Hot lysis method at 20 µg
All lanes: Western blot - Goat Anti-Rabbit IgG H&L (HRP) (Goat Anti-Rabbit IgG H&L (HRP) ab97051) at 1/20000 dilution
Predicted band size: 165 kDa
Observed band size: 165 kDa
Image collected and cropped by CiteAb under a CC-BY license from the publication
NMDAR2A western blot using anti-NMDAR2A antibody [EPR2465(2)] ab124913. Publication image and figure legend from Liang, L., Xie, R., et al., 2020, J Neurochem, PubMed 31705656.
ab124913 was used in this publication in western blot. This may not be the same as the application(s) guaranteed by Abcam. For a full list of applications guaranteed by Abcam for ab124913 please see the product overview.
Effects of antagonizing homodomain interacting protein kinase 2 on the synaptic toxicity of Sev. (a, b) Golgi staining and quantification of spines in control rats, Sev‐treated, A64‐treated, and Sev plus A64‐treated rats. N = 6 rats per group. (c) Synaptic ultrastructure in hippocampus of control rats, A64‐treated, Sev‐treated, and Sev plus A64‐treated rats. Notice that the decrease in spine number and PSD length were partially rescued by A64. N = 6 rats per group. (d, e) Western blot and quantification of Synaptophysin, post‐synaptic density protein 95 (PSD95), calcium/calmodulin‐dependent kinase II (CaMKII), phosphorylation of N‐methyl‐d‐aspartate receptor subunit 2 A (pNR2A), NR2A and vesicular inhibitory amino acid transporter (vGAT). Notice that the decrease in Synaptophysin, PSD95, CaMKII, and pNR2A were partially rescued by A64. N = 6 rats per group. (f–h) Open field assay. N = 8 rats per group. (i–k) Elevated plus maze assay. Notice that A64 treatment alleviated the Sev‐induced anxiety. N = 8 rats per group. (l–n) Morris water maze test. Notice that A64 treatment partially improved the spatial memory of Sev‐treated rats. N = 8 rats per group. Con, control. Sev, Sevoflurane. *p < 0.05. **p < 0.01. ***p < 0.001. ****p < 0.0001. #p < 0.05. One‐way anova (a–n). Bar = 10 μm (a) and 200 nm (c).
Please note: All products are 'FOR RESEARCH USE ONLY. NOT FOR USE IN DIAGNOSTIC OR THERAPEUTIC PROCEDURES'.
For licensing inquiries, please contact partnerships@abcam.com