Review





Similar Products

primary antibodies against gapdh  (Novus Biologicals)
95
Novus Biologicals primary antibodies against gapdh
Expression <t>of</t> <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 <t>GAPDH</t> 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]).
Primary Antibodies Against Gapdh, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/primary antibodies against gapdh/product/Novus Biologicals
Average 95 stars, based on 1 article reviews
primary antibodies against gapdh - by Bioz Stars, 2026-05
95/100 stars
  Buy from Supplier
primary antibodies against gapdh  (Proteintech)
98
Proteintech primary antibodies against gapdh
Expression <t>of</t> <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 <t>GAPDH</t> 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]).
Primary Antibodies Against Gapdh, supplied by Proteintech, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/primary antibodies against gapdh/product/Proteintech
Average 98 stars, based on 1 article reviews
primary antibodies against gapdh - by Bioz Stars, 2026-05
98/100 stars
  Buy from Supplier
primary antibody against gapdh  (Santa Cruz Biotechnology)
97
Santa Cruz Biotechnology primary antibody against gapdh
Expression <t>of</t> <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 <t>GAPDH</t> 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]).
Primary Antibody Against Gapdh, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/primary antibody against gapdh/product/Santa Cruz Biotechnology
Average 97 stars, based on 1 article reviews
primary antibody against gapdh - by Bioz Stars, 2026-05
97/100 stars
  Buy from Supplier
primary antibodies against gapdh  (Cell Signaling Technology Inc)
99
Cell Signaling Technology Inc primary antibodies against gapdh
Untreated Air e −/− mice and Air e −/− mice treated for four weeks with selective JAK1i, JAK2i, or JAK3i were analyzed. Lungs were processed for intracellular cytokine staining, qPCR, ELISA, and immunoblot analyses. ( A-B ) Representative flow cytometry plots showing IFN-γ production by CD4 + and CD8 + T cells. ( C-D ) Frequency (of total CD4 + and CD8 + T cells) and absolute numbers of IFN-γ + CD4 + and IFN-γ + CD8 + T cells in the lung. ( E-F ) Relative Ifng mRNA expression and IFN-γ protein concentrations in lung homogenates. ( G ) <t>Relative</t> <t>Stat1</t> mRNA expression. ( H ) Representative immunoblots of phospho-STAT1 (pSTAT1), total STAT1, and <t>GAPDH.</t> ( I-J ) Quantification of total STAT1 and phospho-STAT1 normalized to GAPDH. For IFN- γ + CD4 + and IFN-γ + CD8 + T cells: n = 9-14 mice per group from four independent experiments. For Ifng and Cxcl9 mRNA: n = 15-22 mice per group from four independent experiments. For Stat1 _mRNA: n = 10-17 mice per group from three independent experiments. For CXCL9 protein: n = 5-10 mice per group from two independent experiments. For STAT1 and pSTAT1 immunoblots: n = 15-22 mice per group from four independent experiments). Statistical analyses were performed using one-way ANOVA or Kruskal-Wallis test with Dunn’s multiple comparisons to the untreated Air e −/− mice. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.
Primary Antibodies Against Gapdh, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/primary antibodies against gapdh/product/Cell Signaling Technology Inc
Average 99 stars, based on 1 article reviews
primary antibodies against gapdh - by Bioz Stars, 2026-05
99/100 stars
  Buy from Supplier
primary antibodies against gapdh  (Huabio Inc)
86
Huabio Inc primary antibodies against gapdh
Untreated Air e −/− mice and Air e −/− mice treated for four weeks with selective JAK1i, JAK2i, or JAK3i were analyzed. Lungs were processed for intracellular cytokine staining, qPCR, ELISA, and immunoblot analyses. ( A-B ) Representative flow cytometry plots showing IFN-γ production by CD4 + and CD8 + T cells. ( C-D ) Frequency (of total CD4 + and CD8 + T cells) and absolute numbers of IFN-γ + CD4 + and IFN-γ + CD8 + T cells in the lung. ( E-F ) Relative Ifng mRNA expression and IFN-γ protein concentrations in lung homogenates. ( G ) <t>Relative</t> <t>Stat1</t> mRNA expression. ( H ) Representative immunoblots of phospho-STAT1 (pSTAT1), total STAT1, and <t>GAPDH.</t> ( I-J ) Quantification of total STAT1 and phospho-STAT1 normalized to GAPDH. For IFN- γ + CD4 + and IFN-γ + CD8 + T cells: n = 9-14 mice per group from four independent experiments. For Ifng and Cxcl9 mRNA: n = 15-22 mice per group from four independent experiments. For Stat1 _mRNA: n = 10-17 mice per group from three independent experiments. For CXCL9 protein: n = 5-10 mice per group from two independent experiments. For STAT1 and pSTAT1 immunoblots: n = 15-22 mice per group from four independent experiments). Statistical analyses were performed using one-way ANOVA or Kruskal-Wallis test with Dunn’s multiple comparisons to the untreated Air e −/− mice. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.
Primary Antibodies Against Gapdh, supplied by Huabio Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/primary antibodies against gapdh/product/Huabio Inc
Average 86 stars, based on 1 article reviews
primary antibodies against gapdh - by Bioz Stars, 2026-05
86/100 stars
  Buy from Supplier
primary antibodies against gapdh  (Santa Cruz Biotechnology)
97
Santa Cruz Biotechnology primary antibodies against gapdh
Untreated Air e −/− mice and Air e −/− mice treated for four weeks with selective JAK1i, JAK2i, or JAK3i were analyzed. Lungs were processed for intracellular cytokine staining, qPCR, ELISA, and immunoblot analyses. ( A-B ) Representative flow cytometry plots showing IFN-γ production by CD4 + and CD8 + T cells. ( C-D ) Frequency (of total CD4 + and CD8 + T cells) and absolute numbers of IFN-γ + CD4 + and IFN-γ + CD8 + T cells in the lung. ( E-F ) Relative Ifng mRNA expression and IFN-γ protein concentrations in lung homogenates. ( G ) <t>Relative</t> <t>Stat1</t> mRNA expression. ( H ) Representative immunoblots of phospho-STAT1 (pSTAT1), total STAT1, and <t>GAPDH.</t> ( I-J ) Quantification of total STAT1 and phospho-STAT1 normalized to GAPDH. For IFN- γ + CD4 + and IFN-γ + CD8 + T cells: n = 9-14 mice per group from four independent experiments. For Ifng and Cxcl9 mRNA: n = 15-22 mice per group from four independent experiments. For Stat1 _mRNA: n = 10-17 mice per group from three independent experiments. For CXCL9 protein: n = 5-10 mice per group from two independent experiments. For STAT1 and pSTAT1 immunoblots: n = 15-22 mice per group from four independent experiments). Statistical analyses were performed using one-way ANOVA or Kruskal-Wallis test with Dunn’s multiple comparisons to the untreated Air e −/− mice. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.
Primary Antibodies Against Gapdh, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/primary antibodies against gapdh/product/Santa Cruz Biotechnology
Average 97 stars, based on 1 article reviews
primary antibodies against gapdh - by Bioz Stars, 2026-05
97/100 stars
  Buy from Supplier

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

Untreated Air e −/− mice and Air e −/− mice treated for four weeks with selective JAK1i, JAK2i, or JAK3i were analyzed. Lungs were processed for intracellular cytokine staining, qPCR, ELISA, and immunoblot analyses. ( A-B ) Representative flow cytometry plots showing IFN-γ production by CD4 + and CD8 + T cells. ( C-D ) Frequency (of total CD4 + and CD8 + T cells) and absolute numbers of IFN-γ + CD4 + and IFN-γ + CD8 + T cells in the lung. ( E-F ) Relative Ifng mRNA expression and IFN-γ protein concentrations in lung homogenates. ( G ) Relative Stat1 mRNA expression. ( H ) Representative immunoblots of phospho-STAT1 (pSTAT1), total STAT1, and GAPDH. ( I-J ) Quantification of total STAT1 and phospho-STAT1 normalized to GAPDH. For IFN- γ + CD4 + and IFN-γ + CD8 + T cells: n = 9-14 mice per group from four independent experiments. For Ifng and Cxcl9 mRNA: n = 15-22 mice per group from four independent experiments. For Stat1 _mRNA: n = 10-17 mice per group from three independent experiments. For CXCL9 protein: n = 5-10 mice per group from two independent experiments. For STAT1 and pSTAT1 immunoblots: n = 15-22 mice per group from four independent experiments). Statistical analyses were performed using one-way ANOVA or Kruskal-Wallis test with Dunn’s multiple comparisons to the untreated Air e −/− mice. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Journal: bioRxiv

Article Title: Selective JAK Inhibition Reveals Paradoxical and Hierarchical Control of interferon-γ-driven Autoimmunity in AIRE Deficiency

doi: 10.64898/2026.03.05.709894

Figure Lengend Snippet: Untreated Air e −/− mice and Air e −/− mice treated for four weeks with selective JAK1i, JAK2i, or JAK3i were analyzed. Lungs were processed for intracellular cytokine staining, qPCR, ELISA, and immunoblot analyses. ( A-B ) Representative flow cytometry plots showing IFN-γ production by CD4 + and CD8 + T cells. ( C-D ) Frequency (of total CD4 + and CD8 + T cells) and absolute numbers of IFN-γ + CD4 + and IFN-γ + CD8 + T cells in the lung. ( E-F ) Relative Ifng mRNA expression and IFN-γ protein concentrations in lung homogenates. ( G ) Relative Stat1 mRNA expression. ( H ) Representative immunoblots of phospho-STAT1 (pSTAT1), total STAT1, and GAPDH. ( I-J ) Quantification of total STAT1 and phospho-STAT1 normalized to GAPDH. For IFN- γ + CD4 + and IFN-γ + CD8 + T cells: n = 9-14 mice per group from four independent experiments. For Ifng and Cxcl9 mRNA: n = 15-22 mice per group from four independent experiments. For Stat1 _mRNA: n = 10-17 mice per group from three independent experiments. For CXCL9 protein: n = 5-10 mice per group from two independent experiments. For STAT1 and pSTAT1 immunoblots: n = 15-22 mice per group from four independent experiments). Statistical analyses were performed using one-way ANOVA or Kruskal-Wallis test with Dunn’s multiple comparisons to the untreated Air e −/− mice. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.

Article Snippet: Primary antibodies against GAPDH (catalog no. 5174S), STAT1 (catalog no. 14995S), and pSTAT1 (catalog no. 9167S) (Cell Signaling Technologies, USA) were used at 1:1,000 dilution, with HRP-conjugated anti-rabbit IgG conjugated with HRP (catalog no.7074S; Cell Signaling Technology) as the secondary antibody.

Techniques: Staining, Enzyme-linked Immunosorbent Assay, Western Blot, Flow Cytometry, Expressing