postsynaptic density protein 95 psd95 Search Results


mouse anti psd 95 upstate  (Alomone Labs)
93
Alomone Labs mouse anti psd 95 upstate
NMDARs and PKC couple to AMPAR complex in dorsal horn. (A) PICK1 co-immunoprecipitates with GluR2 and PKCα (but not PKCβ or PKCγ). (B) GluR2 co-immunoprecipitates with PICK1 and PKCα. (C) <t>PSD-95</t> co-immunoprecipitates with NR2B and stargazin. (D) Stargazin co-immunoprecipitates PSD-95 and GluR2. (E) NR1 (5-nm gold, arrowheads) and GluR2 (15-nm gold) co-localize at superficial dorsal horn synapses. Pre, presynaptic terminal; Post, postsynaptic structure. Scale bar: 100 nm
Mouse Anti Psd 95 Upstate, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mouse anti psd 95 upstate - by Bioz Stars, 2026-03
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psd 95  (StressMarq)
91
StressMarq psd 95
NMDARs and PKC couple to AMPAR complex in dorsal horn. (A) PICK1 co-immunoprecipitates with GluR2 and PKCα (but not PKCβ or PKCγ). (B) GluR2 co-immunoprecipitates with PICK1 and PKCα. (C) <t>PSD-95</t> co-immunoprecipitates with NR2B and stargazin. (D) Stargazin co-immunoprecipitates PSD-95 and GluR2. (E) NR1 (5-nm gold, arrowheads) and GluR2 (15-nm gold) co-localize at superficial dorsal horn synapses. Pre, presynaptic terminal; Post, postsynaptic structure. Scale bar: 100 nm
Psd 95, supplied by StressMarq, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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psd 95 - by Bioz Stars, 2026-03
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psd 95 antibody  (Boster Bio)
93
Boster Bio psd 95 antibody
NMDARs and PKC couple to AMPAR complex in dorsal horn. (A) PICK1 co-immunoprecipitates with GluR2 and PKCα (but not PKCβ or PKCγ). (B) GluR2 co-immunoprecipitates with PICK1 and PKCα. (C) <t>PSD-95</t> co-immunoprecipitates with NR2B and stargazin. (D) Stargazin co-immunoprecipitates PSD-95 and GluR2. (E) NR1 (5-nm gold, arrowheads) and GluR2 (15-nm gold) co-localize at superficial dorsal horn synapses. Pre, presynaptic terminal; Post, postsynaptic structure. Scale bar: 100 nm
Psd 95 Antibody, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/psd 95 antibody/product/Boster Bio
Average 93 stars, based on 1 article reviews
psd 95 antibody - by Bioz Stars, 2026-03
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rabbit anti postsynaptic dense substance 95 psd 95  (Boster Bio)
93
Boster Bio rabbit anti postsynaptic dense substance 95 psd 95
NMDARs and PKC couple to AMPAR complex in dorsal horn. (A) PICK1 co-immunoprecipitates with GluR2 and PKCα (but not PKCβ or PKCγ). (B) GluR2 co-immunoprecipitates with PICK1 and PKCα. (C) <t>PSD-95</t> co-immunoprecipitates with NR2B and stargazin. (D) Stargazin co-immunoprecipitates PSD-95 and GluR2. (E) NR1 (5-nm gold, arrowheads) and GluR2 (15-nm gold) co-localize at superficial dorsal horn synapses. Pre, presynaptic terminal; Post, postsynaptic structure. Scale bar: 100 nm
Rabbit Anti Postsynaptic Dense Substance 95 Psd 95, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/rabbit anti postsynaptic dense substance 95 psd 95/product/Boster Bio
Average 93 stars, based on 1 article reviews
rabbit anti postsynaptic dense substance 95 psd 95 - by Bioz Stars, 2026-03
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anti psd 95  (Alomone Labs)
94
Alomone Labs anti psd 95
NMDARs and PKC couple to AMPAR complex in dorsal horn. (A) PICK1 co-immunoprecipitates with GluR2 and PKCα (but not PKCβ or PKCγ). (B) GluR2 co-immunoprecipitates with PICK1 and PKCα. (C) <t>PSD-95</t> co-immunoprecipitates with NR2B and stargazin. (D) Stargazin co-immunoprecipitates PSD-95 and GluR2. (E) NR1 (5-nm gold, arrowheads) and GluR2 (15-nm gold) co-localize at superficial dorsal horn synapses. Pre, presynaptic terminal; Post, postsynaptic structure. Scale bar: 100 nm
Anti Psd 95, supplied by Alomone Labs, 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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anti psd 95 - by Bioz Stars, 2026-03
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rabbit antipsd95 antibody  (Boster Bio)
93
Boster Bio rabbit antipsd95 antibody
NMDARs and PKC couple to AMPAR complex in dorsal horn. (A) PICK1 co-immunoprecipitates with GluR2 and PKCα (but not PKCβ or PKCγ). (B) GluR2 co-immunoprecipitates with PICK1 and PKCα. (C) <t>PSD-95</t> co-immunoprecipitates with NR2B and stargazin. (D) Stargazin co-immunoprecipitates PSD-95 and GluR2. (E) NR1 (5-nm gold, arrowheads) and GluR2 (15-nm gold) co-localize at superficial dorsal horn synapses. Pre, presynaptic terminal; Post, postsynaptic structure. Scale bar: 100 nm
Rabbit Antipsd95 Antibody, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/rabbit antipsd95 antibody/product/Boster Bio
Average 93 stars, based on 1 article reviews
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postsynaptic density protein 95 (psd95  (Cloud-Clone corp)
90
Cloud-Clone corp postsynaptic density protein 95 (psd95
Early stage daily treatment with NX210 or NX210c reduces pathological hallmarks of Alzheimer’s disease. Mice were treated intraperitoneally once a day with vehicle, NX210 or NX210c (2 mg/kg), or orally with donepezil (DPZ, 1 mg/kg) one hour after intracerebroventricular injection of scrambled control peptides (Ctrl) or amyloid-beta 25 – 35 (Aβ 25 – 35 ) oligomers. They were sacrificed at day 11 (D11) and cerebral structures [hippocampi (A–D) and prefrontal cortices (E–H) ] were collected for biochemical analyses of levels of Aβ 1 – 42 ( A ; ELISA), phosphorylated-tau on threonine 181 [pTau; ( B ; ELISA)], tumor necrosis factor-α [TNFα; ( C ; ELISA)], lipid peroxidation [LPO; ( D; measure of cumene hydroperoxide (CHP) absorbance)], glial fibrillary acidic protein [GFAP; ( E ; ELISA)], caspase-12 [Casp-12; ( F ; ELISA)], synaptophysin [SYP; ( G ; ELISA)] and postsynaptic density <t>protein</t> <t>95</t> <t>[PSD95;</t> ( H ; ELISA)]. NX210 and NX210c decreased the levels of all those pathological hallmarks of AD and increased synaptogenesis. The data are expressed in CHP equivalents (CHPeq) per wet weight of tissue (D) or in pg per mg of tissue ( other items ) and presented as means and SEM. One-way ANOVA followed by Tukey’s multiple comparisons test: ### p < 0.001, # p < 0.05 compared with Ctrl; *** p < 0.001, ** p < 0.01 comp ared with Aβ 25 – 35 ; £££ p < 0.001, £ p < 0.05 compared with Aβ 25 – 35 + DPZ; $$$ p < 0.001 Aβ 25 – 35 + NX210 vs. Aβ 25 – 35 + NX210c, n = 6 Ctrl, n = 5 Aβ 25 – 35 , Aβ 25 – 35 + DPZ, Aβ 25 – 35 + NX210c, n = 4 Aβ 25 – 35 + NX210. These analyses do not include two outliers identified for caspase 12 ELISA using the Grubbs test (red circles) ( p < 0.05).
Postsynaptic Density Protein 95 (Psd95, supplied by Cloud-Clone corp, 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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postsynaptic density protein-95 (psd-95, msd #k250qnd)  (Meso Scale Diagnostics LLC)
90
Meso Scale Diagnostics LLC postsynaptic density protein-95 (psd-95, msd #k250qnd)
Early stage daily treatment with NX210 or NX210c reduces pathological hallmarks of Alzheimer’s disease. Mice were treated intraperitoneally once a day with vehicle, NX210 or NX210c (2 mg/kg), or orally with donepezil (DPZ, 1 mg/kg) one hour after intracerebroventricular injection of scrambled control peptides (Ctrl) or amyloid-beta 25 – 35 (Aβ 25 – 35 ) oligomers. They were sacrificed at day 11 (D11) and cerebral structures [hippocampi (A–D) and prefrontal cortices (E–H) ] were collected for biochemical analyses of levels of Aβ 1 – 42 ( A ; ELISA), phosphorylated-tau on threonine 181 [pTau; ( B ; ELISA)], tumor necrosis factor-α [TNFα; ( C ; ELISA)], lipid peroxidation [LPO; ( D; measure of cumene hydroperoxide (CHP) absorbance)], glial fibrillary acidic protein [GFAP; ( E ; ELISA)], caspase-12 [Casp-12; ( F ; ELISA)], synaptophysin [SYP; ( G ; ELISA)] and postsynaptic density <t>protein</t> <t>95</t> <t>[PSD95;</t> ( H ; ELISA)]. NX210 and NX210c decreased the levels of all those pathological hallmarks of AD and increased synaptogenesis. The data are expressed in CHP equivalents (CHPeq) per wet weight of tissue (D) or in pg per mg of tissue ( other items ) and presented as means and SEM. One-way ANOVA followed by Tukey’s multiple comparisons test: ### p < 0.001, # p < 0.05 compared with Ctrl; *** p < 0.001, ** p < 0.01 comp ared with Aβ 25 – 35 ; £££ p < 0.001, £ p < 0.05 compared with Aβ 25 – 35 + DPZ; $$$ p < 0.001 Aβ 25 – 35 + NX210 vs. Aβ 25 – 35 + NX210c, n = 6 Ctrl, n = 5 Aβ 25 – 35 , Aβ 25 – 35 + DPZ, Aβ 25 – 35 + NX210c, n = 4 Aβ 25 – 35 + NX210. These analyses do not include two outliers identified for caspase 12 ELISA using the Grubbs test (red circles) ( p < 0.05).
Postsynaptic Density Protein 95 (Psd 95, Msd #K250qnd), supplied by Meso Scale Diagnostics LLC, 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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Average 90 stars, based on 1 article reviews
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antibodies to postsynaptic density protein 95 (psd95) (phosphosolutions)  (PhosphoSolutions)
90
PhosphoSolutions antibodies to postsynaptic density protein 95 (psd95) (phosphosolutions)
Early stage daily treatment with NX210 or NX210c reduces pathological hallmarks of Alzheimer’s disease. Mice were treated intraperitoneally once a day with vehicle, NX210 or NX210c (2 mg/kg), or orally with donepezil (DPZ, 1 mg/kg) one hour after intracerebroventricular injection of scrambled control peptides (Ctrl) or amyloid-beta 25 – 35 (Aβ 25 – 35 ) oligomers. They were sacrificed at day 11 (D11) and cerebral structures [hippocampi (A–D) and prefrontal cortices (E–H) ] were collected for biochemical analyses of levels of Aβ 1 – 42 ( A ; ELISA), phosphorylated-tau on threonine 181 [pTau; ( B ; ELISA)], tumor necrosis factor-α [TNFα; ( C ; ELISA)], lipid peroxidation [LPO; ( D; measure of cumene hydroperoxide (CHP) absorbance)], glial fibrillary acidic protein [GFAP; ( E ; ELISA)], caspase-12 [Casp-12; ( F ; ELISA)], synaptophysin [SYP; ( G ; ELISA)] and postsynaptic density <t>protein</t> <t>95</t> <t>[PSD95;</t> ( H ; ELISA)]. NX210 and NX210c decreased the levels of all those pathological hallmarks of AD and increased synaptogenesis. The data are expressed in CHP equivalents (CHPeq) per wet weight of tissue (D) or in pg per mg of tissue ( other items ) and presented as means and SEM. One-way ANOVA followed by Tukey’s multiple comparisons test: ### p < 0.001, # p < 0.05 compared with Ctrl; *** p < 0.001, ** p < 0.01 comp ared with Aβ 25 – 35 ; £££ p < 0.001, £ p < 0.05 compared with Aβ 25 – 35 + DPZ; $$$ p < 0.001 Aβ 25 – 35 + NX210 vs. Aβ 25 – 35 + NX210c, n = 6 Ctrl, n = 5 Aβ 25 – 35 , Aβ 25 – 35 + DPZ, Aβ 25 – 35 + NX210c, n = 4 Aβ 25 – 35 + NX210. These analyses do not include two outliers identified for caspase 12 ELISA using the Grubbs test (red circles) ( p < 0.05).
Antibodies To Postsynaptic Density Protein 95 (Psd95) (Phosphosolutions), supplied by PhosphoSolutions, 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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rabbit anti postsynaptic density protein 95  (Boster Bio)
93
Boster Bio rabbit anti postsynaptic density protein 95
Early stage daily treatment with NX210 or NX210c reduces pathological hallmarks of Alzheimer’s disease. Mice were treated intraperitoneally once a day with vehicle, NX210 or NX210c (2 mg/kg), or orally with donepezil (DPZ, 1 mg/kg) one hour after intracerebroventricular injection of scrambled control peptides (Ctrl) or amyloid-beta 25 – 35 (Aβ 25 – 35 ) oligomers. They were sacrificed at day 11 (D11) and cerebral structures [hippocampi (A–D) and prefrontal cortices (E–H) ] were collected for biochemical analyses of levels of Aβ 1 – 42 ( A ; ELISA), phosphorylated-tau on threonine 181 [pTau; ( B ; ELISA)], tumor necrosis factor-α [TNFα; ( C ; ELISA)], lipid peroxidation [LPO; ( D; measure of cumene hydroperoxide (CHP) absorbance)], glial fibrillary acidic protein [GFAP; ( E ; ELISA)], caspase-12 [Casp-12; ( F ; ELISA)], synaptophysin [SYP; ( G ; ELISA)] and postsynaptic density <t>protein</t> <t>95</t> <t>[PSD95;</t> ( H ; ELISA)]. NX210 and NX210c decreased the levels of all those pathological hallmarks of AD and increased synaptogenesis. The data are expressed in CHP equivalents (CHPeq) per wet weight of tissue (D) or in pg per mg of tissue ( other items ) and presented as means and SEM. One-way ANOVA followed by Tukey’s multiple comparisons test: ### p < 0.001, # p < 0.05 compared with Ctrl; *** p < 0.001, ** p < 0.01 comp ared with Aβ 25 – 35 ; £££ p < 0.001, £ p < 0.05 compared with Aβ 25 – 35 + DPZ; $$$ p < 0.001 Aβ 25 – 35 + NX210 vs. Aβ 25 – 35 + NX210c, n = 6 Ctrl, n = 5 Aβ 25 – 35 , Aβ 25 – 35 + DPZ, Aβ 25 – 35 + NX210c, n = 4 Aβ 25 – 35 + NX210. These analyses do not include two outliers identified for caspase 12 ELISA using the Grubbs test (red circles) ( p < 0.05).
Rabbit Anti Postsynaptic Density Protein 95, supplied by Boster Bio, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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rabbit anti postsynaptic density protein 95 - by Bioz Stars, 2026-03
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psd 95 mouse  (ProSci Incorporated)
90
ProSci Incorporated psd 95 mouse
Early stage daily treatment with NX210 or NX210c reduces pathological hallmarks of Alzheimer’s disease. Mice were treated intraperitoneally once a day with vehicle, NX210 or NX210c (2 mg/kg), or orally with donepezil (DPZ, 1 mg/kg) one hour after intracerebroventricular injection of scrambled control peptides (Ctrl) or amyloid-beta 25 – 35 (Aβ 25 – 35 ) oligomers. They were sacrificed at day 11 (D11) and cerebral structures [hippocampi (A–D) and prefrontal cortices (E–H) ] were collected for biochemical analyses of levels of Aβ 1 – 42 ( A ; ELISA), phosphorylated-tau on threonine 181 [pTau; ( B ; ELISA)], tumor necrosis factor-α [TNFα; ( C ; ELISA)], lipid peroxidation [LPO; ( D; measure of cumene hydroperoxide (CHP) absorbance)], glial fibrillary acidic protein [GFAP; ( E ; ELISA)], caspase-12 [Casp-12; ( F ; ELISA)], synaptophysin [SYP; ( G ; ELISA)] and postsynaptic density <t>protein</t> <t>95</t> <t>[PSD95;</t> ( H ; ELISA)]. NX210 and NX210c decreased the levels of all those pathological hallmarks of AD and increased synaptogenesis. The data are expressed in CHP equivalents (CHPeq) per wet weight of tissue (D) or in pg per mg of tissue ( other items ) and presented as means and SEM. One-way ANOVA followed by Tukey’s multiple comparisons test: ### p < 0.001, # p < 0.05 compared with Ctrl; *** p < 0.001, ** p < 0.01 comp ared with Aβ 25 – 35 ; £££ p < 0.001, £ p < 0.05 compared with Aβ 25 – 35 + DPZ; $$$ p < 0.001 Aβ 25 – 35 + NX210 vs. Aβ 25 – 35 + NX210c, n = 6 Ctrl, n = 5 Aβ 25 – 35 , Aβ 25 – 35 + DPZ, Aβ 25 – 35 + NX210c, n = 4 Aβ 25 – 35 + NX210. These analyses do not include two outliers identified for caspase 12 ELISA using the Grubbs test (red circles) ( p < 0.05).
Psd 95 Mouse, supplied by ProSci Incorporated, 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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psd 95 mouse - by Bioz Stars, 2026-03
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postsynaptic density protein 95 (psd95)  (StemCells Inc)
90
StemCells Inc postsynaptic density protein 95 (psd95)
Early stage daily treatment with NX210 or NX210c reduces pathological hallmarks of Alzheimer’s disease. Mice were treated intraperitoneally once a day with vehicle, NX210 or NX210c (2 mg/kg), or orally with donepezil (DPZ, 1 mg/kg) one hour after intracerebroventricular injection of scrambled control peptides (Ctrl) or amyloid-beta 25 – 35 (Aβ 25 – 35 ) oligomers. They were sacrificed at day 11 (D11) and cerebral structures [hippocampi (A–D) and prefrontal cortices (E–H) ] were collected for biochemical analyses of levels of Aβ 1 – 42 ( A ; ELISA), phosphorylated-tau on threonine 181 [pTau; ( B ; ELISA)], tumor necrosis factor-α [TNFα; ( C ; ELISA)], lipid peroxidation [LPO; ( D; measure of cumene hydroperoxide (CHP) absorbance)], glial fibrillary acidic protein [GFAP; ( E ; ELISA)], caspase-12 [Casp-12; ( F ; ELISA)], synaptophysin [SYP; ( G ; ELISA)] and postsynaptic density <t>protein</t> <t>95</t> <t>[PSD95;</t> ( H ; ELISA)]. NX210 and NX210c decreased the levels of all those pathological hallmarks of AD and increased synaptogenesis. The data are expressed in CHP equivalents (CHPeq) per wet weight of tissue (D) or in pg per mg of tissue ( other items ) and presented as means and SEM. One-way ANOVA followed by Tukey’s multiple comparisons test: ### p < 0.001, # p < 0.05 compared with Ctrl; *** p < 0.001, ** p < 0.01 comp ared with Aβ 25 – 35 ; £££ p < 0.001, £ p < 0.05 compared with Aβ 25 – 35 + DPZ; $$$ p < 0.001 Aβ 25 – 35 + NX210 vs. Aβ 25 – 35 + NX210c, n = 6 Ctrl, n = 5 Aβ 25 – 35 , Aβ 25 – 35 + DPZ, Aβ 25 – 35 + NX210c, n = 4 Aβ 25 – 35 + NX210. These analyses do not include two outliers identified for caspase 12 ELISA using the Grubbs test (red circles) ( p < 0.05).
Postsynaptic Density Protein 95 (Psd95), supplied by StemCells 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


NMDARs and PKC couple to AMPAR complex in dorsal horn. (A) PICK1 co-immunoprecipitates with GluR2 and PKCα (but not PKCβ or PKCγ). (B) GluR2 co-immunoprecipitates with PICK1 and PKCα. (C) PSD-95 co-immunoprecipitates with NR2B and stargazin. (D) Stargazin co-immunoprecipitates PSD-95 and GluR2. (E) NR1 (5-nm gold, arrowheads) and GluR2 (15-nm gold) co-localize at superficial dorsal horn synapses. Pre, presynaptic terminal; Post, postsynaptic structure. Scale bar: 100 nm

Journal:

Article Title: Persistent inflammation induces GluR2 internalization via NMDA receptor-triggered PKC activation in dorsal horn neurons

doi: 10.1523/JNEUROSCI.4514-08.2009

Figure Lengend Snippet: NMDARs and PKC couple to AMPAR complex in dorsal horn. (A) PICK1 co-immunoprecipitates with GluR2 and PKCα (but not PKCβ or PKCγ). (B) GluR2 co-immunoprecipitates with PICK1 and PKCα. (C) PSD-95 co-immunoprecipitates with NR2B and stargazin. (D) Stargazin co-immunoprecipitates PSD-95 and GluR2. (E) NR1 (5-nm gold, arrowheads) and GluR2 (15-nm gold) co-localize at superficial dorsal horn synapses. Pre, presynaptic terminal; Post, postsynaptic structure. Scale bar: 100 nm

Article Snippet: Antibodies The following antibodies were used: rabbit anti-GluR2 (Chemicon, Temecula, CA), mouse anti-GluR2 (Chemicon), rabbit anti-GluR2-p Ser 880 ( Chung et al., 2003 ; Steinberg et al., 2006 ), rabbit ant-PICK1 ( Steinberg et al., 2006 ), rabbit anti-GRIP1 (Upstate, Lake Placid, NY), mouse anti-PSD-95 (Upstate), rabbit anti-PSD-93 (Alomone Labs Ltd, Jerusalem, Israel), rabbit anti-NR2B (Chemicon), rabbit anti-NR1 (Chemicon), rabbit anti-NR2A/2B (Chemicon), rabbit anti-PKCα (Santa Cruz Biotechnology, Santa Cruz, CA), rabbit anti-PKC β (Santa Cruz Biotechnology), rabbit anti-PKCγ (Santa Cruz Biotechnology), rabbit anti- N -cadherin (BD Transduction Laboratories, San Jose, CA), rabbit anti-stargazin (Upstate), mouse anti-α-adaptin (Sigma), and mouse anti-β-actin (Sigma).

Techniques:

Proposed model for the NMDAR/PKC-dependent dorsal horn GluR2 internalization under persistent inflammatory pain conditions. NMDARs couple to AMPARs through PSD-95 (which binds to NR2A/2B) interaction with stargazin (which binds to GluR1, GluR2, and GluR4). Under normal conditions, ABP/GRIP binds to and anchors GluR2 at synapses. Under persistent inflammatory pain conditions, NMDAR activation causes Ca2+ influx and PKCα activation. The latter phosphorylates GluR2 at Ser880 and disrupts GluR2 binding to ABP/GRIP, which leads to GluR2 internalization. GluR2 internalization results in an increase of AMPAR Ca2+ permeability. The increase in [Ca2+]i in dorsal horn neurons should initiate or potentiate a variety of Ca2+-dependent intracellular cascades that are associated with the maintenance of persistent inflammatory pain.

Journal:

Article Title: Persistent inflammation induces GluR2 internalization via NMDA receptor-triggered PKC activation in dorsal horn neurons

doi: 10.1523/JNEUROSCI.4514-08.2009

Figure Lengend Snippet: Proposed model for the NMDAR/PKC-dependent dorsal horn GluR2 internalization under persistent inflammatory pain conditions. NMDARs couple to AMPARs through PSD-95 (which binds to NR2A/2B) interaction with stargazin (which binds to GluR1, GluR2, and GluR4). Under normal conditions, ABP/GRIP binds to and anchors GluR2 at synapses. Under persistent inflammatory pain conditions, NMDAR activation causes Ca2+ influx and PKCα activation. The latter phosphorylates GluR2 at Ser880 and disrupts GluR2 binding to ABP/GRIP, which leads to GluR2 internalization. GluR2 internalization results in an increase of AMPAR Ca2+ permeability. The increase in [Ca2+]i in dorsal horn neurons should initiate or potentiate a variety of Ca2+-dependent intracellular cascades that are associated with the maintenance of persistent inflammatory pain.

Article Snippet: Antibodies The following antibodies were used: rabbit anti-GluR2 (Chemicon, Temecula, CA), mouse anti-GluR2 (Chemicon), rabbit anti-GluR2-p Ser 880 ( Chung et al., 2003 ; Steinberg et al., 2006 ), rabbit ant-PICK1 ( Steinberg et al., 2006 ), rabbit anti-GRIP1 (Upstate, Lake Placid, NY), mouse anti-PSD-95 (Upstate), rabbit anti-PSD-93 (Alomone Labs Ltd, Jerusalem, Israel), rabbit anti-NR2B (Chemicon), rabbit anti-NR1 (Chemicon), rabbit anti-NR2A/2B (Chemicon), rabbit anti-PKCα (Santa Cruz Biotechnology, Santa Cruz, CA), rabbit anti-PKC β (Santa Cruz Biotechnology), rabbit anti-PKCγ (Santa Cruz Biotechnology), rabbit anti- N -cadherin (BD Transduction Laboratories, San Jose, CA), rabbit anti-stargazin (Upstate), mouse anti-α-adaptin (Sigma), and mouse anti-β-actin (Sigma).

Techniques: Activation Assay, Binding Assay, Permeability

Early stage daily treatment with NX210 or NX210c reduces pathological hallmarks of Alzheimer’s disease. Mice were treated intraperitoneally once a day with vehicle, NX210 or NX210c (2 mg/kg), or orally with donepezil (DPZ, 1 mg/kg) one hour after intracerebroventricular injection of scrambled control peptides (Ctrl) or amyloid-beta 25 – 35 (Aβ 25 – 35 ) oligomers. They were sacrificed at day 11 (D11) and cerebral structures [hippocampi (A–D) and prefrontal cortices (E–H) ] were collected for biochemical analyses of levels of Aβ 1 – 42 ( A ; ELISA), phosphorylated-tau on threonine 181 [pTau; ( B ; ELISA)], tumor necrosis factor-α [TNFα; ( C ; ELISA)], lipid peroxidation [LPO; ( D; measure of cumene hydroperoxide (CHP) absorbance)], glial fibrillary acidic protein [GFAP; ( E ; ELISA)], caspase-12 [Casp-12; ( F ; ELISA)], synaptophysin [SYP; ( G ; ELISA)] and postsynaptic density protein 95 [PSD95; ( H ; ELISA)]. NX210 and NX210c decreased the levels of all those pathological hallmarks of AD and increased synaptogenesis. The data are expressed in CHP equivalents (CHPeq) per wet weight of tissue (D) or in pg per mg of tissue ( other items ) and presented as means and SEM. One-way ANOVA followed by Tukey’s multiple comparisons test: ### p < 0.001, # p < 0.05 compared with Ctrl; *** p < 0.001, ** p < 0.01 comp ared with Aβ 25 – 35 ; £££ p < 0.001, £ p < 0.05 compared with Aβ 25 – 35 + DPZ; $$$ p < 0.001 Aβ 25 – 35 + NX210 vs. Aβ 25 – 35 + NX210c, n = 6 Ctrl, n = 5 Aβ 25 – 35 , Aβ 25 – 35 + DPZ, Aβ 25 – 35 + NX210c, n = 4 Aβ 25 – 35 + NX210. These analyses do not include two outliers identified for caspase 12 ELISA using the Grubbs test (red circles) ( p < 0.05).

Journal: Frontiers in Neuroscience

Article Title: Subcommissural Organ-Spondin-Derived Peptide Restores Memory in a Mouse Model of Alzheimer’s Disease

doi: 10.3389/fnins.2021.651094

Figure Lengend Snippet: Early stage daily treatment with NX210 or NX210c reduces pathological hallmarks of Alzheimer’s disease. Mice were treated intraperitoneally once a day with vehicle, NX210 or NX210c (2 mg/kg), or orally with donepezil (DPZ, 1 mg/kg) one hour after intracerebroventricular injection of scrambled control peptides (Ctrl) or amyloid-beta 25 – 35 (Aβ 25 – 35 ) oligomers. They were sacrificed at day 11 (D11) and cerebral structures [hippocampi (A–D) and prefrontal cortices (E–H) ] were collected for biochemical analyses of levels of Aβ 1 – 42 ( A ; ELISA), phosphorylated-tau on threonine 181 [pTau; ( B ; ELISA)], tumor necrosis factor-α [TNFα; ( C ; ELISA)], lipid peroxidation [LPO; ( D; measure of cumene hydroperoxide (CHP) absorbance)], glial fibrillary acidic protein [GFAP; ( E ; ELISA)], caspase-12 [Casp-12; ( F ; ELISA)], synaptophysin [SYP; ( G ; ELISA)] and postsynaptic density protein 95 [PSD95; ( H ; ELISA)]. NX210 and NX210c decreased the levels of all those pathological hallmarks of AD and increased synaptogenesis. The data are expressed in CHP equivalents (CHPeq) per wet weight of tissue (D) or in pg per mg of tissue ( other items ) and presented as means and SEM. One-way ANOVA followed by Tukey’s multiple comparisons test: ### p < 0.001, # p < 0.05 compared with Ctrl; *** p < 0.001, ** p < 0.01 comp ared with Aβ 25 – 35 ; £££ p < 0.001, £ p < 0.05 compared with Aβ 25 – 35 + DPZ; $$$ p < 0.001 Aβ 25 – 35 + NX210 vs. Aβ 25 – 35 + NX210c, n = 6 Ctrl, n = 5 Aβ 25 – 35 , Aβ 25 – 35 + DPZ, Aβ 25 – 35 + NX210c, n = 4 Aβ 25 – 35 + NX210. These analyses do not include two outliers identified for caspase 12 ELISA using the Grubbs test (red circles) ( p < 0.05).

Article Snippet: Based on the manufacturers’ instructions, ELISA for mouse amyloid-beta 1 – 42 (Aβ 1 – 42 ; Cloud-Clone Corp., Houston, TX, United States), phosphorylated-tau on threonine 181 (pTau; Thermo Fisher, Waltham, MA, United States), tumor necrosis factor alpha (TNF-α; Thermo Fisher) (from left hippocampi), glial fibrillary acidic protein (GFAP; Cloud-Clone Corp.), caspase-12 (Cloud-Clone Corp.) (from left prefrontal cortices), synaptophysin (Cloud-Clone Corp.) and postsynaptic density protein 95 (PSD95; Cloud-Clone Corp.) (from right prefrontal cortices) were performed.

Techniques: Injection, Enzyme-linked Immunosorbent Assay