anti psd 93  (Alomone Labs)


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    Alomone Labs anti psd 93
    Altered PSD protein composition in the hippocampal PSD fraction of KI mice during development. A , Immunoblot analyses of PSD fractions from WT and KI mice at the respective developmental ages for the indicated proteins. The following amounts of WT and KI PSD proteins were analyzed per lane: <t>PSD-93,</t> 0.5 μg; SAP102, 0.5 μg; SAP97, 2 μg; GluN2A, 0.5 μg; GluN2B, 0.5 μg; GluA1, 0.5 μg; GluA2/3, 0.5 μg; and γ2/4/8, 2 μg. The arrowhead indicates the degraded bands of PSD-93. For PSD-95, 0.25 μg of WT and 0.5 μg of KI PSD proteins were analyzed for comparison on identical membrane filters and their band intensities were corrected in B . B , Quantitation of various proteins in the PSD fractions based on the results shown in A , normalized to the wild-type level at P30 (set as 100%). The histograms show the mean ± SEM (open bars, WT; filled bars, KI). Three sets of PSD fractions at various ages (P14–P65) were examined. Simple comparison of the means and SEM of WT and KI data was performed using Student’s t-test. * P
    Anti Psd 93, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 92 stars, based on 1 article reviews
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    Images

    1) Product Images from "Impaired synaptic clustering of postsynaptic density proteins and altered signal transmission in hippocampal neurons, and disrupted learning behavior in PDZ1 and PDZ2 ligand binding-deficient PSD-95 knockin mice"

    Article Title: Impaired synaptic clustering of postsynaptic density proteins and altered signal transmission in hippocampal neurons, and disrupted learning behavior in PDZ1 and PDZ2 ligand binding-deficient PSD-95 knockin mice

    Journal: Molecular Brain

    doi: 10.1186/1756-6606-5-43

    Altered PSD protein composition in the hippocampal PSD fraction of KI mice during development. A , Immunoblot analyses of PSD fractions from WT and KI mice at the respective developmental ages for the indicated proteins. The following amounts of WT and KI PSD proteins were analyzed per lane: PSD-93, 0.5 μg; SAP102, 0.5 μg; SAP97, 2 μg; GluN2A, 0.5 μg; GluN2B, 0.5 μg; GluA1, 0.5 μg; GluA2/3, 0.5 μg; and γ2/4/8, 2 μg. The arrowhead indicates the degraded bands of PSD-93. For PSD-95, 0.25 μg of WT and 0.5 μg of KI PSD proteins were analyzed for comparison on identical membrane filters and their band intensities were corrected in B . B , Quantitation of various proteins in the PSD fractions based on the results shown in A , normalized to the wild-type level at P30 (set as 100%). The histograms show the mean ± SEM (open bars, WT; filled bars, KI). Three sets of PSD fractions at various ages (P14–P65) were examined. Simple comparison of the means and SEM of WT and KI data was performed using Student’s t-test. * P
    Figure Legend Snippet: Altered PSD protein composition in the hippocampal PSD fraction of KI mice during development. A , Immunoblot analyses of PSD fractions from WT and KI mice at the respective developmental ages for the indicated proteins. The following amounts of WT and KI PSD proteins were analyzed per lane: PSD-93, 0.5 μg; SAP102, 0.5 μg; SAP97, 2 μg; GluN2A, 0.5 μg; GluN2B, 0.5 μg; GluA1, 0.5 μg; GluA2/3, 0.5 μg; and γ2/4/8, 2 μg. The arrowhead indicates the degraded bands of PSD-93. For PSD-95, 0.25 μg of WT and 0.5 μg of KI PSD proteins were analyzed for comparison on identical membrane filters and their band intensities were corrected in B . B , Quantitation of various proteins in the PSD fractions based on the results shown in A , normalized to the wild-type level at P30 (set as 100%). The histograms show the mean ± SEM (open bars, WT; filled bars, KI). Three sets of PSD fractions at various ages (P14–P65) were examined. Simple comparison of the means and SEM of WT and KI data was performed using Student’s t-test. * P

    Techniques Used: Mouse Assay, Quantitation Assay

    Altered expression of SAP102 and PSD-93 in the hippocampus of KI mice. A , Immunoblot analyses of hippocampal homogenates from WT and KI mice at the respective developmental ages for the indicated proteins. The following amounts of homogenate proteins were analyzed per lane: PSD-93 and SAP102, WT and KI: 5 μg; GluA1 and GluA2/3, WT and KI: 10 μg; and PSD-95, WT: 5 μg, KI: 20 μg. The arrowhead indicates the degraded bands of PSD-93. B , Quantitation of PSD proteins in the hippocampal homogenates based on the results shown in A , normalized to the wild-type levels at P30 (set as 100%). The histograms show the mean ± SEM (open bars, WT; filled bars, KI). Three sets of hippocampal homogenates at various ages (P4–P65) were examined. The means and SEM of WT and KI data were compared using Student’s t-test. * P
    Figure Legend Snippet: Altered expression of SAP102 and PSD-93 in the hippocampus of KI mice. A , Immunoblot analyses of hippocampal homogenates from WT and KI mice at the respective developmental ages for the indicated proteins. The following amounts of homogenate proteins were analyzed per lane: PSD-93 and SAP102, WT and KI: 5 μg; GluA1 and GluA2/3, WT and KI: 10 μg; and PSD-95, WT: 5 μg, KI: 20 μg. The arrowhead indicates the degraded bands of PSD-93. B , Quantitation of PSD proteins in the hippocampal homogenates based on the results shown in A , normalized to the wild-type levels at P30 (set as 100%). The histograms show the mean ± SEM (open bars, WT; filled bars, KI). Three sets of hippocampal homogenates at various ages (P4–P65) were examined. The means and SEM of WT and KI data were compared using Student’s t-test. * P

    Techniques Used: Expressing, Mouse Assay, Quantitation Assay

    2) Product Images from "Adenomatous polyposis coli plays a key role, in vivo , in coordinating assembly of the neuronal nicotinic postsynaptic complex"

    Article Title: Adenomatous polyposis coli plays a key role, in vivo , in coordinating assembly of the neuronal nicotinic postsynaptic complex

    Journal:

    doi: 10.1016/j.mcn.2008.02.006

    Expression of a different blocking peptide, APC::PSD-93-dn, does not alter α3*nAChR surface clusters on CG neurons in vivo
    Figure Legend Snippet: Expression of a different blocking peptide, APC::PSD-93-dn, does not alter α3*nAChR surface clusters on CG neurons in vivo

    Techniques Used: Expressing, Blocking Assay, In Vivo

    3) Product Images from "PSD-93 Deficiency Protects Cultured Cortical Neurons from NMDA Receptor-triggered Neurotoxicity"

    Article Title: PSD-93 Deficiency Protects Cultured Cortical Neurons from NMDA Receptor-triggered Neurotoxicity

    Journal: Neuroscience

    doi: 10.1016/j.neuroscience.2010.01.030

    PSD-93 deficiency attenuates NMDA-stimulated Ca 2+ loading in cultured cortical neurons. Cultures were challenged for 5 or 10 min with 30 μM NMDA, 10 μM CNQX, and 2 μM nimodipine in medium containing 45 CaCl 2 . CMP: counts per minute. * P
    Figure Legend Snippet: PSD-93 deficiency attenuates NMDA-stimulated Ca 2+ loading in cultured cortical neurons. Cultures were challenged for 5 or 10 min with 30 μM NMDA, 10 μM CNQX, and 2 μM nimodipine in medium containing 45 CaCl 2 . CMP: counts per minute. * P

    Techniques Used: Cell Culture

    Efficacy of pCMV-U6-siRNA constructs. (A)RT-PCR analysis showed that a 495 bp product from PSD-93 was inhibited significantly by siP3, GAPDH mRNA was used as a loading Control. siP3 significantly decreased the mRNA of PSD93 by 80.2% of control.(B) Confirmation by western blot analysis of silencing PSD93 expression, The blots were reprobed with anti-GAPDH antibody to verify protein loading. (C) Relative protein level of PSD-93 after siRNA transfection, PSD93 decreased by 79.5% compared to control group when transfected with siP3.
    Figure Legend Snippet: Efficacy of pCMV-U6-siRNA constructs. (A)RT-PCR analysis showed that a 495 bp product from PSD-93 was inhibited significantly by siP3, GAPDH mRNA was used as a loading Control. siP3 significantly decreased the mRNA of PSD93 by 80.2% of control.(B) Confirmation by western blot analysis of silencing PSD93 expression, The blots were reprobed with anti-GAPDH antibody to verify protein loading. (C) Relative protein level of PSD-93 after siRNA transfection, PSD93 decreased by 79.5% compared to control group when transfected with siP3.

    Techniques Used: Construct, Polymerase Chain Reaction, Western Blot, Expressing, Transfection

    PSD-93 deficiency or knockdown protects against NMDA-stimulated neurotoxicity. Cortical neurons were cultured from WT and PSD-93 KO mice and treated with NMDA (0, 10, 20, 30, 40, and 60 μM) in the presence of 10 μM CNQX and 2 μM nimodipine. (A) Neuronal viability was assessed by MTT assay. (B) Percentage of neuronal death was determined by propidium iodide and calcein AM staining. * P
    Figure Legend Snippet: PSD-93 deficiency or knockdown protects against NMDA-stimulated neurotoxicity. Cortical neurons were cultured from WT and PSD-93 KO mice and treated with NMDA (0, 10, 20, 30, 40, and 60 μM) in the presence of 10 μM CNQX and 2 μM nimodipine. (A) Neuronal viability was assessed by MTT assay. (B) Percentage of neuronal death was determined by propidium iodide and calcein AM staining. * P

    Techniques Used: Cell Culture, Mouse Assay, MTT Assay, Staining

    MK-801 attenuates NMDA-induced neurotoxicity in cultured cortical neurons from WT but not from PSD-93 KO mice. Percentage of neuronal death was determined by propidium iodide and calcein AM staining (top) and neuronal viability by MTT assay (bottom). * P
    Figure Legend Snippet: MK-801 attenuates NMDA-induced neurotoxicity in cultured cortical neurons from WT but not from PSD-93 KO mice. Percentage of neuronal death was determined by propidium iodide and calcein AM staining (top) and neuronal viability by MTT assay (bottom). * P

    Techniques Used: Cell Culture, Mouse Assay, Staining, MTT Assay

    PSD-93 deficiency has no effect on non-NMDA receptor-triggered neurotoxicity in cultured cortical neurons. Cultured neurons were treated with kainate at the doses shown in the presence of 10 μM MK-801 and 2 μM nimodipine. Percentage of neuronal death was determined by propidium iodide and calcein AM staining (top) and neuronal viability by MTT assay (bottom). n = 6 repeats.
    Figure Legend Snippet: PSD-93 deficiency has no effect on non-NMDA receptor-triggered neurotoxicity in cultured cortical neurons. Cultured neurons were treated with kainate at the doses shown in the presence of 10 μM MK-801 and 2 μM nimodipine. Percentage of neuronal death was determined by propidium iodide and calcein AM staining (top) and neuronal viability by MTT assay (bottom). n = 6 repeats.

    Techniques Used: Cell Culture, Staining, MTT Assay

    PSD-93 deficiency decreases NMDA-stimulated increase in cGMP in cultured cortical neurons. (A) NMDA-induced neurotoxicity was NOS-dependent in cultured cortical neurons. Cultured neurons were treated with NMDA (30 μM or 60 μM) with or without L-NAME (10 μM or 30 μM). Neuronal viability was determined by MTT assay (top) and percentage of neuronal death by propidium iodide and calcein AM staining (bottom). * P
    Figure Legend Snippet: PSD-93 deficiency decreases NMDA-stimulated increase in cGMP in cultured cortical neurons. (A) NMDA-induced neurotoxicity was NOS-dependent in cultured cortical neurons. Cultured neurons were treated with NMDA (30 μM or 60 μM) with or without L-NAME (10 μM or 30 μM). Neuronal viability was determined by MTT assay (top) and percentage of neuronal death by propidium iodide and calcein AM staining (bottom). * P

    Techniques Used: Cell Culture, MTT Assay, Staining

    PSD-93 deficiency significantly reduces synaptic expression of NR2A and NR2B in cultured cortical neurons. (A) Representative Western blots showing the levels of PSD-93, PSD-95, NR2A, and NR2B in the total soluble and synaptosomal fractions. (B) Statistical summary of the densitometric analysis expressed relative to WT mice after normalization to corresponding β-actin or N-cadherin. ** P
    Figure Legend Snippet: PSD-93 deficiency significantly reduces synaptic expression of NR2A and NR2B in cultured cortical neurons. (A) Representative Western blots showing the levels of PSD-93, PSD-95, NR2A, and NR2B in the total soluble and synaptosomal fractions. (B) Statistical summary of the densitometric analysis expressed relative to WT mice after normalization to corresponding β-actin or N-cadherin. ** P

    Techniques Used: Expressing, Cell Culture, Western Blot, Mouse Assay

    4) Product Images from "Phosphoprotein Associated with Glycosphingolipid-Enriched Microdomains Differentially Modulates Src Kinase Activity in Brain Maturation"

    Article Title: Phosphoprotein Associated with Glycosphingolipid-Enriched Microdomains Differentially Modulates Src Kinase Activity in Brain Maturation

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0023978

    Developmental expression and Csk-binding of PSD93. A ) Whole brain lysates from WT mice of the indicated ages were Western blotted and stained for PSD93. B ) Brains of P1 wild type and Pag1 -/- mice and 3 month old WT/ Pag1 -/- littermate pairs were lysed at concentrations of 3 ml/g and 4.5 ml/g, respectively, in GEM-lysis buffer and subjected to sucrose-density centrifugation. Fractions were analyzed by Western blotting and staining for PSD93. Lipid raft fractions were identified by binding of cholera toxin subunit B (Ctx) binding to GM1-lipids in a dot blot from the fractions. C ) Densitometric quantification of the PSD93 signal in GEM-fractions as percentage of the total PSD93-signal. For both time points, the PSD93 signal in fractions 2-5 was expressed as a ratio to control. This most likely overestimates the lipid raft localized material in P1, as only fraction 2 and 3 contain rafts (n = 3 independent experiments for each time point) D ) Csk-immunoprecipitates from whole brain lysates of WT mice (ages as indicated), stained for PSD93 and Csk. Densitometric quantification of the relative amount of PSD93 bound to Csk in brains of P1 and 3 month old mice (n = 3 independent experiments) E ) Csk-immunoprecipitates from whole brain lysates of 3 month old WT and Pag1 -/- mice stained for PSD93 and Csk. Two exposures are given for the PSD93-signal in the left panel. Comparison of whole brain lysates of 3 month old WT and Pag1 -/- to P1. Given are the means +/- SEM, n.s. not significant, Student's t-test.
    Figure Legend Snippet: Developmental expression and Csk-binding of PSD93. A ) Whole brain lysates from WT mice of the indicated ages were Western blotted and stained for PSD93. B ) Brains of P1 wild type and Pag1 -/- mice and 3 month old WT/ Pag1 -/- littermate pairs were lysed at concentrations of 3 ml/g and 4.5 ml/g, respectively, in GEM-lysis buffer and subjected to sucrose-density centrifugation. Fractions were analyzed by Western blotting and staining for PSD93. Lipid raft fractions were identified by binding of cholera toxin subunit B (Ctx) binding to GM1-lipids in a dot blot from the fractions. C ) Densitometric quantification of the PSD93 signal in GEM-fractions as percentage of the total PSD93-signal. For both time points, the PSD93 signal in fractions 2-5 was expressed as a ratio to control. This most likely overestimates the lipid raft localized material in P1, as only fraction 2 and 3 contain rafts (n = 3 independent experiments for each time point) D ) Csk-immunoprecipitates from whole brain lysates of WT mice (ages as indicated), stained for PSD93 and Csk. Densitometric quantification of the relative amount of PSD93 bound to Csk in brains of P1 and 3 month old mice (n = 3 independent experiments) E ) Csk-immunoprecipitates from whole brain lysates of 3 month old WT and Pag1 -/- mice stained for PSD93 and Csk. Two exposures are given for the PSD93-signal in the left panel. Comparison of whole brain lysates of 3 month old WT and Pag1 -/- to P1. Given are the means +/- SEM, n.s. not significant, Student's t-test.

    Techniques Used: Expressing, Binding Assay, Mouse Assay, Western Blot, Staining, Lysis, Centrifugation, Dot Blot

    5) Product Images from "Localization of kainate receptors in inner and outer hair cell synapses"

    Article Title: Localization of kainate receptors in inner and outer hair cell synapses

    Journal: Hearing research

    doi: 10.1016/j.heares.2014.05.001

    GluRs show a developmental change of expression in OHCs. The apical turn (a) and basal turn (b) of whole-mount rat cochleae at P8 were used. Afferent synapses were visualized using PSD-93 (A-H, K, L) or ribeye/CtBP2 (I, J, M, N). The strial side is on
    Figure Legend Snippet: GluRs show a developmental change of expression in OHCs. The apical turn (a) and basal turn (b) of whole-mount rat cochleae at P8 were used. Afferent synapses were visualized using PSD-93 (A-H, K, L) or ribeye/CtBP2 (I, J, M, N). The strial side is on

    Techniques Used: Expressing

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    Alomone Labs anti psd 93
    Altered PSD protein composition in the hippocampal PSD fraction of KI mice during development. A , Immunoblot analyses of PSD fractions from WT and KI mice at the respective developmental ages for the indicated proteins. The following amounts of WT and KI PSD proteins were analyzed per lane: <t>PSD-93,</t> 0.5 μg; SAP102, 0.5 μg; SAP97, 2 μg; GluN2A, 0.5 μg; GluN2B, 0.5 μg; GluA1, 0.5 μg; GluA2/3, 0.5 μg; and γ2/4/8, 2 μg. The arrowhead indicates the degraded bands of PSD-93. For PSD-95, 0.25 μg of WT and 0.5 μg of KI PSD proteins were analyzed for comparison on identical membrane filters and their band intensities were corrected in B . B , Quantitation of various proteins in the PSD fractions based on the results shown in A , normalized to the wild-type level at P30 (set as 100%). The histograms show the mean ± SEM (open bars, WT; filled bars, KI). Three sets of PSD fractions at various ages (P14–P65) were examined. Simple comparison of the means and SEM of WT and KI data was performed using Student’s t-test. * P
    Anti Psd 93, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti psd 93/product/Alomone Labs
    Average 92 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    anti psd 93 - by Bioz Stars, 2022-05
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    Altered PSD protein composition in the hippocampal PSD fraction of KI mice during development. A , Immunoblot analyses of PSD fractions from WT and KI mice at the respective developmental ages for the indicated proteins. The following amounts of WT and KI PSD proteins were analyzed per lane: PSD-93, 0.5 μg; SAP102, 0.5 μg; SAP97, 2 μg; GluN2A, 0.5 μg; GluN2B, 0.5 μg; GluA1, 0.5 μg; GluA2/3, 0.5 μg; and γ2/4/8, 2 μg. The arrowhead indicates the degraded bands of PSD-93. For PSD-95, 0.25 μg of WT and 0.5 μg of KI PSD proteins were analyzed for comparison on identical membrane filters and their band intensities were corrected in B . B , Quantitation of various proteins in the PSD fractions based on the results shown in A , normalized to the wild-type level at P30 (set as 100%). The histograms show the mean ± SEM (open bars, WT; filled bars, KI). Three sets of PSD fractions at various ages (P14–P65) were examined. Simple comparison of the means and SEM of WT and KI data was performed using Student’s t-test. * P

    Journal: Molecular Brain

    Article Title: Impaired synaptic clustering of postsynaptic density proteins and altered signal transmission in hippocampal neurons, and disrupted learning behavior in PDZ1 and PDZ2 ligand binding-deficient PSD-95 knockin mice

    doi: 10.1186/1756-6606-5-43

    Figure Lengend Snippet: Altered PSD protein composition in the hippocampal PSD fraction of KI mice during development. A , Immunoblot analyses of PSD fractions from WT and KI mice at the respective developmental ages for the indicated proteins. The following amounts of WT and KI PSD proteins were analyzed per lane: PSD-93, 0.5 μg; SAP102, 0.5 μg; SAP97, 2 μg; GluN2A, 0.5 μg; GluN2B, 0.5 μg; GluA1, 0.5 μg; GluA2/3, 0.5 μg; and γ2/4/8, 2 μg. The arrowhead indicates the degraded bands of PSD-93. For PSD-95, 0.25 μg of WT and 0.5 μg of KI PSD proteins were analyzed for comparison on identical membrane filters and their band intensities were corrected in B . B , Quantitation of various proteins in the PSD fractions based on the results shown in A , normalized to the wild-type level at P30 (set as 100%). The histograms show the mean ± SEM (open bars, WT; filled bars, KI). Three sets of PSD fractions at various ages (P14–P65) were examined. Simple comparison of the means and SEM of WT and KI data was performed using Student’s t-test. * P

    Article Snippet: Immunoblot analyses and immunohistochemistry The following antibodies were used: anti-PSD-95 (mouse monoclonal; K28/43; 1:1000; NeuroMab), anti-PSD-93 (rabbit polyclonal; 1:200; Alomone Labs), anti-SAP97 (mouse monoclonal; K64/15; 1:200; NeuroMab), anti-GluA1 (rabbit polyclonal; 1:400; Chemicon), anti-GluA2/3 (rabbit polyclonal; 1:500; Chemicon), anti-GluN2A (mouse monoclonal; 1:500; BD Transduction Laboratories), anti-GluN2B (mouse monoclonal; 1:250; BD Transduction Laboratories), anti-TARPGamma2/4/8 (mouse monoclonal; N245/36; 1:200; NeuroMab), and anti-SynGAP (rabbit polyclonal; 1:1000; Affinity BioReagents), anti-AKAP150 (rabbit polyclonal; 1:1000; Millipore), anti-pan-Shank (mouse monoclonal; 1:1000; StressMarq Biosciences), anti-mGluR5 (rabbit polyclonal; 1:2000; Millipore), anti-Homer antiserum (rabbit polyclonal; 1:10000).

    Techniques: Mouse Assay, Quantitation Assay

    Altered expression of SAP102 and PSD-93 in the hippocampus of KI mice. A , Immunoblot analyses of hippocampal homogenates from WT and KI mice at the respective developmental ages for the indicated proteins. The following amounts of homogenate proteins were analyzed per lane: PSD-93 and SAP102, WT and KI: 5 μg; GluA1 and GluA2/3, WT and KI: 10 μg; and PSD-95, WT: 5 μg, KI: 20 μg. The arrowhead indicates the degraded bands of PSD-93. B , Quantitation of PSD proteins in the hippocampal homogenates based on the results shown in A , normalized to the wild-type levels at P30 (set as 100%). The histograms show the mean ± SEM (open bars, WT; filled bars, KI). Three sets of hippocampal homogenates at various ages (P4–P65) were examined. The means and SEM of WT and KI data were compared using Student’s t-test. * P

    Journal: Molecular Brain

    Article Title: Impaired synaptic clustering of postsynaptic density proteins and altered signal transmission in hippocampal neurons, and disrupted learning behavior in PDZ1 and PDZ2 ligand binding-deficient PSD-95 knockin mice

    doi: 10.1186/1756-6606-5-43

    Figure Lengend Snippet: Altered expression of SAP102 and PSD-93 in the hippocampus of KI mice. A , Immunoblot analyses of hippocampal homogenates from WT and KI mice at the respective developmental ages for the indicated proteins. The following amounts of homogenate proteins were analyzed per lane: PSD-93 and SAP102, WT and KI: 5 μg; GluA1 and GluA2/3, WT and KI: 10 μg; and PSD-95, WT: 5 μg, KI: 20 μg. The arrowhead indicates the degraded bands of PSD-93. B , Quantitation of PSD proteins in the hippocampal homogenates based on the results shown in A , normalized to the wild-type levels at P30 (set as 100%). The histograms show the mean ± SEM (open bars, WT; filled bars, KI). Three sets of hippocampal homogenates at various ages (P4–P65) were examined. The means and SEM of WT and KI data were compared using Student’s t-test. * P

    Article Snippet: Immunoblot analyses and immunohistochemistry The following antibodies were used: anti-PSD-95 (mouse monoclonal; K28/43; 1:1000; NeuroMab), anti-PSD-93 (rabbit polyclonal; 1:200; Alomone Labs), anti-SAP97 (mouse monoclonal; K64/15; 1:200; NeuroMab), anti-GluA1 (rabbit polyclonal; 1:400; Chemicon), anti-GluA2/3 (rabbit polyclonal; 1:500; Chemicon), anti-GluN2A (mouse monoclonal; 1:500; BD Transduction Laboratories), anti-GluN2B (mouse monoclonal; 1:250; BD Transduction Laboratories), anti-TARPGamma2/4/8 (mouse monoclonal; N245/36; 1:200; NeuroMab), and anti-SynGAP (rabbit polyclonal; 1:1000; Affinity BioReagents), anti-AKAP150 (rabbit polyclonal; 1:1000; Millipore), anti-pan-Shank (mouse monoclonal; 1:1000; StressMarq Biosciences), anti-mGluR5 (rabbit polyclonal; 1:2000; Millipore), anti-Homer antiserum (rabbit polyclonal; 1:10000).

    Techniques: Expressing, Mouse Assay, Quantitation Assay

    Expression of a different blocking peptide, APC::PSD-93-dn, does not alter α3*nAChR surface clusters on CG neurons in vivo

    Journal:

    Article Title: Adenomatous polyposis coli plays a key role, in vivo , in coordinating assembly of the neuronal nicotinic postsynaptic complex

    doi: 10.1016/j.mcn.2008.02.006

    Figure Lengend Snippet: Expression of a different blocking peptide, APC::PSD-93-dn, does not alter α3*nAChR surface clusters on CG neurons in vivo

    Article Snippet: Primary antibodies used were: C-20 to APC C-terminus (Santa Cruz Biotechnology, Santa Cruz, CA); ab58 to APC N-terminus (abcam, Cambridge, MA); anti-Chapsyn-110/PSD-93 (Alomone Labs, Jerusalem, Israel); anti-EB1 (Transduction Laboratories, Lexington, KY); anti-β-catenin and anti-N-cadherin (Zymed Laboratories, San Francisco, CA); for α3-nAChRs: mAb35 (Developmental Studies Hybridoma Bank, Iowa City, IA) which detects an extracellular epitope and mAb313 (Covance, Berkeley, CA) which detects an intracellular epitope; for α7-nAChRs: biotinylated α-bungarotoxin (Molecular Probes-Invitrogen, Eugene, OR); mAb2b for GlyRs (Synaptic Systems, Göttingen, Germany); anti-SV2 for synaptic vesicles (Developmental Studies Hybridoma Bank); anti-14-3-3β (K-19)(a pan-subunit 14-3-3 antibody, Santa Cruz); Alexa Fluor 568-phalloidin (Molecular Probes) to detect F-actin; neuronal specific tubulin tuj-1 (Covance); anti-IQGAP1 (gift from David Sacks, Harvard Medical School, Boston, MA, and BD Transduction Laboratories, San Diego, CA); anti-kakapo which detects macrophin (MACF) (gift of Talila Volk, Weizmann Institute of Science, Rehovot, Israel); anti-myc (Cell Signaling, Danvers, MA); anti-MBP antibody (New England Biolabs, Ipswich, MA); anti-GST (GRASP Center, Tufts University) and anti-HA (clone 3F10, Roche Diagnostics, Indianapolis, IN, and Y-11, Santa Cruz Biotechnology).

    Techniques: Expressing, Blocking Assay, In Vivo

    PSD-93 deficiency attenuates NMDA-stimulated Ca 2+ loading in cultured cortical neurons. Cultures were challenged for 5 or 10 min with 30 μM NMDA, 10 μM CNQX, and 2 μM nimodipine in medium containing 45 CaCl 2 . CMP: counts per minute. * P

    Journal: Neuroscience

    Article Title: PSD-93 Deficiency Protects Cultured Cortical Neurons from NMDA Receptor-triggered Neurotoxicity

    doi: 10.1016/j.neuroscience.2010.01.030

    Figure Lengend Snippet: PSD-93 deficiency attenuates NMDA-stimulated Ca 2+ loading in cultured cortical neurons. Cultures were challenged for 5 or 10 min with 30 μM NMDA, 10 μM CNQX, and 2 μM nimodipine in medium containing 45 CaCl 2 . CMP: counts per minute. * P

    Article Snippet: Membranes were blocked with 3% non-fat dry milk for 1 h and incubated overnight at 4°C with rabbit anti-PSD-93 (1:1,000; Alomone Labs Ltd, Jerusalem, Israel), rabbit anti-NR2A (1:200, Upstate/Chemicon, Temecula, CA), rabbit anti-NR2B (1:200, Upstate/Chemicon), mouse anti-PSD-95 (1:1,000; Upstate/Chemicon), rabbit anti- N -cadherin (1:1,000; BD Biosciences, Palo Alto, CA), or monoclonal mouse anti-β-actin (1:10,000; Santa Cruz Biotechnology, Inc., Santa Cruz, CA).

    Techniques: Cell Culture

    Efficacy of pCMV-U6-siRNA constructs. (A)RT-PCR analysis showed that a 495 bp product from PSD-93 was inhibited significantly by siP3, GAPDH mRNA was used as a loading Control. siP3 significantly decreased the mRNA of PSD93 by 80.2% of control.(B) Confirmation by western blot analysis of silencing PSD93 expression, The blots were reprobed with anti-GAPDH antibody to verify protein loading. (C) Relative protein level of PSD-93 after siRNA transfection, PSD93 decreased by 79.5% compared to control group when transfected with siP3.

    Journal: Neuroscience

    Article Title: PSD-93 Deficiency Protects Cultured Cortical Neurons from NMDA Receptor-triggered Neurotoxicity

    doi: 10.1016/j.neuroscience.2010.01.030

    Figure Lengend Snippet: Efficacy of pCMV-U6-siRNA constructs. (A)RT-PCR analysis showed that a 495 bp product from PSD-93 was inhibited significantly by siP3, GAPDH mRNA was used as a loading Control. siP3 significantly decreased the mRNA of PSD93 by 80.2% of control.(B) Confirmation by western blot analysis of silencing PSD93 expression, The blots were reprobed with anti-GAPDH antibody to verify protein loading. (C) Relative protein level of PSD-93 after siRNA transfection, PSD93 decreased by 79.5% compared to control group when transfected with siP3.

    Article Snippet: Membranes were blocked with 3% non-fat dry milk for 1 h and incubated overnight at 4°C with rabbit anti-PSD-93 (1:1,000; Alomone Labs Ltd, Jerusalem, Israel), rabbit anti-NR2A (1:200, Upstate/Chemicon, Temecula, CA), rabbit anti-NR2B (1:200, Upstate/Chemicon), mouse anti-PSD-95 (1:1,000; Upstate/Chemicon), rabbit anti- N -cadherin (1:1,000; BD Biosciences, Palo Alto, CA), or monoclonal mouse anti-β-actin (1:10,000; Santa Cruz Biotechnology, Inc., Santa Cruz, CA).

    Techniques: Construct, Polymerase Chain Reaction, Western Blot, Expressing, Transfection

    PSD-93 deficiency or knockdown protects against NMDA-stimulated neurotoxicity. Cortical neurons were cultured from WT and PSD-93 KO mice and treated with NMDA (0, 10, 20, 30, 40, and 60 μM) in the presence of 10 μM CNQX and 2 μM nimodipine. (A) Neuronal viability was assessed by MTT assay. (B) Percentage of neuronal death was determined by propidium iodide and calcein AM staining. * P

    Journal: Neuroscience

    Article Title: PSD-93 Deficiency Protects Cultured Cortical Neurons from NMDA Receptor-triggered Neurotoxicity

    doi: 10.1016/j.neuroscience.2010.01.030

    Figure Lengend Snippet: PSD-93 deficiency or knockdown protects against NMDA-stimulated neurotoxicity. Cortical neurons were cultured from WT and PSD-93 KO mice and treated with NMDA (0, 10, 20, 30, 40, and 60 μM) in the presence of 10 μM CNQX and 2 μM nimodipine. (A) Neuronal viability was assessed by MTT assay. (B) Percentage of neuronal death was determined by propidium iodide and calcein AM staining. * P

    Article Snippet: Membranes were blocked with 3% non-fat dry milk for 1 h and incubated overnight at 4°C with rabbit anti-PSD-93 (1:1,000; Alomone Labs Ltd, Jerusalem, Israel), rabbit anti-NR2A (1:200, Upstate/Chemicon, Temecula, CA), rabbit anti-NR2B (1:200, Upstate/Chemicon), mouse anti-PSD-95 (1:1,000; Upstate/Chemicon), rabbit anti- N -cadherin (1:1,000; BD Biosciences, Palo Alto, CA), or monoclonal mouse anti-β-actin (1:10,000; Santa Cruz Biotechnology, Inc., Santa Cruz, CA).

    Techniques: Cell Culture, Mouse Assay, MTT Assay, Staining

    MK-801 attenuates NMDA-induced neurotoxicity in cultured cortical neurons from WT but not from PSD-93 KO mice. Percentage of neuronal death was determined by propidium iodide and calcein AM staining (top) and neuronal viability by MTT assay (bottom). * P

    Journal: Neuroscience

    Article Title: PSD-93 Deficiency Protects Cultured Cortical Neurons from NMDA Receptor-triggered Neurotoxicity

    doi: 10.1016/j.neuroscience.2010.01.030

    Figure Lengend Snippet: MK-801 attenuates NMDA-induced neurotoxicity in cultured cortical neurons from WT but not from PSD-93 KO mice. Percentage of neuronal death was determined by propidium iodide and calcein AM staining (top) and neuronal viability by MTT assay (bottom). * P

    Article Snippet: Membranes were blocked with 3% non-fat dry milk for 1 h and incubated overnight at 4°C with rabbit anti-PSD-93 (1:1,000; Alomone Labs Ltd, Jerusalem, Israel), rabbit anti-NR2A (1:200, Upstate/Chemicon, Temecula, CA), rabbit anti-NR2B (1:200, Upstate/Chemicon), mouse anti-PSD-95 (1:1,000; Upstate/Chemicon), rabbit anti- N -cadherin (1:1,000; BD Biosciences, Palo Alto, CA), or monoclonal mouse anti-β-actin (1:10,000; Santa Cruz Biotechnology, Inc., Santa Cruz, CA).

    Techniques: Cell Culture, Mouse Assay, Staining, MTT Assay

    PSD-93 deficiency has no effect on non-NMDA receptor-triggered neurotoxicity in cultured cortical neurons. Cultured neurons were treated with kainate at the doses shown in the presence of 10 μM MK-801 and 2 μM nimodipine. Percentage of neuronal death was determined by propidium iodide and calcein AM staining (top) and neuronal viability by MTT assay (bottom). n = 6 repeats.

    Journal: Neuroscience

    Article Title: PSD-93 Deficiency Protects Cultured Cortical Neurons from NMDA Receptor-triggered Neurotoxicity

    doi: 10.1016/j.neuroscience.2010.01.030

    Figure Lengend Snippet: PSD-93 deficiency has no effect on non-NMDA receptor-triggered neurotoxicity in cultured cortical neurons. Cultured neurons were treated with kainate at the doses shown in the presence of 10 μM MK-801 and 2 μM nimodipine. Percentage of neuronal death was determined by propidium iodide and calcein AM staining (top) and neuronal viability by MTT assay (bottom). n = 6 repeats.

    Article Snippet: Membranes were blocked with 3% non-fat dry milk for 1 h and incubated overnight at 4°C with rabbit anti-PSD-93 (1:1,000; Alomone Labs Ltd, Jerusalem, Israel), rabbit anti-NR2A (1:200, Upstate/Chemicon, Temecula, CA), rabbit anti-NR2B (1:200, Upstate/Chemicon), mouse anti-PSD-95 (1:1,000; Upstate/Chemicon), rabbit anti- N -cadherin (1:1,000; BD Biosciences, Palo Alto, CA), or monoclonal mouse anti-β-actin (1:10,000; Santa Cruz Biotechnology, Inc., Santa Cruz, CA).

    Techniques: Cell Culture, Staining, MTT Assay

    PSD-93 deficiency decreases NMDA-stimulated increase in cGMP in cultured cortical neurons. (A) NMDA-induced neurotoxicity was NOS-dependent in cultured cortical neurons. Cultured neurons were treated with NMDA (30 μM or 60 μM) with or without L-NAME (10 μM or 30 μM). Neuronal viability was determined by MTT assay (top) and percentage of neuronal death by propidium iodide and calcein AM staining (bottom). * P

    Journal: Neuroscience

    Article Title: PSD-93 Deficiency Protects Cultured Cortical Neurons from NMDA Receptor-triggered Neurotoxicity

    doi: 10.1016/j.neuroscience.2010.01.030

    Figure Lengend Snippet: PSD-93 deficiency decreases NMDA-stimulated increase in cGMP in cultured cortical neurons. (A) NMDA-induced neurotoxicity was NOS-dependent in cultured cortical neurons. Cultured neurons were treated with NMDA (30 μM or 60 μM) with or without L-NAME (10 μM or 30 μM). Neuronal viability was determined by MTT assay (top) and percentage of neuronal death by propidium iodide and calcein AM staining (bottom). * P

    Article Snippet: Membranes were blocked with 3% non-fat dry milk for 1 h and incubated overnight at 4°C with rabbit anti-PSD-93 (1:1,000; Alomone Labs Ltd, Jerusalem, Israel), rabbit anti-NR2A (1:200, Upstate/Chemicon, Temecula, CA), rabbit anti-NR2B (1:200, Upstate/Chemicon), mouse anti-PSD-95 (1:1,000; Upstate/Chemicon), rabbit anti- N -cadherin (1:1,000; BD Biosciences, Palo Alto, CA), or monoclonal mouse anti-β-actin (1:10,000; Santa Cruz Biotechnology, Inc., Santa Cruz, CA).

    Techniques: Cell Culture, MTT Assay, Staining

    PSD-93 deficiency significantly reduces synaptic expression of NR2A and NR2B in cultured cortical neurons. (A) Representative Western blots showing the levels of PSD-93, PSD-95, NR2A, and NR2B in the total soluble and synaptosomal fractions. (B) Statistical summary of the densitometric analysis expressed relative to WT mice after normalization to corresponding β-actin or N-cadherin. ** P

    Journal: Neuroscience

    Article Title: PSD-93 Deficiency Protects Cultured Cortical Neurons from NMDA Receptor-triggered Neurotoxicity

    doi: 10.1016/j.neuroscience.2010.01.030

    Figure Lengend Snippet: PSD-93 deficiency significantly reduces synaptic expression of NR2A and NR2B in cultured cortical neurons. (A) Representative Western blots showing the levels of PSD-93, PSD-95, NR2A, and NR2B in the total soluble and synaptosomal fractions. (B) Statistical summary of the densitometric analysis expressed relative to WT mice after normalization to corresponding β-actin or N-cadherin. ** P

    Article Snippet: Membranes were blocked with 3% non-fat dry milk for 1 h and incubated overnight at 4°C with rabbit anti-PSD-93 (1:1,000; Alomone Labs Ltd, Jerusalem, Israel), rabbit anti-NR2A (1:200, Upstate/Chemicon, Temecula, CA), rabbit anti-NR2B (1:200, Upstate/Chemicon), mouse anti-PSD-95 (1:1,000; Upstate/Chemicon), rabbit anti- N -cadherin (1:1,000; BD Biosciences, Palo Alto, CA), or monoclonal mouse anti-β-actin (1:10,000; Santa Cruz Biotechnology, Inc., Santa Cruz, CA).

    Techniques: Expressing, Cell Culture, Western Blot, Mouse Assay

    Developmental expression and Csk-binding of PSD93. A ) Whole brain lysates from WT mice of the indicated ages were Western blotted and stained for PSD93. B ) Brains of P1 wild type and Pag1 -/- mice and 3 month old WT/ Pag1 -/- littermate pairs were lysed at concentrations of 3 ml/g and 4.5 ml/g, respectively, in GEM-lysis buffer and subjected to sucrose-density centrifugation. Fractions were analyzed by Western blotting and staining for PSD93. Lipid raft fractions were identified by binding of cholera toxin subunit B (Ctx) binding to GM1-lipids in a dot blot from the fractions. C ) Densitometric quantification of the PSD93 signal in GEM-fractions as percentage of the total PSD93-signal. For both time points, the PSD93 signal in fractions 2-5 was expressed as a ratio to control. This most likely overestimates the lipid raft localized material in P1, as only fraction 2 and 3 contain rafts (n = 3 independent experiments for each time point) D ) Csk-immunoprecipitates from whole brain lysates of WT mice (ages as indicated), stained for PSD93 and Csk. Densitometric quantification of the relative amount of PSD93 bound to Csk in brains of P1 and 3 month old mice (n = 3 independent experiments) E ) Csk-immunoprecipitates from whole brain lysates of 3 month old WT and Pag1 -/- mice stained for PSD93 and Csk. Two exposures are given for the PSD93-signal in the left panel. Comparison of whole brain lysates of 3 month old WT and Pag1 -/- to P1. Given are the means +/- SEM, n.s. not significant, Student's t-test.

    Journal: PLoS ONE

    Article Title: Phosphoprotein Associated with Glycosphingolipid-Enriched Microdomains Differentially Modulates Src Kinase Activity in Brain Maturation

    doi: 10.1371/journal.pone.0023978

    Figure Lengend Snippet: Developmental expression and Csk-binding of PSD93. A ) Whole brain lysates from WT mice of the indicated ages were Western blotted and stained for PSD93. B ) Brains of P1 wild type and Pag1 -/- mice and 3 month old WT/ Pag1 -/- littermate pairs were lysed at concentrations of 3 ml/g and 4.5 ml/g, respectively, in GEM-lysis buffer and subjected to sucrose-density centrifugation. Fractions were analyzed by Western blotting and staining for PSD93. Lipid raft fractions were identified by binding of cholera toxin subunit B (Ctx) binding to GM1-lipids in a dot blot from the fractions. C ) Densitometric quantification of the PSD93 signal in GEM-fractions as percentage of the total PSD93-signal. For both time points, the PSD93 signal in fractions 2-5 was expressed as a ratio to control. This most likely overestimates the lipid raft localized material in P1, as only fraction 2 and 3 contain rafts (n = 3 independent experiments for each time point) D ) Csk-immunoprecipitates from whole brain lysates of WT mice (ages as indicated), stained for PSD93 and Csk. Densitometric quantification of the relative amount of PSD93 bound to Csk in brains of P1 and 3 month old mice (n = 3 independent experiments) E ) Csk-immunoprecipitates from whole brain lysates of 3 month old WT and Pag1 -/- mice stained for PSD93 and Csk. Two exposures are given for the PSD93-signal in the left panel. Comparison of whole brain lysates of 3 month old WT and Pag1 -/- to P1. Given are the means +/- SEM, n.s. not significant, Student's t-test.

    Article Snippet: Antibodies and reagents Rabbit phosphor-specific anti-Src (pY418), recognizing both Y423 in mouse Src and Y419 in mouse Fyn, as well as anti-Src (pY529), recognizing both Y534 in mouse Src and Y530 in mouse Fyn due to the highly conserved sequence of these residues were purchased from BioSource, rabbit anti-Csk (C-20) and anti-Ctk from Santa Cruz, mouse-anti-Csk (clone 52) and mouse anti-CHK from BD BioSciences, mouse anti-Src (clone GD11) from Upstate (Lake Placid, NY), rabbit anti-PSD93 from Alomone Labs Ltd., rabbit anti-c-Src (Y215) from ECM Biosciences, and mouse anti-β-actin (clone AC-15) from Sigma.

    Techniques: Expressing, Binding Assay, Mouse Assay, Western Blot, Staining, Lysis, Centrifugation, Dot Blot