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mouse anti-glun2a antibody  (Millipore)


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    Structured Review

    Millipore mouse anti-glun2a antibody
    Mouse Anti Glun2a Antibody, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+anti-glun2a/glun2a+antibody/pm37930965-80-47-50
    Average 90 stars, based on 1 article reviews
    mouse anti-glun2a antibody - by Bioz Stars, 2026-10
    90/100 stars

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    other:

    Article Title: miR-146a and miR-200b alter cognition by targeting NMDA receptor subunits
    Article Snippet: The primary antibodies used were: rabbit anti-GluN1 (1:1000, Abcam), rabbit anti-GluN2B (1:1000, Abcam), mouse anti-GluN2A (1:1000, Millipore), mouse anti-GluR1 (1:750, Santacruz), mouse anti-beta actin (1:3000, Sigma) and rabbit anti-NRG1 (1:1000, Santacruz).

    Article Title: Subtype selective NMDA receptor antagonists induce recovery of synapses lost following exposure to HIV-1 Tat.
    Article Snippet: After permeabilization, the cells were incubated with mouse anti-GluN2A (1:200, Chemicon/Millipore, Billerica, MA, USA) or mouse antiGluN2B (1:200, BD Transduction Laboratories, San Jose, CA, USA) in TBS + 0.2% Tween-20 (Sigma) for 1 h at room temperature.

    Article Title: Intracellular zinc signaling influences NMDA receptor function by enhancing the interaction of ZnT1 with GluN2A.
    Article Snippet: Zinc, loaded into glutamate-containing presynaptic vesicles and released into the synapse in an activitydependent manner, modulates neurotransmission through its actions on postsynaptic targets, prominently via high-affinity inhibition of GluN2A-containing NMDA receptors.. Recently, we identified a postsynaptic transport mechanism that regulates endogenous zinc inhibition of NMDARs.. In this new model of zinc regulation, the postsynaptic transporter ZnT1 mediates zinc inhibition of NMDARs by binding to GluN2A.

    Article Title: Subtype selective NMDA receptor antagonists induce recovery of synapses lost following exposure to HIV-1 Tat
    Article Snippet: After permeabilization, the cells were incubated with mouse anti-GluN2A (1:200, Chemicon/Millipore, Billerica, MA, USA) or mouse anti-GluN2B (1:200, BD Transduction Laboratories, San Jose, CA, USA) in TBS + 0.2% Tween-20 (Sigma) for 1 h at room temperature.

    Article Title: Immunohistochemical localization of ionotropic glutamate receptors in the rat red nucleus
    Article Snippet: The sections were incubated in rabbit anti-GluA1 (1:250, AB1504, Chemicon, USA), mouse anti-GluA2 (1:500, MAB 397, Chemicon, USA), mouse anti-GluA3 (1:250, MAB5416, Chemicon, USA), rabbit anti-GluA4 (1:250, AB1508, Chemicon, USA), goat anti-GluK1 (1:250, sc-7617, Santa Cruz, USA) rabbit anti-GluK5 (1:2000, Jennes and Eyigor, R52-4) [ 30 ], and guinea pig anti-GluK2/3 (1:500, Jennes and Eyigor) [ 31 ], mouse anti-GluN1 (1:500, 556308, BD Pharmingen, USA) or mouse anti-GluN2A (1:3000, MAB5216, Millipore, USA) for 48 hours at room temperature.



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    R&D Systems glun2a
    Expression of <t>GluN2A</t> (A) and GluN2B (B) and basal extracellular levels of L‐glutamate (C) and D‐serine (D) in 4‐weeks and 8‐weeks of age S286L‐TG and wild‐type littermate. Ordinates indicate mean ± SD ( n = 6) of (A) expression levels of GluN2A relative to GAPDH in the plasma membrane fraction (B) expression levels of GluN2B relative to GAPDH in the plasma membrane fraction, (C) basal extracellular L‐glutamate level (μM) and (D) basal extracellular D‐serine level (μM) in the frontal cortex of wild‐type (gray column) and S286L‐TG (blue column). The lower‐side panels in A and B indicate pseudo‐gel images of capillary immunoblotting. Circles indicate the values of each individual rat. * p < 0.05, relative to 4‐weeks of age (4 W) and # p < 0.05 relative to wild‐type using two‐way ANOVA with Scheffe's post hoc test. F ‐values were in (A) expression of GluN2A ( F age [1, 20] = 46.7 [ p < 0.05], F genotype [1, 20] = 5.34 [ p < 0.05], F age*genotype [1, 20] = 1.1 [ p > 0.05]), (B) expression of GluN2B ( F age [1, 20] = 22.4 [ p < 0.05], F genotype [1, 20] = 8.3 [ p < 0.05], F age*genotype [1, 20] = 2.0 [ p > 0.05]), (C) L‐glutamate level ( F age [1, 20] = 3.2 [ p > 0.05], F genotype [1, 20] = 21.2 [ p < 0.05], F age*genotype [1, 20] = 1.9 [ p > 0.05]) and (D) D‐serine level ( F age [1, 20] = 8.4 [ p < 0.05], F genotype [1, 20] = 21.6 [ p < 0.05], F age*genotype [1, 20] = 2.8 [ p > 0.05]).
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    Millipore mouse anti-glun2a antibody
    Expression of <t>GluN2A</t> (A) and GluN2B (B) and basal extracellular levels of L‐glutamate (C) and D‐serine (D) in 4‐weeks and 8‐weeks of age S286L‐TG and wild‐type littermate. Ordinates indicate mean ± SD ( n = 6) of (A) expression levels of GluN2A relative to GAPDH in the plasma membrane fraction (B) expression levels of GluN2B relative to GAPDH in the plasma membrane fraction, (C) basal extracellular L‐glutamate level (μM) and (D) basal extracellular D‐serine level (μM) in the frontal cortex of wild‐type (gray column) and S286L‐TG (blue column). The lower‐side panels in A and B indicate pseudo‐gel images of capillary immunoblotting. Circles indicate the values of each individual rat. * p < 0.05, relative to 4‐weeks of age (4 W) and # p < 0.05 relative to wild‐type using two‐way ANOVA with Scheffe's post hoc test. F ‐values were in (A) expression of GluN2A ( F age [1, 20] = 46.7 [ p < 0.05], F genotype [1, 20] = 5.34 [ p < 0.05], F age*genotype [1, 20] = 1.1 [ p > 0.05]), (B) expression of GluN2B ( F age [1, 20] = 22.4 [ p < 0.05], F genotype [1, 20] = 8.3 [ p < 0.05], F age*genotype [1, 20] = 2.0 [ p > 0.05]), (C) L‐glutamate level ( F age [1, 20] = 3.2 [ p > 0.05], F genotype [1, 20] = 21.2 [ p < 0.05], F age*genotype [1, 20] = 1.9 [ p > 0.05]) and (D) D‐serine level ( F age [1, 20] = 8.4 [ p < 0.05], F genotype [1, 20] = 21.6 [ p < 0.05], F age*genotype [1, 20] = 2.8 [ p > 0.05]).
    Mouse Anti Glun2a Antibody, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    NeuroMab mouse anti glun2a
    Expression of <t>GluN2A</t> (A) and GluN2B (B) and basal extracellular levels of L‐glutamate (C) and D‐serine (D) in 4‐weeks and 8‐weeks of age S286L‐TG and wild‐type littermate. Ordinates indicate mean ± SD ( n = 6) of (A) expression levels of GluN2A relative to GAPDH in the plasma membrane fraction (B) expression levels of GluN2B relative to GAPDH in the plasma membrane fraction, (C) basal extracellular L‐glutamate level (μM) and (D) basal extracellular D‐serine level (μM) in the frontal cortex of wild‐type (gray column) and S286L‐TG (blue column). The lower‐side panels in A and B indicate pseudo‐gel images of capillary immunoblotting. Circles indicate the values of each individual rat. * p < 0.05, relative to 4‐weeks of age (4 W) and # p < 0.05 relative to wild‐type using two‐way ANOVA with Scheffe's post hoc test. F ‐values were in (A) expression of GluN2A ( F age [1, 20] = 46.7 [ p < 0.05], F genotype [1, 20] = 5.34 [ p < 0.05], F age*genotype [1, 20] = 1.1 [ p > 0.05]), (B) expression of GluN2B ( F age [1, 20] = 22.4 [ p < 0.05], F genotype [1, 20] = 8.3 [ p < 0.05], F age*genotype [1, 20] = 2.0 [ p > 0.05]), (C) L‐glutamate level ( F age [1, 20] = 3.2 [ p > 0.05], F genotype [1, 20] = 21.2 [ p < 0.05], F age*genotype [1, 20] = 1.9 [ p > 0.05]) and (D) D‐serine level ( F age [1, 20] = 8.4 [ p < 0.05], F genotype [1, 20] = 21.6 [ p < 0.05], F age*genotype [1, 20] = 2.8 [ p > 0.05]).
    Mouse Anti Glun2a, supplied by NeuroMab, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    NeuroMab mouse monoclonal igg2a
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    Millipore mouse anti-glun2a
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    NeuroMab mouse antiglun2a antibody
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    Millipore mouse anti-glun2a h-060-50
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    Image Search Results


    Expression of GluN2A (A) and GluN2B (B) and basal extracellular levels of L‐glutamate (C) and D‐serine (D) in 4‐weeks and 8‐weeks of age S286L‐TG and wild‐type littermate. Ordinates indicate mean ± SD ( n = 6) of (A) expression levels of GluN2A relative to GAPDH in the plasma membrane fraction (B) expression levels of GluN2B relative to GAPDH in the plasma membrane fraction, (C) basal extracellular L‐glutamate level (μM) and (D) basal extracellular D‐serine level (μM) in the frontal cortex of wild‐type (gray column) and S286L‐TG (blue column). The lower‐side panels in A and B indicate pseudo‐gel images of capillary immunoblotting. Circles indicate the values of each individual rat. * p < 0.05, relative to 4‐weeks of age (4 W) and # p < 0.05 relative to wild‐type using two‐way ANOVA with Scheffe's post hoc test. F ‐values were in (A) expression of GluN2A ( F age [1, 20] = 46.7 [ p < 0.05], F genotype [1, 20] = 5.34 [ p < 0.05], F age*genotype [1, 20] = 1.1 [ p > 0.05]), (B) expression of GluN2B ( F age [1, 20] = 22.4 [ p < 0.05], F genotype [1, 20] = 8.3 [ p < 0.05], F age*genotype [1, 20] = 2.0 [ p > 0.05]), (C) L‐glutamate level ( F age [1, 20] = 3.2 [ p > 0.05], F genotype [1, 20] = 21.2 [ p < 0.05], F age*genotype [1, 20] = 1.9 [ p > 0.05]) and (D) D‐serine level ( F age [1, 20] = 8.4 [ p < 0.05], F genotype [1, 20] = 21.6 [ p < 0.05], F age*genotype [1, 20] = 2.8 [ p > 0.05]).

    Journal: Pharmacology Research & Perspectives

    Article Title: Combined Inhibition of TRPM 4/ NMDA Receptor Complex and Extrasynaptic NMDA Receptors Is Candidate Therapeutic Target for Suppression of Epileptic Seizures and Improvement of Cognitive Impairments

    doi: 10.1002/prp2.70256

    Figure Lengend Snippet: Expression of GluN2A (A) and GluN2B (B) and basal extracellular levels of L‐glutamate (C) and D‐serine (D) in 4‐weeks and 8‐weeks of age S286L‐TG and wild‐type littermate. Ordinates indicate mean ± SD ( n = 6) of (A) expression levels of GluN2A relative to GAPDH in the plasma membrane fraction (B) expression levels of GluN2B relative to GAPDH in the plasma membrane fraction, (C) basal extracellular L‐glutamate level (μM) and (D) basal extracellular D‐serine level (μM) in the frontal cortex of wild‐type (gray column) and S286L‐TG (blue column). The lower‐side panels in A and B indicate pseudo‐gel images of capillary immunoblotting. Circles indicate the values of each individual rat. * p < 0.05, relative to 4‐weeks of age (4 W) and # p < 0.05 relative to wild‐type using two‐way ANOVA with Scheffe's post hoc test. F ‐values were in (A) expression of GluN2A ( F age [1, 20] = 46.7 [ p < 0.05], F genotype [1, 20] = 5.34 [ p < 0.05], F age*genotype [1, 20] = 1.1 [ p > 0.05]), (B) expression of GluN2B ( F age [1, 20] = 22.4 [ p < 0.05], F genotype [1, 20] = 8.3 [ p < 0.05], F age*genotype [1, 20] = 2.0 [ p > 0.05]), (C) L‐glutamate level ( F age [1, 20] = 3.2 [ p > 0.05], F genotype [1, 20] = 21.2 [ p < 0.05], F age*genotype [1, 20] = 1.9 [ p > 0.05]) and (D) D‐serine level ( F age [1, 20] = 8.4 [ p < 0.05], F genotype [1, 20] = 21.6 [ p < 0.05], F age*genotype [1, 20] = 2.8 [ p > 0.05]).

    Article Snippet: Primary antibodies against GAPDH (NB300‐327, RRID:AB_10001915, 1:300; Novus Biologicals, Littleton, CO, USA), GluN2A (PPS012, RRID:AB_2112297, 1:100, R&D Systems, Minneapolis, MN, USA), GluN2B (PPS013, RRID:AB_562667, 1:100, R&D Systems), cAMP response element binding protein (CREB) (#4820, 1:50, Cell Signaling Technology, Danvers, MA, USA), and pCREB (#9198, 1:50, Cell Signaling) were used.

    Techniques: Expressing, Clinical Proteomics, Membrane, Western Blot

    Effects of chronic administration of probenecid, MK‐801, memantine, and FP802 on expression of GluN2A and GluN2B in S286L‐TG and wild‐type littermates. All rats were chronically administered by vehicle (control), probenecid (PBN: 100 mg/kg/day), MK‐801 (0.1 mg/kg/day), memantine (MEM: 10 mg/kg/day) and FP802 (40 mg/kg/day) for 2‐weeks (from 6‐weeks to 8‐weeks of age). Ordinates indicate mean ± SD ( n = 6) of expression levels of GluN2A (A1‐A4) and GluN2B (B1‐B4) relative to GAPDH in wild‐type (A1‐A2, B1‐B2) and S286L‐TG (A3‐A4, B3‐B4). The right‐side panels indicate pseudo‐gel images of capillary immunoblotting. Circles indicate the values of each individual rat. * p < 0.05, relative to control using one‐way ANOVA with Scheffe's post hoc test. F ‐values regarding effects of probenecid and MK‐801 on GluN2A expression in wild‐type (A1) ( F [2, 15] = 7.8 [ p < 0.05]), GluN2A in S286L (A3) ( F [2, 15] = 19.4 [ p < 0.05]), GluN2B in wild‐type (B1) ( F [2, 15] = 12.1 [ p < 0.05]) and GluN2B in S286L‐TG (B3) ( F [2, 15] = 18.2 [ p < 0.05]). F ‐values regarding effects of memantine and FP802 on GluN2A in wild‐type (A2) ( F [2, 15] = 0.4 [ p > 0.05]), GluN2A in S286L‐TG (A4) ( F [2, 15] = 7.1 [ p < 0.05]), GluN2B in wild‐type (B2) ( F [2, 15] = 0.2 [ p > 0.05]) and GluN2B in S286L‐TG (B4) ( F [2, 15] = 4.8 [ p < 0.05]).

    Journal: Pharmacology Research & Perspectives

    Article Title: Combined Inhibition of TRPM 4/ NMDA Receptor Complex and Extrasynaptic NMDA Receptors Is Candidate Therapeutic Target for Suppression of Epileptic Seizures and Improvement of Cognitive Impairments

    doi: 10.1002/prp2.70256

    Figure Lengend Snippet: Effects of chronic administration of probenecid, MK‐801, memantine, and FP802 on expression of GluN2A and GluN2B in S286L‐TG and wild‐type littermates. All rats were chronically administered by vehicle (control), probenecid (PBN: 100 mg/kg/day), MK‐801 (0.1 mg/kg/day), memantine (MEM: 10 mg/kg/day) and FP802 (40 mg/kg/day) for 2‐weeks (from 6‐weeks to 8‐weeks of age). Ordinates indicate mean ± SD ( n = 6) of expression levels of GluN2A (A1‐A4) and GluN2B (B1‐B4) relative to GAPDH in wild‐type (A1‐A2, B1‐B2) and S286L‐TG (A3‐A4, B3‐B4). The right‐side panels indicate pseudo‐gel images of capillary immunoblotting. Circles indicate the values of each individual rat. * p < 0.05, relative to control using one‐way ANOVA with Scheffe's post hoc test. F ‐values regarding effects of probenecid and MK‐801 on GluN2A expression in wild‐type (A1) ( F [2, 15] = 7.8 [ p < 0.05]), GluN2A in S286L (A3) ( F [2, 15] = 19.4 [ p < 0.05]), GluN2B in wild‐type (B1) ( F [2, 15] = 12.1 [ p < 0.05]) and GluN2B in S286L‐TG (B3) ( F [2, 15] = 18.2 [ p < 0.05]). F ‐values regarding effects of memantine and FP802 on GluN2A in wild‐type (A2) ( F [2, 15] = 0.4 [ p > 0.05]), GluN2A in S286L‐TG (A4) ( F [2, 15] = 7.1 [ p < 0.05]), GluN2B in wild‐type (B2) ( F [2, 15] = 0.2 [ p > 0.05]) and GluN2B in S286L‐TG (B4) ( F [2, 15] = 4.8 [ p < 0.05]).

    Article Snippet: Primary antibodies against GAPDH (NB300‐327, RRID:AB_10001915, 1:300; Novus Biologicals, Littleton, CO, USA), GluN2A (PPS012, RRID:AB_2112297, 1:100, R&D Systems, Minneapolis, MN, USA), GluN2B (PPS013, RRID:AB_562667, 1:100, R&D Systems), cAMP response element binding protein (CREB) (#4820, 1:50, Cell Signaling Technology, Danvers, MA, USA), and pCREB (#9198, 1:50, Cell Signaling) were used.

    Techniques: Expressing, Control, Western Blot

    Effects of chronic combined administration of memantine with FP802 on ADSHE seizure frequency (A), sucrose preference (B), expression of GluN2A (C1) and GluN2B (C2), and basal extracellular levels of L‐glutamate (D) and D‐serine (E) in S286L‐TG and wild‐type littermate. All rats were chronically administered by vehicle (control) and combined of memantine (MEM: 10 mg/kg/day) with FP802 (40 mg/kg/day) for 2‐weeks (from 6‐weeks to 8‐weeks of age). Ordinates indicate mean ± SD ( n = 6) of (A) ADSHE seizure frequency (count h −1 ), (B) consumption of sucrose preference (%), (C1) expression levels of GluN2A relative to GAPDH, (C2) expression levels of GluN2B relative to GAPDH, (D) basal extracellular L‐glutamate level (μM) and (E) basal extracellular D‐serine level (μM). The right‐side panels in C1‐C2 indicate pseudo‐gel images of capillary immunoblotting. Circles indicate the values of each individual rat. * p < 0.05, relative to control and # p < 0.05 relative to wild‐type using student T ‐test or one‐way or two‐way ANOVA with Scheffe's post hoc test. F ‐values were in (B) sucrose preference: MEM ( F memantine+FP802 [1, 20] = 21.3 [ p < 0.05], F genotype [1, 20] = 5.1 [ p < 0.05], F rmemantine+FP802*genotype [1, 20] = 5.3 [ p < 0.05]), (D) L‐glutamate level: ( F memantine+FP802 [1, 20] = 5.3 [ p < 0.05], F genotype [1, 20] = 15.9 [ p < 0.05], F rmemantine+FP802*genotype [1, 20] = 4.8 [ p < 0.05]), (E) D‐serine level: ( F memantine+FP802 [1, 20] = 7.6 [ p < 0.05], F genotype [1, 20] = 22.4 [ p < 0.05], F rmemantine+FP802*genotype [1, 20] = 10.4 [ p < 0.05]).

    Journal: Pharmacology Research & Perspectives

    Article Title: Combined Inhibition of TRPM 4/ NMDA Receptor Complex and Extrasynaptic NMDA Receptors Is Candidate Therapeutic Target for Suppression of Epileptic Seizures and Improvement of Cognitive Impairments

    doi: 10.1002/prp2.70256

    Figure Lengend Snippet: Effects of chronic combined administration of memantine with FP802 on ADSHE seizure frequency (A), sucrose preference (B), expression of GluN2A (C1) and GluN2B (C2), and basal extracellular levels of L‐glutamate (D) and D‐serine (E) in S286L‐TG and wild‐type littermate. All rats were chronically administered by vehicle (control) and combined of memantine (MEM: 10 mg/kg/day) with FP802 (40 mg/kg/day) for 2‐weeks (from 6‐weeks to 8‐weeks of age). Ordinates indicate mean ± SD ( n = 6) of (A) ADSHE seizure frequency (count h −1 ), (B) consumption of sucrose preference (%), (C1) expression levels of GluN2A relative to GAPDH, (C2) expression levels of GluN2B relative to GAPDH, (D) basal extracellular L‐glutamate level (μM) and (E) basal extracellular D‐serine level (μM). The right‐side panels in C1‐C2 indicate pseudo‐gel images of capillary immunoblotting. Circles indicate the values of each individual rat. * p < 0.05, relative to control and # p < 0.05 relative to wild‐type using student T ‐test or one‐way or two‐way ANOVA with Scheffe's post hoc test. F ‐values were in (B) sucrose preference: MEM ( F memantine+FP802 [1, 20] = 21.3 [ p < 0.05], F genotype [1, 20] = 5.1 [ p < 0.05], F rmemantine+FP802*genotype [1, 20] = 5.3 [ p < 0.05]), (D) L‐glutamate level: ( F memantine+FP802 [1, 20] = 5.3 [ p < 0.05], F genotype [1, 20] = 15.9 [ p < 0.05], F rmemantine+FP802*genotype [1, 20] = 4.8 [ p < 0.05]), (E) D‐serine level: ( F memantine+FP802 [1, 20] = 7.6 [ p < 0.05], F genotype [1, 20] = 22.4 [ p < 0.05], F rmemantine+FP802*genotype [1, 20] = 10.4 [ p < 0.05]).

    Article Snippet: Primary antibodies against GAPDH (NB300‐327, RRID:AB_10001915, 1:300; Novus Biologicals, Littleton, CO, USA), GluN2A (PPS012, RRID:AB_2112297, 1:100, R&D Systems, Minneapolis, MN, USA), GluN2B (PPS013, RRID:AB_562667, 1:100, R&D Systems), cAMP response element binding protein (CREB) (#4820, 1:50, Cell Signaling Technology, Danvers, MA, USA), and pCREB (#9198, 1:50, Cell Signaling) were used.

    Techniques: Expressing, Control, Western Blot

    Key resources table

    Journal: Cell reports

    Article Title: A synaptic molecular dependency network revealed by knockdown of autism- and schizophrenia-associated genes

    doi: 10.1016/j.celrep.2023.112430

    Figure Lengend Snippet: Key resources table

    Article Snippet: anti-NR2A, mouse monoclonal IgG2a , Neuromab , Cat#75–288 Clone: N327/95.

    Techniques: Recombinant, Gene Expression, Modification, Imaging, Software