postsynaptic ampa receptor glua2 Search Results


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A single ECS but not chronic ECS increases the level of Tyr 876 -phosphorylated <t>GluA2</t> in the hippocampus. Immunoblot analysis for phosphorylation of GluA2 at Tyr 876 (Y 876 ) or 3Tyr (3Y: Tyr 869 , Tyr 873 , and Tyr 876 ) and total GluA2 expression in the hippocampal crude membrane (P2) fraction following a single ECS ( n = 5 rats per time point) (a–c) and chronic ECS ( n = 5 rats for 72 h time point and n = 6 rats per all other time points) (d–f). The ratio of the phosphorylated GluA2 band intensity over the β -actin band intensity (a-b, d-e) and the ratio of total GluA2 band intensity over the β -actin band intensity (c, f) were calculated per each time point and normalized to that of “no seizure” (NS) sham group. Data shown represent the mean band intensity ± SEM. (a–c) A single ECS increases the level of Tyr 876 -phosphorylated GluA2 at 96 h time point ((b) ∗ p < 0.05) but does not alter the level of 3Tyr-phosphorylated GluA2 and total GluA2. (d–f) Chronic ECS does not change Tyr-phosphorylation of GluA2 (d-e) and total GluA2 expression (f).
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Boster Bio rabbit polyclonal anti glur2
A single ECS but not chronic ECS increases the level of Tyr 876 -phosphorylated <t>GluA2</t> in the hippocampus. Immunoblot analysis for phosphorylation of GluA2 at Tyr 876 (Y 876 ) or 3Tyr (3Y: Tyr 869 , Tyr 873 , and Tyr 876 ) and total GluA2 expression in the hippocampal crude membrane (P2) fraction following a single ECS ( n = 5 rats per time point) (a–c) and chronic ECS ( n = 5 rats for 72 h time point and n = 6 rats per all other time points) (d–f). The ratio of the phosphorylated GluA2 band intensity over the β -actin band intensity (a-b, d-e) and the ratio of total GluA2 band intensity over the β -actin band intensity (c, f) were calculated per each time point and normalized to that of “no seizure” (NS) sham group. Data shown represent the mean band intensity ± SEM. (a–c) A single ECS increases the level of Tyr 876 -phosphorylated GluA2 at 96 h time point ((b) ∗ p < 0.05) but does not alter the level of 3Tyr-phosphorylated GluA2 and total GluA2. (d–f) Chronic ECS does not change Tyr-phosphorylation of GluA2 (d-e) and total GluA2 expression (f).
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Thermo Fisher gene exp gria2 rn00568514 m1
A single ECS but not chronic ECS increases the level of Tyr 876 -phosphorylated <t>GluA2</t> in the hippocampus. Immunoblot analysis for phosphorylation of GluA2 at Tyr 876 (Y 876 ) or 3Tyr (3Y: Tyr 869 , Tyr 873 , and Tyr 876 ) and total GluA2 expression in the hippocampal crude membrane (P2) fraction following a single ECS ( n = 5 rats per time point) (a–c) and chronic ECS ( n = 5 rats for 72 h time point and n = 6 rats per all other time points) (d–f). The ratio of the phosphorylated GluA2 band intensity over the β -actin band intensity (a-b, d-e) and the ratio of total GluA2 band intensity over the β -actin band intensity (c, f) were calculated per each time point and normalized to that of “no seizure” (NS) sham group. Data shown represent the mean band intensity ± SEM. (a–c) A single ECS increases the level of Tyr 876 -phosphorylated GluA2 at 96 h time point ((b) ∗ p < 0.05) but does not alter the level of 3Tyr-phosphorylated GluA2 and total GluA2. (d–f) Chronic ECS does not change Tyr-phosphorylation of GluA2 (d-e) and total GluA2 expression (f).
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Cell Signaling Technology Inc anti glua2
A single ECS but not chronic ECS increases the level of Tyr 876 -phosphorylated <t>GluA2</t> in the hippocampus. Immunoblot analysis for phosphorylation of GluA2 at Tyr 876 (Y 876 ) or 3Tyr (3Y: Tyr 869 , Tyr 873 , and Tyr 876 ) and total GluA2 expression in the hippocampal crude membrane (P2) fraction following a single ECS ( n = 5 rats per time point) (a–c) and chronic ECS ( n = 5 rats for 72 h time point and n = 6 rats per all other time points) (d–f). The ratio of the phosphorylated GluA2 band intensity over the β -actin band intensity (a-b, d-e) and the ratio of total GluA2 band intensity over the β -actin band intensity (c, f) were calculated per each time point and normalized to that of “no seizure” (NS) sham group. Data shown represent the mean band intensity ± SEM. (a–c) A single ECS increases the level of Tyr 876 -phosphorylated GluA2 at 96 h time point ((b) ∗ p < 0.05) but does not alter the level of 3Tyr-phosphorylated GluA2 and total GluA2. (d–f) Chronic ECS does not change Tyr-phosphorylation of GluA2 (d-e) and total GluA2 expression (f).
Anti Glua2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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A single ECS but not chronic ECS increases the level of Tyr 876 -phosphorylated <t>GluA2</t> in the hippocampus. Immunoblot analysis for phosphorylation of GluA2 at Tyr 876 (Y 876 ) or 3Tyr (3Y: Tyr 869 , Tyr 873 , and Tyr 876 ) and total GluA2 expression in the hippocampal crude membrane (P2) fraction following a single ECS ( n = 5 rats per time point) (a–c) and chronic ECS ( n = 5 rats for 72 h time point and n = 6 rats per all other time points) (d–f). The ratio of the phosphorylated GluA2 band intensity over the β -actin band intensity (a-b, d-e) and the ratio of total GluA2 band intensity over the β -actin band intensity (c, f) were calculated per each time point and normalized to that of “no seizure” (NS) sham group. Data shown represent the mean band intensity ± SEM. (a–c) A single ECS increases the level of Tyr 876 -phosphorylated GluA2 at 96 h time point ((b) ∗ p < 0.05) but does not alter the level of 3Tyr-phosphorylated GluA2 and total GluA2. (d–f) Chronic ECS does not change Tyr-phosphorylation of GluA2 (d-e) and total GluA2 expression (f).
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Cell Signaling Technology Inc p gria2 y869 873 876
Effects of PDI knockdown on PP2A bindings to PDI and <t>GluA2</t> in the hippocampus following KA injection. KA increases PDI:PP2A and GluA2:PP2A bindings in control siRNA-infused animals, but not in PDI siRNA-infused animals. ( a ) Representative Western blot images for the PDI:PP2A and GluA2:PP2A bindings. ( b – c ) Quantitative analyses of the effects of PDI siRNA on PP2A level ( b ) and PDI:PP2A binding ( c ) following KA injection (*, # p < 0.05 vs. control siRNA vs. saline; n = 7, respectively; Kruskal–Wallis test followed by Tukey post-hoc test).
P Gria2 Y869 873 876, supplied by Cell Signaling Technology Inc, 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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Thermo Fisher gene exp gria2 hs00181331 m1
Effects of PDI knockdown on PP2A bindings to PDI and <t>GluA2</t> in the hippocampus following KA injection. KA increases PDI:PP2A and GluA2:PP2A bindings in control siRNA-infused animals, but not in PDI siRNA-infused animals. ( a ) Representative Western blot images for the PDI:PP2A and GluA2:PP2A bindings. ( b – c ) Quantitative analyses of the effects of PDI siRNA on PP2A level ( b ) and PDI:PP2A binding ( c ) following KA injection (*, # p < 0.05 vs. control siRNA vs. saline; n = 7, respectively; Kruskal–Wallis test followed by Tukey post-hoc test).
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Cell Signaling Technology Inc ampa receptor (glutamate receptors glur2/glur3/glur4) antibody
Effects of PDI knockdown on PP2A bindings to PDI and <t>GluA2</t> in the hippocampus following KA injection. KA increases PDI:PP2A and GluA2:PP2A bindings in control siRNA-infused animals, but not in PDI siRNA-infused animals. ( a ) Representative Western blot images for the PDI:PP2A and GluA2:PP2A bindings. ( b – c ) Quantitative analyses of the effects of PDI siRNA on PP2A level ( b ) and PDI:PP2A binding ( c ) following KA injection (*, # p < 0.05 vs. control siRNA vs. saline; n = 7, respectively; Kruskal–Wallis test followed by Tukey post-hoc test).
Ampa Receptor (Glutamate Receptors Glur2/Glur3/Glur4) Antibody, supplied by Cell Signaling Technology Inc, 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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Image Search Results


A single ECS but not chronic ECS increases the level of Tyr 876 -phosphorylated GluA2 in the hippocampus. Immunoblot analysis for phosphorylation of GluA2 at Tyr 876 (Y 876 ) or 3Tyr (3Y: Tyr 869 , Tyr 873 , and Tyr 876 ) and total GluA2 expression in the hippocampal crude membrane (P2) fraction following a single ECS ( n = 5 rats per time point) (a–c) and chronic ECS ( n = 5 rats for 72 h time point and n = 6 rats per all other time points) (d–f). The ratio of the phosphorylated GluA2 band intensity over the β -actin band intensity (a-b, d-e) and the ratio of total GluA2 band intensity over the β -actin band intensity (c, f) were calculated per each time point and normalized to that of “no seizure” (NS) sham group. Data shown represent the mean band intensity ± SEM. (a–c) A single ECS increases the level of Tyr 876 -phosphorylated GluA2 at 96 h time point ((b) ∗ p < 0.05) but does not alter the level of 3Tyr-phosphorylated GluA2 and total GluA2. (d–f) Chronic ECS does not change Tyr-phosphorylation of GluA2 (d-e) and total GluA2 expression (f).

Journal: Neural Plasticity

Article Title: Seizure-Induced Regulations of Amyloid- β , STEP 61 , and STEP 61 Substrates Involved in Hippocampal Synaptic Plasticity

doi: 10.1155/2016/2123748

Figure Lengend Snippet: A single ECS but not chronic ECS increases the level of Tyr 876 -phosphorylated GluA2 in the hippocampus. Immunoblot analysis for phosphorylation of GluA2 at Tyr 876 (Y 876 ) or 3Tyr (3Y: Tyr 869 , Tyr 873 , and Tyr 876 ) and total GluA2 expression in the hippocampal crude membrane (P2) fraction following a single ECS ( n = 5 rats per time point) (a–c) and chronic ECS ( n = 5 rats for 72 h time point and n = 6 rats per all other time points) (d–f). The ratio of the phosphorylated GluA2 band intensity over the β -actin band intensity (a-b, d-e) and the ratio of total GluA2 band intensity over the β -actin band intensity (c, f) were calculated per each time point and normalized to that of “no seizure” (NS) sham group. Data shown represent the mean band intensity ± SEM. (a–c) A single ECS increases the level of Tyr 876 -phosphorylated GluA2 at 96 h time point ((b) ∗ p < 0.05) but does not alter the level of 3Tyr-phosphorylated GluA2 and total GluA2. (d–f) Chronic ECS does not change Tyr-phosphorylation of GluA2 (d-e) and total GluA2 expression (f).

Article Snippet: Phosphorylation site specific antibodies used include anti-GluN2B-pTyr 1472 which recognizes phosphorylated Tyr-1472 of GluN2B (P1516-1472, PhosphoSolutions), anti-ERK1/2-pThr 202 /Tyr 204 which recognizes phosphorylated Thr 202 /Tyr 204 of ERK1 and Thr 185 /Tyr 187 of ERK2 (#9106, Cell Signaling), anti-GluA2-p3Y which recognizes phosphorylated Tyr 869 , Tyr 873 , and Tyr 876 (3Y) of GluA2 (#3921S, Cell Signaling), and anti-GluA2-pY 876 which recognizes phosphorylated Tyr 876 of GluA2 (#4027S, Cell Signaling).

Techniques: Western Blot, Expressing

Effects of PDI knockdown on PP2A bindings to PDI and GluA2 in the hippocampus following KA injection. KA increases PDI:PP2A and GluA2:PP2A bindings in control siRNA-infused animals, but not in PDI siRNA-infused animals. ( a ) Representative Western blot images for the PDI:PP2A and GluA2:PP2A bindings. ( b – c ) Quantitative analyses of the effects of PDI siRNA on PP2A level ( b ) and PDI:PP2A binding ( c ) following KA injection (*, # p < 0.05 vs. control siRNA vs. saline; n = 7, respectively; Kruskal–Wallis test followed by Tukey post-hoc test).

Journal: Scientific Reports

Article Title: PDI augments kainic acid-induced seizure activity and neuronal death by inhibiting PP2A-GluA2-PICK1-mediated AMPA receptor internalization in the mouse hippocampus

doi: 10.1038/s41598-023-41014-7

Figure Lengend Snippet: Effects of PDI knockdown on PP2A bindings to PDI and GluA2 in the hippocampus following KA injection. KA increases PDI:PP2A and GluA2:PP2A bindings in control siRNA-infused animals, but not in PDI siRNA-infused animals. ( a ) Representative Western blot images for the PDI:PP2A and GluA2:PP2A bindings. ( b – c ) Quantitative analyses of the effects of PDI siRNA on PP2A level ( b ) and PDI:PP2A binding ( c ) following KA injection (*, # p < 0.05 vs. control siRNA vs. saline; n = 7, respectively; Kruskal–Wallis test followed by Tukey post-hoc test).

Article Snippet: p-GRIA2 Y869/873/876 , Rabbit , Cell signaling (#3921) , 1:1,000 (WB).

Techniques: Knockdown, Injection, Control, Western Blot, Binding Assay, Saline

Effects of PDI knockdown on PICK1 bindings to GluA2 in the hippocampus following KA injection. PDI siRNA does not influence PICK1 level in both saline- and KA-treated groups. As compared to control siRNA, PDI siRNA increases GluA2A:PICK1 binding in saline-treated group. Although KA does not affect GluA2:PICK1 binding in control siRNA-infused group, it increases it in PDI siRNA-infused group. ( a ) Representative Western blot images for the GluA2:PICK1 binding. ( b – c ) Quantitative analyses of the effects of PDI siRNA on PICK1 level ( b ) and GluA2:PICK1 binding ( c ) following KA injection (*, # p < 0.05 vs. control siRNA vs. saline; n = 7, respectively; Kruskal–Wallis test followed by Tukey post-hoc test). ( d ) Scheme of the role of PDI in AMPAR internalization. PDI may reduce lead to reduction-induced PP2A activation, which would abolish PICK1-mediated AMPAR internalization by dephosphorylating GluA2 S880 and CaMKII T286 sites.

Journal: Scientific Reports

Article Title: PDI augments kainic acid-induced seizure activity and neuronal death by inhibiting PP2A-GluA2-PICK1-mediated AMPA receptor internalization in the mouse hippocampus

doi: 10.1038/s41598-023-41014-7

Figure Lengend Snippet: Effects of PDI knockdown on PICK1 bindings to GluA2 in the hippocampus following KA injection. PDI siRNA does not influence PICK1 level in both saline- and KA-treated groups. As compared to control siRNA, PDI siRNA increases GluA2A:PICK1 binding in saline-treated group. Although KA does not affect GluA2:PICK1 binding in control siRNA-infused group, it increases it in PDI siRNA-infused group. ( a ) Representative Western blot images for the GluA2:PICK1 binding. ( b – c ) Quantitative analyses of the effects of PDI siRNA on PICK1 level ( b ) and GluA2:PICK1 binding ( c ) following KA injection (*, # p < 0.05 vs. control siRNA vs. saline; n = 7, respectively; Kruskal–Wallis test followed by Tukey post-hoc test). ( d ) Scheme of the role of PDI in AMPAR internalization. PDI may reduce lead to reduction-induced PP2A activation, which would abolish PICK1-mediated AMPAR internalization by dephosphorylating GluA2 S880 and CaMKII T286 sites.

Article Snippet: p-GRIA2 Y869/873/876 , Rabbit , Cell signaling (#3921) , 1:1,000 (WB).

Techniques: Knockdown, Injection, Saline, Control, Binding Assay, Western Blot, Activation Assay

Primary antibodies used in the present study.

Journal: Scientific Reports

Article Title: PDI augments kainic acid-induced seizure activity and neuronal death by inhibiting PP2A-GluA2-PICK1-mediated AMPA receptor internalization in the mouse hippocampus

doi: 10.1038/s41598-023-41014-7

Figure Lengend Snippet: Primary antibodies used in the present study.

Article Snippet: p-GRIA2 Y869/873/876 , Rabbit , Cell signaling (#3921) , 1:1,000 (WB).

Techniques: