glua2 m clone l21 Search Results


fabp3 antibody  (NSJ Bioreagents)
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1999 homer1 gp  (Synaptic Systems)
95
Synaptic Systems 1999 homer1 gp
Figure 4. Reduced synaptic availability of GluA1 as well as reduced electrophysiological AMPAR activity is accompanied by increased AMPAR mobility upon syndapin I deficiency. (A–G) Primary hippocampal neurons from WT and syndapin I KO mice (DIV 16–20) stained for surface-localized GluA1 together with <t>Homer1,</t> Bassoon (A,D–G), or MAP2 (C) that were subjected to surface reconstructions using Imaris software. (A) Exemplary coimmunolabeling of surface GluA1, Homer1, Bassoon. Bars, 10 μm. (B) Illustration of analyzed clusters and spheres. Synaptic clusters, GluA1 clusters overlapping with Homer1–Bassoon-positive spheres. Non-synaptic clusters, Homer1–Bassoon-negative GluA1 clusters. Spheres were derived from Homer1–Bassoon colocalization channels with a diameter of 0.5 μm resembling PSD-like areas. (C) Quantitation of densities of GluA1 surface–reconstructed clusters in MAP2-stained dendrites. (D–F) GluA1 clusters grouped into synaptic and non-synaptic clusters.
1999 Homer1 Gp, supplied by Synaptic Systems, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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citation wb if bassoon rb  (Synaptic Systems)
94
Synaptic Systems citation wb if bassoon rb
Figure 4. Reduced synaptic availability of GluA1 as well as reduced electrophysiological AMPAR activity is accompanied by increased AMPAR mobility upon syndapin I deficiency. (A–G) Primary hippocampal neurons from WT and syndapin I KO mice (DIV 16–20) stained for surface-localized GluA1 together with <t>Homer1,</t> Bassoon (A,D–G), or MAP2 (C) that were subjected to surface reconstructions using Imaris software. (A) Exemplary coimmunolabeling of surface GluA1, Homer1, Bassoon. Bars, 10 μm. (B) Illustration of analyzed clusters and spheres. Synaptic clusters, GluA1 clusters overlapping with Homer1–Bassoon-positive spheres. Non-synaptic clusters, Homer1–Bassoon-negative GluA1 clusters. Spheres were derived from Homer1–Bassoon colocalization channels with a diameter of 0.5 μm resembling PSD-like areas. (C) Quantitation of densities of GluA1 surface–reconstructed clusters in MAP2-stained dendrites. (D–F) GluA1 clusters grouped into synaptic and non-synaptic clusters.
Citation Wb If Bassoon Rb, supplied by Synaptic Systems, 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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synaptic systems map2 gp  (Synaptic Systems)
97
Synaptic Systems synaptic systems map2 gp
Figure 4. Reduced synaptic availability of GluA1 as well as reduced electrophysiological AMPAR activity is accompanied by increased AMPAR mobility upon syndapin I deficiency. (A–G) Primary hippocampal neurons from WT and syndapin I KO mice (DIV 16–20) stained for surface-localized GluA1 together with Homer1, Bassoon (A,D–G), or <t>MAP2</t> (C) that were subjected to surface reconstructions using Imaris software. (A) Exemplary coimmunolabeling of surface GluA1, Homer1, Bassoon. Bars, 10 μm. (B) Illustration of analyzed clusters and spheres. Synaptic clusters, GluA1 clusters overlapping with Homer1–Bassoon-positive spheres. Non-synaptic clusters, Homer1–Bassoon-negative GluA1 clusters. Spheres were derived from Homer1–Bassoon colocalization channels with a diameter of 0.5 μm resembling PSD-like areas. (C) Quantitation of densities of GluA1 surface–reconstructed clusters in MAP2-stained dendrites. (D–F) GluA1 clusters grouped into synaptic and non-synaptic clusters.
Synaptic Systems Map2 Gp, supplied by Synaptic Systems, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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neuromab prosap1 shank2 rb  (Synaptic Systems)
91
Synaptic Systems neuromab prosap1 shank2 rb
Figure 4. Reduced synaptic availability of GluA1 as well as reduced electrophysiological AMPAR activity is accompanied by increased AMPAR mobility upon syndapin I deficiency. (A–G) Primary hippocampal neurons from WT and syndapin I KO mice (DIV 16–20) stained for surface-localized GluA1 together with Homer1, Bassoon (A,D–G), or <t>MAP2</t> (C) that were subjected to surface reconstructions using Imaris software. (A) Exemplary coimmunolabeling of surface GluA1, Homer1, Bassoon. Bars, 10 μm. (B) Illustration of analyzed clusters and spheres. Synaptic clusters, GluA1 clusters overlapping with Homer1–Bassoon-positive spheres. Non-synaptic clusters, Homer1–Bassoon-negative GluA1 clusters. Spheres were derived from Homer1–Bassoon colocalization channels with a diameter of 0.5 μm resembling PSD-like areas. (C) Quantitation of densities of GluA1 surface–reconstructed clusters in MAP2-stained dendrites. (D–F) GluA1 clusters grouped into synaptic and non-synaptic clusters.
Neuromab Prosap1 Shank2 Rb, supplied by Synaptic Systems, 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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synaptic systems prosap2 shank3 rb  (Synaptic Systems)
93
Synaptic Systems synaptic systems prosap2 shank3 rb
Figure 4. Reduced synaptic availability of GluA1 as well as reduced electrophysiological AMPAR activity is accompanied by increased AMPAR mobility upon syndapin I deficiency. (A–G) Primary hippocampal neurons from WT and syndapin I KO mice (DIV 16–20) stained for surface-localized GluA1 together with Homer1, Bassoon (A,D–G), or <t>MAP2</t> (C) that were subjected to surface reconstructions using Imaris software. (A) Exemplary coimmunolabeling of surface GluA1, Homer1, Bassoon. Bars, 10 μm. (B) Illustration of analyzed clusters and spheres. Synaptic clusters, GluA1 clusters overlapping with Homer1–Bassoon-positive spheres. Non-synaptic clusters, Homer1–Bassoon-negative GluA1 clusters. Spheres were derived from Homer1–Bassoon colocalization channels with a diameter of 0.5 μm resembling PSD-like areas. (C) Quantitation of densities of GluA1 surface–reconstructed clusters in MAP2-stained dendrites. (D–F) GluA1 clusters grouped into synaptic and non-synaptic clusters.
Synaptic Systems Prosap2 Shank3 Rb, supplied by Synaptic Systems, 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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erc1b 2 rb 143 003  (Synaptic Systems)
92
Synaptic Systems erc1b 2 rb 143 003
Figure 4. Reduced synaptic availability of GluA1 as well as reduced electrophysiological AMPAR activity is accompanied by increased AMPAR mobility upon syndapin I deficiency. (A–G) Primary hippocampal neurons from WT and syndapin I KO mice (DIV 16–20) stained for surface-localized GluA1 together with Homer1, Bassoon (A,D–G), or <t>MAP2</t> (C) that were subjected to surface reconstructions using Imaris software. (A) Exemplary coimmunolabeling of surface GluA1, Homer1, Bassoon. Bars, 10 μm. (B) Illustration of analyzed clusters and spheres. Synaptic clusters, GluA1 clusters overlapping with Homer1–Bassoon-positive spheres. Non-synaptic clusters, Homer1–Bassoon-negative GluA1 clusters. Spheres were derived from Homer1–Bassoon colocalization channels with a diameter of 0.5 μm resembling PSD-like areas. (C) Quantitation of densities of GluA1 surface–reconstructed clusters in MAP2-stained dendrites. (D–F) GluA1 clusters grouped into synaptic and non-synaptic clusters.
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Image Search Results


Figure 4. Reduced synaptic availability of GluA1 as well as reduced electrophysiological AMPAR activity is accompanied by increased AMPAR mobility upon syndapin I deficiency. (A–G) Primary hippocampal neurons from WT and syndapin I KO mice (DIV 16–20) stained for surface-localized GluA1 together with Homer1, Bassoon (A,D–G), or MAP2 (C) that were subjected to surface reconstructions using Imaris software. (A) Exemplary coimmunolabeling of surface GluA1, Homer1, Bassoon. Bars, 10 μm. (B) Illustration of analyzed clusters and spheres. Synaptic clusters, GluA1 clusters overlapping with Homer1–Bassoon-positive spheres. Non-synaptic clusters, Homer1–Bassoon-negative GluA1 clusters. Spheres were derived from Homer1–Bassoon colocalization channels with a diameter of 0.5 μm resembling PSD-like areas. (C) Quantitation of densities of GluA1 surface–reconstructed clusters in MAP2-stained dendrites. (D–F) GluA1 clusters grouped into synaptic and non-synaptic clusters.

Journal: Cerebral cortex (New York, N.Y. : 1991)

Article Title: Syndapin I Loss-of-Function in Mice Leads to Schizophrenia-Like Symptoms.

doi: 10.1093/cercor/bhaa013

Figure Lengend Snippet: Figure 4. Reduced synaptic availability of GluA1 as well as reduced electrophysiological AMPAR activity is accompanied by increased AMPAR mobility upon syndapin I deficiency. (A–G) Primary hippocampal neurons from WT and syndapin I KO mice (DIV 16–20) stained for surface-localized GluA1 together with Homer1, Bassoon (A,D–G), or MAP2 (C) that were subjected to surface reconstructions using Imaris software. (A) Exemplary coimmunolabeling of surface GluA1, Homer1, Bassoon. Bars, 10 μm. (B) Illustration of analyzed clusters and spheres. Synaptic clusters, GluA1 clusters overlapping with Homer1–Bassoon-positive spheres. Non-synaptic clusters, Homer1–Bassoon-negative GluA1 clusters. Spheres were derived from Homer1–Bassoon colocalization channels with a diameter of 0.5 μm resembling PSD-like areas. (C) Quantitation of densities of GluA1 surface–reconstructed clusters in MAP2-stained dendrites. (D–F) GluA1 clusters grouped into synaptic and non-synaptic clusters.

Article Snippet: D ow nloaded from https://academ ic.oup.com /cercor/advance-article-abstract/doi/10.1093/cercor/bhaa013/5799015 by U niversity of Edinburgh user on 13 M arch 2020 Table 1 Primary antibodies used Protein recognized Species Clone/name/ordering # Dilutions used Company, citation WB IF Bassoon rb 141 002 1:300 Synaptic Systems ERC1b/2 rb 143 003 1:1000 Synaptic Systems FLAG rb F7425 1:500 Sigma GFP m Clone JL-8 1:8000 Clontech GFP m Clone B34 1:1000 BioLegend GluA1 m Clone RH95 1:1000 1:100 Millipore GluA1 rb Clone C3T 1:500 Millipore GluA2 m Clone 6C4 1:100 Millipore GluA2 m Clone L21/32 1:500 1:500 NeuroMab GluA3 m Clone 3B3 1:1000 Millipore GluN2A m clone N327/95 1:300 NeuroMab GluN2B m clone N59/36 1:500 NeuroMab GST rb - 1:1000 (Qualmann et al. 1999) Homer1 gp 160 004 1:1000 1:300 Synaptic Systems MAP2 gp 188 004 1:500 Synaptic Systems MAP2 rb ab24640 1:500 Abcam N-WASP gp P337 1:1000 (Kessels and Qualmann 2002) PICK1 m clone L20/8 1:1000 NeuroMab ProSAP1/Shank2 rb 162 202 1:1000 Synaptic Systems ProSAP2/Shank3 rb 162 002 1:1000 Synaptic Systems Shank1 m Clone N22/21 1:1000 NeuroMab Syndapin I gp – 1:2500 (Braun et al. 2005)

Techniques: Activity Assay, Staining, Software, Derivative Assay, Quantitation Assay

Figure 6. AMPAR and NMDAR hypofunction in syndapin I KO mice. (A) Quantitative Western blot analysis of PSD fractions (10 μg protein each) from WT and syndapin I KO cortices. Signals were normalized to anti-Homer1 immunoblotting signals on the same membrane. n = 4–6 detections/protein. (B) NMDAR-mediated eEPSCs evoked at Vh = +40 mV in the presence of 20 μM CNQX and 100 μM picrotoxin (same neurons as presented in Fig. 4H). (C) Quantitative analyses showing significantly reduced NMDAR eEPSCs upon syndapin I KO. n = 26/27 cells (WT/KO) from 10 mice/genotype. (D) Decreased ratio of NMDA/AMPA eEPSCs in syndapin I KO mice. Data, mean + SEM. Mann–Whitney U (A) or unpaired t-test (C,D) for WT versus KO; ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001. See also Fig. S6.

Journal: Cerebral cortex (New York, N.Y. : 1991)

Article Title: Syndapin I Loss-of-Function in Mice Leads to Schizophrenia-Like Symptoms.

doi: 10.1093/cercor/bhaa013

Figure Lengend Snippet: Figure 6. AMPAR and NMDAR hypofunction in syndapin I KO mice. (A) Quantitative Western blot analysis of PSD fractions (10 μg protein each) from WT and syndapin I KO cortices. Signals were normalized to anti-Homer1 immunoblotting signals on the same membrane. n = 4–6 detections/protein. (B) NMDAR-mediated eEPSCs evoked at Vh = +40 mV in the presence of 20 μM CNQX and 100 μM picrotoxin (same neurons as presented in Fig. 4H). (C) Quantitative analyses showing significantly reduced NMDAR eEPSCs upon syndapin I KO. n = 26/27 cells (WT/KO) from 10 mice/genotype. (D) Decreased ratio of NMDA/AMPA eEPSCs in syndapin I KO mice. Data, mean + SEM. Mann–Whitney U (A) or unpaired t-test (C,D) for WT versus KO; ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001. See also Fig. S6.

Article Snippet: D ow nloaded from https://academ ic.oup.com /cercor/advance-article-abstract/doi/10.1093/cercor/bhaa013/5799015 by U niversity of Edinburgh user on 13 M arch 2020 Table 1 Primary antibodies used Protein recognized Species Clone/name/ordering # Dilutions used Company, citation WB IF Bassoon rb 141 002 1:300 Synaptic Systems ERC1b/2 rb 143 003 1:1000 Synaptic Systems FLAG rb F7425 1:500 Sigma GFP m Clone JL-8 1:8000 Clontech GFP m Clone B34 1:1000 BioLegend GluA1 m Clone RH95 1:1000 1:100 Millipore GluA1 rb Clone C3T 1:500 Millipore GluA2 m Clone 6C4 1:100 Millipore GluA2 m Clone L21/32 1:500 1:500 NeuroMab GluA3 m Clone 3B3 1:1000 Millipore GluN2A m clone N327/95 1:300 NeuroMab GluN2B m clone N59/36 1:500 NeuroMab GST rb - 1:1000 (Qualmann et al. 1999) Homer1 gp 160 004 1:1000 1:300 Synaptic Systems MAP2 gp 188 004 1:500 Synaptic Systems MAP2 rb ab24640 1:500 Abcam N-WASP gp P337 1:1000 (Kessels and Qualmann 2002) PICK1 m clone L20/8 1:1000 NeuroMab ProSAP1/Shank2 rb 162 202 1:1000 Synaptic Systems ProSAP2/Shank3 rb 162 002 1:1000 Synaptic Systems Shank1 m Clone N22/21 1:1000 NeuroMab Syndapin I gp – 1:2500 (Braun et al. 2005)

Techniques: Western Blot, Membrane, MANN-WHITNEY

Figure 4. Reduced synaptic availability of GluA1 as well as reduced electrophysiological AMPAR activity is accompanied by increased AMPAR mobility upon syndapin I deficiency. (A–G) Primary hippocampal neurons from WT and syndapin I KO mice (DIV 16–20) stained for surface-localized GluA1 together with Homer1, Bassoon (A,D–G), or MAP2 (C) that were subjected to surface reconstructions using Imaris software. (A) Exemplary coimmunolabeling of surface GluA1, Homer1, Bassoon. Bars, 10 μm. (B) Illustration of analyzed clusters and spheres. Synaptic clusters, GluA1 clusters overlapping with Homer1–Bassoon-positive spheres. Non-synaptic clusters, Homer1–Bassoon-negative GluA1 clusters. Spheres were derived from Homer1–Bassoon colocalization channels with a diameter of 0.5 μm resembling PSD-like areas. (C) Quantitation of densities of GluA1 surface–reconstructed clusters in MAP2-stained dendrites. (D–F) GluA1 clusters grouped into synaptic and non-synaptic clusters.

Journal: Cerebral cortex (New York, N.Y. : 1991)

Article Title: Syndapin I Loss-of-Function in Mice Leads to Schizophrenia-Like Symptoms.

doi: 10.1093/cercor/bhaa013

Figure Lengend Snippet: Figure 4. Reduced synaptic availability of GluA1 as well as reduced electrophysiological AMPAR activity is accompanied by increased AMPAR mobility upon syndapin I deficiency. (A–G) Primary hippocampal neurons from WT and syndapin I KO mice (DIV 16–20) stained for surface-localized GluA1 together with Homer1, Bassoon (A,D–G), or MAP2 (C) that were subjected to surface reconstructions using Imaris software. (A) Exemplary coimmunolabeling of surface GluA1, Homer1, Bassoon. Bars, 10 μm. (B) Illustration of analyzed clusters and spheres. Synaptic clusters, GluA1 clusters overlapping with Homer1–Bassoon-positive spheres. Non-synaptic clusters, Homer1–Bassoon-negative GluA1 clusters. Spheres were derived from Homer1–Bassoon colocalization channels with a diameter of 0.5 μm resembling PSD-like areas. (C) Quantitation of densities of GluA1 surface–reconstructed clusters in MAP2-stained dendrites. (D–F) GluA1 clusters grouped into synaptic and non-synaptic clusters.

Article Snippet: D ow nloaded from https://academ ic.oup.com /cercor/advance-article-abstract/doi/10.1093/cercor/bhaa013/5799015 by U niversity of Edinburgh user on 13 M arch 2020 Table 1 Primary antibodies used Protein recognized Species Clone/name/ordering # Dilutions used Company, citation WB IF Bassoon rb 141 002 1:300 Synaptic Systems ERC1b/2 rb 143 003 1:1000 Synaptic Systems FLAG rb F7425 1:500 Sigma GFP m Clone JL-8 1:8000 Clontech GFP m Clone B34 1:1000 BioLegend GluA1 m Clone RH95 1:1000 1:100 Millipore GluA1 rb Clone C3T 1:500 Millipore GluA2 m Clone 6C4 1:100 Millipore GluA2 m Clone L21/32 1:500 1:500 NeuroMab GluA3 m Clone 3B3 1:1000 Millipore GluN2A m clone N327/95 1:300 NeuroMab GluN2B m clone N59/36 1:500 NeuroMab GST rb - 1:1000 (Qualmann et al. 1999) Homer1 gp 160 004 1:1000 1:300 Synaptic Systems MAP2 gp 188 004 1:500 Synaptic Systems MAP2 rb ab24640 1:500 Abcam N-WASP gp P337 1:1000 (Kessels and Qualmann 2002) PICK1 m clone L20/8 1:1000 NeuroMab ProSAP1/Shank2 rb 162 202 1:1000 Synaptic Systems ProSAP2/Shank3 rb 162 002 1:1000 Synaptic Systems Shank1 m Clone N22/21 1:1000 NeuroMab Syndapin I gp – 1:2500 (Braun et al. 2005)

Techniques: Activity Assay, Staining, Software, Derivative Assay, Quantitation Assay