glun2b (Proteintech)
Proteintech is a verified supplier 
96
Structured Review
Proteintech
glun2b
Glun2b, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 158 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/glun2b/product/Proteintech
Average 96 stars, based on 158 article reviews
Glun2b, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 158 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/glun2b/product/Proteintech
Average 96 stars, based on 158 article reviews
glun2b - by Bioz Stars,
2026-06
96/100 stars
Images
1) Product Images from "HMGCS2-dependent β-OHB/H3K9bhb ameliorates synaptic plasticity and cognition in Alzheimer’s disease"
Article Title: HMGCS2-dependent β-OHB/H3K9bhb ameliorates synaptic plasticity and cognition in Alzheimer’s disease
Journal: Experimental & Molecular Medicine
doi: 10.1038/s12276-026-01664-9
Figure Legend Snippet: a , b , The representative immunoblots ( a ) and quantitative analyses ( b ) of Glun1, Glun2A, Glun2B and Syn1 in the hippocampus of the WT, 3xTg-AD and 3xTg-AD+β-OHB mice, n = 4 per group. c , RT–qPCR assays mRNA expression of the Glun1, Glun2A, Glun2B and Syn1 in the hippocampus of the WT, 3xTg-AD and 3xTg-AD+β-OHB mice, n = 5 per group. d , ChIP–qPCR analysis of the enrichment of H3K9bhb at Glun1, Glun2A, Glun2B, Glun2C and Syn1 promoters in the hippocampus of the WT, 3xTg-AD and 3xTg-AD+β-OHB mice, n = 5 per group. e , f , Supplementing with β-OHB could increase the density of 3xTg-AD dendritic spines detected by Golgi-cox staining; the representative images ( e ) and quantitative analysis ( f ) of spine, n = 5 per group, three fields per mice. Scale bar, 5 μm. g – j , The Sholl analysis showed the synaptic complexity of neurons after supplementing with β-OHB in 3xTg-AD mice; the representative images ( g and i ) and the quantitative analysis ( h and j ), n = 5 per group, two fields per mice. Scale bar, 50 μm. Data are shown as mean ± s.e.m. One-way ANOVA followed by Bonferroni’s post hoc test for b – d and f . Two-way ANOVA followed by Bonferroni’s post hoc test for i and k . * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001; ns, not significant.
Techniques Used: Western Blot, Quantitative RT-PCR, Expressing, ChIP-qPCR, Staining
Figure Legend Snippet: a – c , The HMGCS2 upregulation promotes the protein ( a and b ) and mRNA ( c ) expression of H3K9bhb, Glun1, Glun2A, Glun2B, Syn1 and PSD95, n = 4 or 5 per group. d , e , ChIP–qPCR analyses of the enrichment of H3K9bhb at Glun1, Glun2A, Glun2B and Syn1 promoters in the primary neurons of the WT, 3xTg-AD and 3xTg-AD + HMGCS2 mice n = 5 per group ( d ) and representative gel images from ChIP–qPCR assays ( e ). f – j , The HMGCS2 upregulation promotes the expression of Syn1 (scale bar, 25 μm) ( f ); n = 10 cells per group in MAP2 immunofluorescence ( g ) and quantitative analysis ( h ), n = 10 cells per group and SYP ( i and j ), n = 10 cells per group, scale bar, 15 μm. Data are shown as mean ± s.e.m. One-way ANOVA followed by Bonferroni’s post hoc test for b – d and j . Two-way ANOVA followed by Bonferroni’s post hoc test for h . * P < 0.05, ** P < 0.01 , *** P < 0.001, **** P < 0.0001; ns, not significant.
Techniques Used: Expressing, ChIP-qPCR, Immunofluorescence
Figure Legend Snippet: a , b , A western blot analysis ( a ) of hippocampal lysates shows that HMGCS2 upregulation increases the protein levels ( b ) of H3K9bhb, Glun1, Glun2A, Glun2B, Syn1 and PSD95, n = 3 per group. c , The ChIP–qPCR analysis of H3K9bhb enrichment at the promoters of Glun2A , Glun2B , Syn1 and PSD95 in the four groups, n = 5 per group. d , The mRNA levels of Glun1, Glun2A, Glun2B, Syn1 and PSD95 in the hippocampus, as determined by RT–qPCR, n = 5 per group. e , f , Golgi staining reveals increased dendritic spine density in 3xTg-AD mice following overexpression of HMGCS2; representative images ( e ) and quantification ( f ) are shown, n = 5 per group, three fields per mice. Scale bar, 5 μm. g – j , A behavioral assessment of spatial learning and memory using the MWM, NOR and contextual fear conditioning tests: area under the curve (AUC) of escape latency during MWM training of day 1–6 ( g ), escape latency on day 7 of the MWM test ( h ), NOR discrimination index ( i ), freezing time on day 7 in the contextual fear conditioning test ( j ), n = 8 per group. Data are shown as mean ± s.e.m. One-way ANOVA followed by Bonferroni’s post hoc test for b – d , f and g – j . * P < 0.05, ** P < 0.01 , *** P < 0.001, **** P < 0.0001; ns, not significant.
Techniques Used: Western Blot, ChIP-qPCR, Quantitative RT-PCR, Staining, Over Expression
![Expression of GluN2A (A) and <t>GluN2B</t> (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)