Invitrogen

NMDAR2A Polyclonal Antibody

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NMDAR2A Antibody in Immunohistochemistry (IHC) — Immunohistochemistry analysis of NMDAR2A in rabbit retina showing NMDAR2A polyclonal antibody (Product # OpA1-04021) using a dilution of 1:1,000 (green) in the rod and cone photoreceptors in the outer plexiform layer as well as the entire inner plexiform layer.

NMDAR2A Antibody in Western Blot (WB) — Western blot of NMDAR2A in rat hippocampal lysate (10 µg), showing specific immunolabeling of a ~180 kDa band corresponding to the NR2A subunit of the NMDAR2A polyclonal antibody (Product # OPA1-04021) receptor.

NMDAR2A Antibody in Immunocytochemistry, Immunohistochemistry (ICC/IF, IHC) — Figure 3 Representative double immunofluorescent photos for localization of PSD95, NR2A and PDI in the outer molecular layer of the upper blade of the dentate gyrus following acute seizures. ( A ) Low magnification photos of PSD95 and MAP2 in the upper blade of dentate gyrus. Bar = 50 mum. Abbreviations: OML, outer molecular layer; MML, middle molecular layer; IML, inner molecular layer; DG, dentate granule cell layer. ( B ) The reduced PSD95 puncta on MAP2-positive dendrites induced by acute seizures. Arrows indicate beading (damaging) dendrite induced by seizure activity. The right panels are high magnification images for rectangles. Bar = 10 (the left three panels) and 2.5 (the right panel) mum. ( C ) The changed colocalization of PSD95, NR2A and PDI in the molecular layer of the dentate gyrus. Following acute seizures, colocalization of NR2A:PSD95 is reduced. Acute seizure activity increases the colocalization of PDI:NR2A, while it does not affect colocalization of PDI:PSD95. Bar = 5 mum. The right panels indicate quantification of colocalized fluorescent intensity. Open circles indicate each individual value. Horizontal bars indicate mean value. Error bars indicate SEM (* p < 0.05 vs. saline, Student's t -test, n = 7, respectively).

NMDAR2A Antibody in Immunocytochemistry, Immunohistochemistry (ICC/IF, IHC) — Figure 7 Effect of PDI knockdown on localization of PSD95, NR2A and PDI in the outer molecular layer of the upper blade of the dentate gyrus of epileptic rats. ( A ) PDI siRNA does not affect the density of PSD95 puncta on MAP2-positive dendrites in epileptic rats. Arrows indicate beading (damaging) dendrite induced by seizure activity. The right panels are high magnification images for rectangles. Bar = 10 and 2.5 mum. ( B ) The changed colocalization of PSD95, NR2A and PDI in the molecular layer of the dentate gyrus. As compared to control animals (see Figure 3 B), colocalizations of NR2A:PSD95, PDI:PSD95 and PDI:NR2A are elevated in epileptic animals. PDI siRNA significantly reduced them, as compared to control siRNA. Bar = 5 mum. The right panels indicate quantification of colocalized fluorescent intensity. Open circles indicate each individual value. Horizontal bars indicate mean value. Error bars indicate SEM ( *, # p < 0.05 vs. control animals and control siRNA, respectively, one-way ANOVA, n = 7, respectively).

NMDAR2A Antibody in Western Blot, Immunoprecipitation (WB, IP) — Figure 4 The amounts of total- and SNO-thiols on PSD95 and NR2A, and the bindings of NR2A-PSD95, PDI-PSD95 and PDI-NR2A in the hippocampus of epilepsy rats. ( A ) Representative Western blot for expression and the amounts of total- and SNO-thiol on PSD95 and NR2A. As compared to control animals, epilepsy rats show the increases in the total- and SNO-thiol levels on PSD95 without altered PSD95 expression. In addition, they show the increases in total- and SNO-thiol levels on NR2A, in spite of the reduced NR2A expression. ( B , C ) Quantification of Western blot data. Open circles indicate each individual value. Horizontal bars indicate mean value. Error bars indicate SEM (* p < 0.05 vs. saline, Student's t -test, n = 7, respectively). ( D ) Co-immunoprecipitation analysis of NR2A-PSD95 interaction in epileptic rats. The NR2A-PSD95 binding is significantly increased, as compared to control animals. ( E ) Quantification of Western blot data. Open circles indicate each individual value. Horizontal bars indicate mean value. Error bars indicate SEM (* p < 0.05 vs. saline, Student's t -test, n = 7, respectively). ( F ) Co-immunoprecipitation analyses of PDI-PSD95 and PDI-NR2A co-assemblies in epileptic rats. The bindings of PDI-PSD95 and PDI-NR2A are elevated in epileptic rats, as compared to control animals. ( G ) Quantification of Western blot data. Open circles indicate each individual value. Horizontal bars indicate mean value. Error bars indicate SEM (* p < 0.05 vs. saline, Stu

NMDAR2A Antibody in Western Blot, Immunoprecipitation (WB, IP) — Figure 6 Effects of PDI knockdown on the amounts of total- and SNO-thiols on PSD95 and NR2A, and the bindings of NR2A-PSD95, PDI-PSD95 and PDI-NR2A in the hippocampus of epilepsy rats. ( A ) Representative Western blot for expression and the amounts of total- and SNO-thiols on PSD95. As compared to control siRNA, PDI siRNA reduces PDI protein level and the total thiol level on PSD95, without altering PSD95 expression. PDI siRNA also effectively decreases the total thiol level, but not SNO-thiol level, on NR2A in epilepsy rats. ( B , C ) Quantification of Western blot data. Open circles indicate each individual value. Horizontal bars indicate mean value. Error bars indicate SEM (* p < 0.05 vs. saline, Student''s t -test, n = 7, respectively). ( D ) Co-immunoprecipitation analysis of NR2A-PSD95 interaction in epileptic rats. The NR2A-PSD95 binding is significantly reduced by PDI knockdown. ( E ) Quantification of Western blot data. Open circles indicate each individual value. Horizontal bars indicate mean value. Error bars indicate SEM (* p < 0.05 vs. saline, Student''s t -test, n = 7, respectively). ( F ) Co-immunoprecipitation analyses of PDI-PSD95 and PDI-NR2A co-assemblies in epileptic rats. The PDI-PSD95 and PDI-NR2A bindings are diminished by PDI siRNA. ( G ) Quantification of Western blot data. Open circles indicate each individual value. Horizontal bars indicate mean value. Error bars indicate SEM (* p < 0.05 vs. saline, Student''s t -test, n = 7, respectively).

NMDAR2A Antibody in Western Blot, Immunoprecipitation (WB, IP) — Figure 2 The effect of acute seizures on the total- and SNO-thiol levels on PSD95 and NR2A, and the bindings of NR2A-PSD95, PDI-PSD95 and PDI-NR2A in the hippocampus. ( A ) Representative Western blot for expression and the amounts of total- and SNO-thiols on PSD95 and NR2A. Acute seizures increase the number of SNO-thiols, but not total thiols, on PSD95. ( B , C ) Quantification of Western blot data. Open circles indicate each individual value. Horizontal bars indicate mean value. Error bars indicate SEM (* p < 0.05 vs. saline, Student's t -test, n = 7, respectively). ( D ) Co-immunoprecipitation analysis of NR2A-PSD95 interaction following acute seizures. Acute seizure reduces both PSD95 and NR2A expression. However, the NR2A-PSD95 bindings are significantly reduced, as compared to saline-treated animals. ( E ) Quantification of Western blot data. Open circles indicate each individual value. Horizontal bars indicate mean value. Error bars indicate SEM (* p < 0.05 vs. saline, Student's t -test, n = 7, respectively). ( F ) Co-immunoprecipitation analyses of PDI interactions with PSD95 and NR2A. Acute seizure increases PDI expression and PDI-NR2A binding, without altering PDI-PSD95 binding. ( G ) Quantification of Western blot data. Open circles indicate each individual value. Horizontal bars indicate mean value. Error bars indicate SEM (* p < 0.05 vs. saline, Student's t -test, n = 7, respectively).

NMDAR2A Antibody in Western Blot, Immunoprecipitation (WB, IP) — Figure 6 Effect of PDI knockdown on spontaneous seizure activity in epileptic (6 week-post SE) rats. ( A ) Representative EEGs for control siRNA- and PDI siRNA-infused epileptic animals. ( B-D ) Anticonvulsive effect of PDI siRNA on spontaneous seizure activity: ( B ) the mean seizure frequency, ( C ) seizure duration and ( D ) behavioral seizure score (Open circles indicate each individual value. Closed circles indicate mean value. * p < 0.05 vs. control siRNA; n = 5, respectively). PDI knockdown inhibits the spontaneous seizure activity in chronic epileptic rats. ( E ) Co-immunoprecipitation analyses of NR1 or NR2A interaction with PDI in control siRNA- and PDI siRNA-infused epileptic animals. M, molecular weight marker. ( F ) The quantitative analyses of co-immunoprecipitation of PDI bound to NR1 and NR2A (* p < 0.05 vs. control siRNA; n = 7, respectively). ( G ) Western blot data for the amounts of -SH + -SNO on NR1 and NR2A subunits in normal (N), control siRNA- and PDI siRNA-infused epileptic animals. M, molecular weight marker. ( H,I ) Quantification of effects of PDI siRNA on the amount of -SH + -SNO on NR1 and NR2A subunit and PDI expression in epileptic rats (mean +- S.E.M.; *p < 0.05 vs. normal; n = 7, respectively). PDI siRNA infusion reduces the binding of PDI to NMDAR, the amount of -SH + -SNO of NMDAR subunits and PDI expression level in epileptic animals.

NMDAR2A Antibody in Western Blot (WB) — Figure 3 The role of PDI in redox status of NMDAR. ( A ) Co-immunoprecipitation analyses of PDI interaction with IP3R, NR2A, NR2B, NR1 and M1R in the hippocampus. M, molecular weight marker. ( B ) The quantitative analyses of co-immunoprecipitation of PDI with NR1, NR2A, NR2B, M1R and IP3. PDI binds to NR1 and NR2A more than NR2B. ( C ) Schematics of modified biotin switch technique for the measurement of the amount of free thiols (-SH) and S-nitrosothiols (-SNO). ( D ) Representative western blot for the amount of -SH + -SNO in total protein extracts. M, molecular weight marker. ( E-G ) Effects of PDI siRNA, DTNB and bacitracin on thiols on NR1 and NR2. The amount of -SH + -SNO on NR1 and NR2A subunits are significantly reduced by PDI siRNA, DTNB and bacitracin. ( E ) Western blot representing the amount of -SH + -SNO on NR1 and NR2A subunit. M, molecular weight marker. ( F,G ) Quantification of effects of PDI siRNA, DTNB and bacitracin on the amount of -SH + -SNO on NR1 and NR2A subunit and PDI expression (mean +- S.E.M.; *p < 0.05 vs. control; n = 7, respectively).

NMDAR2A Antibody in Western Blot, Immunoprecipitation (WB, IP) — Figure 5 Changed redox status of NMDAR by PDI in epileptic rats. ( A ) Western blot data for the amounts of -SH + -SNO of NR1 and NR2A subunits in non-SE (N), 3 day-post SE (3D), 1 week-post SE (1W) and chronic epileptic (6 week-post SE, Epil) animals. M, molecular weight marker. ( B ) Quantification of the amount of -SH + -SNO on NR1 and NR2A (mean +- S.E.M.; *p < 0.05 vs. normal; n = 7, respectively). The amounts of -SH + -SNO of NR1 and NR2A are increased 3 days after SE, and subsequently recovered to normal normal level 1 week after SE. ( C ) Representative photos for PDI expression in the normal and epileptic hippocampus. Bar = 300 mum. ( D ) Co-immunoprecipitation analyses of NR1 and NR2A interaction with PDI in normal and epileptic animals. M, molecular weight marker. ( E ) The quantitative analyses of co-immunoprecipitation of PDI with NR1 and NR2A in normal and epileptic animals (* p < 0.05 vs. normal; n = 7, respectively). In chronic epileptic animals, the amount of -SH + -SNO of NR1 is increased, as compared to normal animals.

NMDAR2A Antibody in Western Blot (WB) — Figure 7 Effects of PDI knockdown on ER stress induction and excitatory receptor expressions. ( A ) Western blot data for ER stress makers including pPERK, pIRE1alpha, IRE1alpha and ATF6 at 7 days after PDI siRNA infusion. M, molecular weight marker. ( B ) Western blot data for excitatory receptors including IP3R, NR2A, NR2B, NR1, M1R and CIB1 at 7 days after PDI siRNA infusion. M, molecular weight marker. ( C ) Quantification of effects of PDI siRNA on levels of ER stress markers and receptor expressions (n = 7, respectively). PDI knockdown does not induce ER stress and alterations in excitatory receptor expressions.

NMDAR2A Antibody in Western Blot (WB) — Published figure using NMDAR2A polyclonal antibody (Product # OPA1-04021) in Western Blot

NMDAR2A Antibody in Western Blot (WB) — Published figure using NMDAR2A polyclonal antibody (Product # OPA1-04021) in Western Blot

NMDAR2A Antibody in Immunoprecipitation (IP) — Published figure using NMDAR2A polyclonal antibody (Product # OPA1-04021) in Immunoprecipitation

Product Details

OPA1-04021

Applications	Tested Dilution	Publications
Western Blot (WB)	1:1,000	View 4 publications 4 publications
Immunohistochemistry (IHC)	1:1,000	View 1 publication 1 publication
Immunoprecipitation (IP)	3 µL/200 µg lysate	View 3 publications 3 publications
Immunocytochemistry (ICC/IF)	-	View 1 publication 1 publication

Product Specifications
Species Reactivity	Human, Mouse, Rabbit, Rat
Published species	Mouse, Rat
Host/Isotype	Rabbit / IgG
Class	Polyclonal
Type	Antibody
Immunogen	Fusion protein from the C-terminal region of the NR2A subunit of rat GRIN2A View immunogen
Conjugate	Unconjugated
Form	Lyophilized
Purification	Affinity chromatography
Contains	no preservative
Storage conditions	-20° C, Avoid Freeze/Thaw Cycles
RRID	AB_2112313

Product Specific Information

In Western blot, this antibody detects a single ~180 kDa protein representing NR2A in rat brain homogenate. It shows no cross-reactivity with NR2B.

Reconstitute with 50 µL of PBS.

Target Information

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.

For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.

Product References

PDI-Mediated Reduction of Disulfide Bond on PSD95 Increases Spontaneous Seizure Activity by Regulating NR2A-PSD95 Interaction in Epileptic Rats Independent of S-Nitrosylation.

International journal of molecular sciences

Lee DS,Kim JE

OPA1-04021 was used in Immunohistochemistry to indicate that PDI-mediated reduction of disulfide-bond formations may facilitate the NR2A-PSD95 binding and contribute to spontaneous seizure generation in epileptic animals.

Wed Mar 18 00:00:00 EDT 2020

PDI-Mediated Reduction of Disulfide Bond on PSD95 Increases Spontaneous Seizure Activity by Regulating NR2A-PSD95 Interaction in Epileptic Rats Independent of S-Nitrosylation.

International journal of molecular sciences

Lee DS,Kim JE

OPA1-04021 was used in Immunohistochemistry to indicate that PDI-mediated reduction of disulfide-bond formations may facilitate the NR2A-PSD95 binding and contribute to spontaneous seizure generation in epileptic animals.

Wed Mar 18 00:00:00 EDT 2020

PDI-Mediated Reduction of Disulfide Bond on PSD95 Increases Spontaneous Seizure Activity by Regulating NR2A-PSD95 Interaction in Epileptic Rats Independent of S-Nitrosylation.

International journal of molecular sciences

Lee DS,Kim JE

OPA1-04021 was used in Immunohistochemistry to indicate that PDI-mediated reduction of disulfide-bond formations may facilitate the NR2A-PSD95 binding and contribute to spontaneous seizure generation in epileptic animals.

Wed Mar 18 00:00:00 EDT 2020

PDI-Mediated Reduction of Disulfide Bond on PSD95 Increases Spontaneous Seizure Activity by Regulating NR2A-PSD95 Interaction in Epileptic Rats Independent of S-Nitrosylation.

International journal of molecular sciences

Lee DS,Kim JE

OPA1-04021 was used in Immunohistochemistry to indicate that PDI-mediated reduction of disulfide-bond formations may facilitate the NR2A-PSD95 binding and contribute to spontaneous seizure generation in epileptic animals.

Wed Mar 18 00:00:00 EDT 2020

PDI-Mediated Reduction of Disulfide Bond on PSD95 Increases Spontaneous Seizure Activity by Regulating NR2A-PSD95 Interaction in Epileptic Rats Independent of S-Nitrosylation.

International journal of molecular sciences

Lee DS,Kim JE

OPA1-04021 was used in Immunohistochemistry to indicate that PDI-mediated reduction of disulfide-bond formations may facilitate the NR2A-PSD95 binding and contribute to spontaneous seizure generation in epileptic animals.

Wed Mar 18 00:00:00 EDT 2020

PDI-Mediated Reduction of Disulfide Bond on PSD95 Increases Spontaneous Seizure Activity by Regulating NR2A-PSD95 Interaction in Epileptic Rats Independent of S-Nitrosylation.

International journal of molecular sciences

Lee DS,Kim JE

OPA1-04021 was used in Immunohistochemistry to indicate that PDI-mediated reduction of disulfide-bond formations may facilitate the NR2A-PSD95 binding and contribute to spontaneous seizure generation in epileptic animals.

Wed Mar 18 00:00:00 EDT 2020

A simple DMSO-based method for cryopreservation of primary hippocampal and cortical neurons.

Journal of neuroscience methods

Ishizuka Y,Bramham CR

OPA1-04021 was used in Western Blot to present a simplified cryopreservation method for rodent primary hippocampal and cortical neurons from embryonic day 18.5 fetuses, using DMSO-containing traditional cell freezing medium.

Sun Mar 01 00:00:00 EST 2020

SorCS2-mediated NR2A trafficking regulates motor deficits in Huntington's disease.

JCI insight

Ma Q,Yang J,Milner TA,Vonsattel JG,Palko ME,Tessarollo L,Hempstead BL

Published figure using NMDAR2A polyclonal antibody (Product # OPA1-04021) in Immunoprecipitation

Thu May 04 00:00:00 EDT 2017

PDI regulates seizure activity via NMDA receptor redox in rats.

Scientific reports

Kim JY,Ko AR,Hyun HW,Min SJ,Kim JE

OPA104021 was used in western blot to show protein disulfide isomerases bind to N-methyl-D-aspartate receptor in the normal hippocampus, and that this binding is increased in chronic epileptic rats

Wed Feb 15 00:00:00 EST 2017

PDI regulates seizure activity via NMDA receptor redox in rats.

Scientific reports

Kim JY,Ko AR,Hyun HW,Min SJ,Kim JE

OPA104021 was used in western blot to show protein disulfide isomerases bind to N-methyl-D-aspartate receptor in the normal hippocampus, and that this binding is increased in chronic epileptic rats

Wed Feb 15 00:00:00 EST 2017

In vivo composition of NMDA receptor signaling complexes differs between membrane subdomains and is modulated by PSD-95 and PSD-93.

The Journal of neuroscience : the official journal of the Society for Neuroscience

Delint-Ramirez I,Fernández E,Bayés A,Kicsi E,Komiyama NH,Grant SG

OPA1-04021 was used in western blot to investigate the composition of NMDAR-PSD-95 complexes in lipid rafts

Wed Jun 16 00:00:00 EDT 2010

Bioinformatics

Protein Aliases: GluN2A; GluRepsilon1; Glutamate [NMDA] receptor subunit epsilon-1; glutamate receptor; Glutamate receptor ionotropic, NMDA 2A; glutamate receptor, ionotropic, N-methyl D-aspartate 2A; hNR2A; 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 2A; NMDAR 2A; NMDAR2A; OTTHUMP00000160135; OTTHUMP00000174531

Gene Aliases: EPND; FESD; GluN2A; GRIN2A; LKS; NMDAR2A; NR2A

UniProt ID: (Human) Q12879, (Mouse) P35436, (Rat) Q00959

Entrez Gene ID: (Human) 2903, (Rabbit) 100337889, (Mouse) 14811, (Rat) 24409

Molecular Function: transmembrane signal receptor

MAPK cascade startle response response to amphetamine transport glutamate receptor signaling pathway chemical synaptic transmission learning or memory memory protein localization visual learning response to wounding sensory perception of pain neurogenesis sleep directional locomotion ionotropic glutamate receptor signaling pathway negative regulation of protein catabolic process dopamine metabolic process serotonin metabolic process response to drug positive regulation of apoptotic process positive regulation of GTPase activity response to ethanol regulation of sensory perception of pain excitatory postsynaptic potential long-term synaptic potentiation calcium ion transmembrane transport positive regulation of long-term synaptic potentiation action potential ion transport cation transport calcium ion transport learning locomotory behavior positive regulation of cell death ion transmembrane transport regulation of ion transmembrane transport synaptic transmission, glutamatergic locomotion regulation of membrane potential regulation of synaptic plasticity regulation of long-term neuronal synaptic plasticity rhythmic process modulation of synaptic transmission detection of mechanical stimulus involved in sensory perception of pain protein tetramerization regulation of postsynaptic membrane potential cellular response to amino acid stimulus cellular response to zinc ion cation transmembrane transport positive regulation of excitatory postsynaptic potential response to light stimulus response to carbohydrate response to manganese ion response to organic cyclic compound response to amine spinal cord development hippocampus development cerebral cortex development response to cocaine response to calcium ion response to methylmercury response to other organism response to ammonium ion response to fungicide cellular response to magnesium ion cellular response to manganese ion cellular response to dsRNA cellular response to growth factor stimulus cellular response to lipid

Process(es)

NMDA glutamate receptor activity Ras guanyl-nucleotide exchange factor activity extracellular-glutamate-gated ion channel activity calcium channel activity protein binding zinc ion binding receptor activity ionotropic glutamate receptor activity receptor binding ion channel activity cation channel activity glutamate binding protein kinase binding voltage-gated cation channel activity protein complex binding glutamate receptor binding neurotransmitter binding metal ion binding protein heterodimerization activity protein dimerization activity cell adhesion molecule binding ATPase binding scaffold protein binding