anti glun2a (Alomone Labs)
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anti glun2a
Anti Glun2a, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 29 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+glun2a/Anti-NMDAR2A+(GluN2A)+(extracellular)+Antibody/pmc12802853-251-13-15
Average 94 stars, based on 29 article reviews
Anti Glun2a, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 94/100, based on 29 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+glun2a/Anti-NMDAR2A+(GluN2A)+(extracellular)+Antibody/pmc12802853-251-13-15
Average 94 stars, based on 29 article reviews
anti glun2a - by Bioz Stars,
2026-10
94/100 stars
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other:Article Title: eNOS-dependent S-nitrosylation of the NF-κB subunit p65 has neuroprotective effects. Article Snippet: Anti-phospho-p65 was obtained from Cell signaling (Cat. No.: 3033) (Danvers, MA, USA), Anti-MAP2A/2B was obtained from Millipore (Cat. No.: MAB378) (Burlington, MA, USA), Anti-GFAP was obtained from US Biological (Cat. No.: G2032-28B-PE) (Swampscott, MA, USA), AntiβIII tubulin was obtained from Promega (Cat. No.: G712A) (Madison, WI, USA), In Vivo:Article Title: Synaptic rearrangement of NMDA receptors controls memory engram formation and malleability in the cortex Article Snippet: Prevention of NMDAR surface redistributions was achieved using an antibody-based x-link strategy in which cultured hippocampal neurons were exposed for 30 min to high concentrations (0.08 mg/ml) of rabbit polyclonal immunoglobulins directed against extracellular epitopes of GluN2B subunits (RRID:AB_2040028; catalog number: AGC-003, Alomone Labs; epitopes corresponding to residues 323-337 of the GluN2B subunit, Jerusalem, Israel) to aggregate the receptors and limit their movements within the membrane plane, as previously described and figs. S17 to S21) ( ). .. The same strategy was also applied in vivo by injecting 0.8 μl of anti-GluN2B same as above) or Article Title: Synaptic rearrangement of NMDA receptors controls memory engram formation and malleability in the cortex. Article Snippet: Antibody- based x- link of NMDARs Prevention of NMDAR surface redistributions was achieved using an antibody- based x- link strategy in which cultured hippocampal neurons were exposed for 30 min to high concentrations (0.08 mg/ ml) of rabbit polyclonal immunoglobulins directed against extracellular epitopes of GluN2B subunits (RRID:AB_2040028; catalog number: AGC- 003, Alomone Labs; epitopes corresponding to residues 323- 337 of the GluN2B subunit, Jerusalem, Israel) to aggregate the receptors and limit their movements within the membrane plane, as previously described Fig. 6 and figs. S17 to S21) (20). .. The same strategy was also applied in vivo by injecting 0.8 μl of antiGluN2B same as above) or Western Blot:Article Title: Cryo-EM of autoantibody-bound NMDA receptors reveals antigenic hotspots in an active immunization model of anti-NMDAR encephalitis. Article Snippet: .. Immunoblotting was performed using the following primary antibodies: anti- GluN1 (1:600; Alomone Labs, AGC- 001), Article Title: Cryo-EM of autoantibody-bound NMDA receptors reveals antigenic hotspots in an active immunization model of anti-NMDAR encephalitis Article Snippet: .. Immunoblotting was performed using the following primary antibodies: anti-GluN1 (1:600; Alomone Labs, AGC-001), Incubation:Article Title: RAGE signaling is required for AMPA receptor dysfunction in the hippocampus of hyperglycemic mice. Article Snippet: Diabetes in humans has been associated for a long time with cognitive dysfunction.. In rodent animal models, cognitive dysfunction can manifest as impaired hippocampal synaptic plasticity.. Particular attention has been concentrated on the receptor for advanced glycation end products (RAGE), which is implicated in multiple diabetic complications involving the development of vascular and peripheral nerve abnormalities. Control:Article Title: RAGE signaling is required for AMPA receptor dysfunction in the hippocampus of hyperglycemic mice. Article Snippet: Diabetes in humans has been associated for a long time with cognitive dysfunction.. In rodent animal models, cognitive dysfunction can manifest as impaired hippocampal synaptic plasticity.. Particular attention has been concentrated on the receptor for advanced glycation end products (RAGE), which is implicated in multiple diabetic complications involving the development of vascular and peripheral nerve abnormalities. Saline:Article Title: RAGE signaling is required for AMPA receptor dysfunction in the hippocampus of hyperglycemic mice. Article Snippet: Diabetes in humans has been associated for a long time with cognitive dysfunction.. In rodent animal models, cognitive dysfunction can manifest as impaired hippocampal synaptic plasticity.. Particular attention has been concentrated on the receptor for advanced glycation end products (RAGE), which is implicated in multiple diabetic complications involving the development of vascular and peripheral nerve abnormalities. |
![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]).](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_9079/pmc13109079/pmc13109079__PRP2-14-e70256-g002.jpg)
![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]).](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_9079/pmc13109079/pmc13109079__PRP2-14-e70256-g003.jpg)
![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]).](https://pub-med-central-images-cdn.bioz.com/pub_med_central_ids_ending_with_9079/pmc13109079/pmc13109079__PRP2-14-e70256-g007.jpg)
