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anti psd95 primary  (Proteintech)


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    Structured Review

    Proteintech anti psd95 primary
    Anti Psd95 Primary, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 452 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+antibodies+psd95/PSD95-Specific%2CDLG4+Antibody/pm41933661-135-5-8
    Average 96 stars, based on 452 article reviews
    anti psd95 primary - by Bioz Stars, 2026-09
    96/100 stars

    Images

    Related Articles

    Centrifugation:

    Article Title: The regulatory role of NAAG-mGluR3 signaling on cortical synaptic plasticity after hypoxic ischemia
    Article Snippet: Further, after centrifugation the supernatant was collected for protein concentration determination followed by denaturation using 5X loading buffer at 100 °C for 5 min. SDS-PAGE electrophoresis was performed by loading 30 μg of protein to each lane with electrophoresis conditions at 140 V for 60 min. Further, the sample were transferred to a PVDF membrane and blocked with 5% skim milk for 2 h. The membrane was further incubated with primary antibodies such as GCPII (1:2000, ab133579), syph(1:1000, ab52636), PSD95 (1: 1000, ab18258), β-actin (1: 1000, ab8226), at 4 °C overnight and then incubated with horseradish peroxidase (HRP) conjugated rabbit and mouse IgG secondary antibody (1: 10,000, proteintech, SA00001-1; SA00001-2) for 2 h at room temperature.

    Protein Concentration:

    Article Title: The regulatory role of NAAG-mGluR3 signaling on cortical synaptic plasticity after hypoxic ischemia
    Article Snippet: Further, after centrifugation the supernatant was collected for protein concentration determination followed by denaturation using 5X loading buffer at 100 °C for 5 min. SDS-PAGE electrophoresis was performed by loading 30 μg of protein to each lane with electrophoresis conditions at 140 V for 60 min. Further, the sample were transferred to a PVDF membrane and blocked with 5% skim milk for 2 h. The membrane was further incubated with primary antibodies such as GCPII (1:2000, ab133579), syph(1:1000, ab52636), PSD95 (1: 1000, ab18258), β-actin (1: 1000, ab8226), at 4 °C overnight and then incubated with horseradish peroxidase (HRP) conjugated rabbit and mouse IgG secondary antibody (1: 10,000, proteintech, SA00001-1; SA00001-2) for 2 h at room temperature.

    SDS Page:

    Article Title: The regulatory role of NAAG-mGluR3 signaling on cortical synaptic plasticity after hypoxic ischemia
    Article Snippet: Further, after centrifugation the supernatant was collected for protein concentration determination followed by denaturation using 5X loading buffer at 100 °C for 5 min. SDS-PAGE electrophoresis was performed by loading 30 μg of protein to each lane with electrophoresis conditions at 140 V for 60 min. Further, the sample were transferred to a PVDF membrane and blocked with 5% skim milk for 2 h. The membrane was further incubated with primary antibodies such as GCPII (1:2000, ab133579), syph(1:1000, ab52636), PSD95 (1: 1000, ab18258), β-actin (1: 1000, ab8226), at 4 °C overnight and then incubated with horseradish peroxidase (HRP) conjugated rabbit and mouse IgG secondary antibody (1: 10,000, proteintech, SA00001-1; SA00001-2) for 2 h at room temperature.

    Electrophoresis:

    Article Title: The regulatory role of NAAG-mGluR3 signaling on cortical synaptic plasticity after hypoxic ischemia
    Article Snippet: Further, after centrifugation the supernatant was collected for protein concentration determination followed by denaturation using 5X loading buffer at 100 °C for 5 min. SDS-PAGE electrophoresis was performed by loading 30 μg of protein to each lane with electrophoresis conditions at 140 V for 60 min. Further, the sample were transferred to a PVDF membrane and blocked with 5% skim milk for 2 h. The membrane was further incubated with primary antibodies such as GCPII (1:2000, ab133579), syph(1:1000, ab52636), PSD95 (1: 1000, ab18258), β-actin (1: 1000, ab8226), at 4 °C overnight and then incubated with horseradish peroxidase (HRP) conjugated rabbit and mouse IgG secondary antibody (1: 10,000, proteintech, SA00001-1; SA00001-2) for 2 h at room temperature.

    Membrane:

    Article Title: The regulatory role of NAAG-mGluR3 signaling on cortical synaptic plasticity after hypoxic ischemia
    Article Snippet: Further, after centrifugation the supernatant was collected for protein concentration determination followed by denaturation using 5X loading buffer at 100 °C for 5 min. SDS-PAGE electrophoresis was performed by loading 30 μg of protein to each lane with electrophoresis conditions at 140 V for 60 min. Further, the sample were transferred to a PVDF membrane and blocked with 5% skim milk for 2 h. The membrane was further incubated with primary antibodies such as GCPII (1:2000, ab133579), syph(1:1000, ab52636), PSD95 (1: 1000, ab18258), β-actin (1: 1000, ab8226), at 4 °C overnight and then incubated with horseradish peroxidase (HRP) conjugated rabbit and mouse IgG secondary antibody (1: 10,000, proteintech, SA00001-1; SA00001-2) for 2 h at room temperature.

    Incubation:

    Article Title: The regulatory role of NAAG-mGluR3 signaling on cortical synaptic plasticity after hypoxic ischemia
    Article Snippet: Further, after centrifugation the supernatant was collected for protein concentration determination followed by denaturation using 5X loading buffer at 100 °C for 5 min. SDS-PAGE electrophoresis was performed by loading 30 μg of protein to each lane with electrophoresis conditions at 140 V for 60 min. Further, the sample were transferred to a PVDF membrane and blocked with 5% skim milk for 2 h. The membrane was further incubated with primary antibodies such as GCPII (1:2000, ab133579), syph(1:1000, ab52636), PSD95 (1: 1000, ab18258), β-actin (1: 1000, ab8226), at 4 °C overnight and then incubated with horseradish peroxidase (HRP) conjugated rabbit and mouse IgG secondary antibody (1: 10,000, proteintech, SA00001-1; SA00001-2) for 2 h at room temperature.



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    (A–H) Synaptic density analysis with Emerin KD and OE. (A and B) Experimental workflow (A). DIV12 neuronal cultures were immunolabeled with synaptic markers (B). (C) Color-code for data in (E) and (H). (D) Representative images of Synaptophysin and <t>PSD95</t> immunolabeling with Emerin KD (2 top rows) and Emerin OE in excitatory (2 center rows) and inhibitory neurons (2 bottom rows). (E) Quantification of Synaptophysin and PSD95 puncta and their colocalization with Emerin KD (top row), Emerin OE in excitatory (center row), and inhibitory neurons (bottom row). (F and G) Representative images of Homer1 and Gephyrin with Emerin KD (F) and Emerin OE in excitatory neurons (G). Boxed regions in DAPI images are shown enlarged for Homer1 and Gephyrin. (H) Quantification of Homer1 and Gephyrin puncta with Emerin KD (top row) and Emerin OE in excitatory (center row) and inhibitory neurons (bottom row). (E and H) Quantification of postsynaptic components is highlighted in gray. Punctum counts are normalized to neuron numbers, based on DAPI. n = 12 individual wells from 4 independent culture preparations, Mann-Whitney test. Lines indicate median and 95% CI. (I–N) Spine morphology analysis with Emerin KD. (I) Representative image of a sparsely labeled neuron expressing EGFP. Blue rectangle, a representative secondary dendrite selected for analysis. (J) Representative dendritic stretches from Emerin KD and sham KD neurons. Examples of the four spine types quantified are labeled. (K–N) Counts of all spine types (K), filopodia (L), mushroom (M), and all types excluding filopodia (N). n = 10–11 ~45-mm dendritic stretches, each from one individual neuron. 3 independent culture preparations, Mann-Whitney test. Lines indicate median and 95% CI. Scale bars: 50 μm (D), 100 μm (I), and 10 μm (J). The scale bars in (G) (50 μm) apply to (F).
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    Acute sleep deprivation caused Ca 2+ overload and impaired synaptic plasticity in the PL of mice with memory impairment. (A) Timeline of tissue collection for measuring Ca 2+ concentration and <t>PSD95</t> expression. (B) Ca 2+ concentration in the PL was significantly higher in the ASD FC group. (C) PSD95 mRNA level was significantly lower in the ASD FC group. (D) Representative immunoblot images of PSD95. (E) The expression of PSD95 proteins was significantly reduced in sleep deprived mice. (F) Representative immunofluorescence of PSD95 in two groups. (G) Quantitative analysis showed that PSD95 protein expression was significantly decreased. (H) Timeline for dendrite spine density analysis. (I) Schematic diagram showing the dendritic spines of PL neurons. Secondary basal spine dendrites were analyzed. Scale bar: 10 μm (J) Representative dendrites spines of PL neurons from control and sleep-deprived mice. Scale bar: 2 μm. (K) Dendritic spine densities of PL neurons in control and sleep-deprived mice were quantified. n ​= ​12–15 dendrites from 3 mice per group. FC: fear conditioned; ASD: acute sleep deprivation; Mean ±SEM. ∗ p ​< ​0.05, ∗∗ p ​< ​0.01, ∗∗∗∗ p < 0.0001. Scale bar: 40 μm.
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    Acute sleep deprivation caused Ca 2+ overload and impaired synaptic plasticity in the PL of mice with memory impairment. (A) Timeline of tissue collection for measuring Ca 2+ concentration and <t>PSD95</t> expression. (B) Ca 2+ concentration in the PL was significantly higher in the ASD FC group. (C) PSD95 mRNA level was significantly lower in the ASD FC group. (D) Representative immunoblot images of PSD95. (E) The expression of PSD95 proteins was significantly reduced in sleep deprived mice. (F) Representative immunofluorescence of PSD95 in two groups. (G) Quantitative analysis showed that PSD95 protein expression was significantly decreased. (H) Timeline for dendrite spine density analysis. (I) Schematic diagram showing the dendritic spines of PL neurons. Secondary basal spine dendrites were analyzed. Scale bar: 10 μm (J) Representative dendrites spines of PL neurons from control and sleep-deprived mice. Scale bar: 2 μm. (K) Dendritic spine densities of PL neurons in control and sleep-deprived mice were quantified. n ​= ​12–15 dendrites from 3 mice per group. FC: fear conditioned; ASD: acute sleep deprivation; Mean ±SEM. ∗ p ​< ​0.05, ∗∗ p ​< ​0.01, ∗∗∗∗ p < 0.0001. Scale bar: 40 μm.
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    Acute sleep deprivation caused Ca 2+ overload and impaired synaptic plasticity in the PL of mice with memory impairment. (A) Timeline of tissue collection for measuring Ca 2+ concentration and <t>PSD95</t> expression. (B) Ca 2+ concentration in the PL was significantly higher in the ASD FC group. (C) PSD95 mRNA level was significantly lower in the ASD FC group. (D) Representative immunoblot images of PSD95. (E) The expression of PSD95 proteins was significantly reduced in sleep deprived mice. (F) Representative immunofluorescence of PSD95 in two groups. (G) Quantitative analysis showed that PSD95 protein expression was significantly decreased. (H) Timeline for dendrite spine density analysis. (I) Schematic diagram showing the dendritic spines of PL neurons. Secondary basal spine dendrites were analyzed. Scale bar: 10 μm (J) Representative dendrites spines of PL neurons from control and sleep-deprived mice. Scale bar: 2 μm. (K) Dendritic spine densities of PL neurons in control and sleep-deprived mice were quantified. n ​= ​12–15 dendrites from 3 mice per group. FC: fear conditioned; ASD: acute sleep deprivation; Mean ±SEM. ∗ p ​< ​0.05, ∗∗ p ​< ​0.01, ∗∗∗∗ p < 0.0001. Scale bar: 40 μm.
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    Image Search Results


    Assessment of synaptic (S) and non-synaptic (NS) mitochondrial proteins associated with mitochondrial bioenergetics and Ca 2+ handling. Representative immunoblots (A) and quantification of the relative protein expressions of mCU (B) , VDAC (C) , ANT1 (D) and CyP D (E) in synaptic and non-synaptic mitochondria normalized to the mitochondrial housekeeping protein, COX IV. Error bars represent mean ± SEM ( * p < 0.05 and ** p < 0.01).

    Journal: Frontiers in Synaptic Neuroscience

    Article Title: Differential Ca 2+ handling by isolated synaptic and non-synaptic mitochondria: roles of Ca 2+ buffering and efflux

    doi: 10.3389/fnsyn.2025.1562065

    Figure Lengend Snippet: Assessment of synaptic (S) and non-synaptic (NS) mitochondrial proteins associated with mitochondrial bioenergetics and Ca 2+ handling. Representative immunoblots (A) and quantification of the relative protein expressions of mCU (B) , VDAC (C) , ANT1 (D) and CyP D (E) in synaptic and non-synaptic mitochondria normalized to the mitochondrial housekeeping protein, COX IV. Error bars represent mean ± SEM ( * p < 0.05 and ** p < 0.01).

    Article Snippet: The membranes were blotted with the following primary antibodies: mCU, Synaptophysin, PSD95, VDAC, ANT1, (Cell Signaling Technology) and Cyp D (abcam).

    Techniques: Western Blot

    (A–H) Synaptic density analysis with Emerin KD and OE. (A and B) Experimental workflow (A). DIV12 neuronal cultures were immunolabeled with synaptic markers (B). (C) Color-code for data in (E) and (H). (D) Representative images of Synaptophysin and PSD95 immunolabeling with Emerin KD (2 top rows) and Emerin OE in excitatory (2 center rows) and inhibitory neurons (2 bottom rows). (E) Quantification of Synaptophysin and PSD95 puncta and their colocalization with Emerin KD (top row), Emerin OE in excitatory (center row), and inhibitory neurons (bottom row). (F and G) Representative images of Homer1 and Gephyrin with Emerin KD (F) and Emerin OE in excitatory neurons (G). Boxed regions in DAPI images are shown enlarged for Homer1 and Gephyrin. (H) Quantification of Homer1 and Gephyrin puncta with Emerin KD (top row) and Emerin OE in excitatory (center row) and inhibitory neurons (bottom row). (E and H) Quantification of postsynaptic components is highlighted in gray. Punctum counts are normalized to neuron numbers, based on DAPI. n = 12 individual wells from 4 independent culture preparations, Mann-Whitney test. Lines indicate median and 95% CI. (I–N) Spine morphology analysis with Emerin KD. (I) Representative image of a sparsely labeled neuron expressing EGFP. Blue rectangle, a representative secondary dendrite selected for analysis. (J) Representative dendritic stretches from Emerin KD and sham KD neurons. Examples of the four spine types quantified are labeled. (K–N) Counts of all spine types (K), filopodia (L), mushroom (M), and all types excluding filopodia (N). n = 10–11 ~45-mm dendritic stretches, each from one individual neuron. 3 independent culture preparations, Mann-Whitney test. Lines indicate median and 95% CI. Scale bars: 50 μm (D), 100 μm (I), and 10 μm (J). The scale bars in (G) (50 μm) apply to (F).

    Journal: Cell reports

    Article Title: Activity-dependent synthesis of Emerin gates neuronal plasticity by regulating proteostasis

    doi: 10.1016/j.celrep.2025.115439

    Figure Lengend Snippet: (A–H) Synaptic density analysis with Emerin KD and OE. (A and B) Experimental workflow (A). DIV12 neuronal cultures were immunolabeled with synaptic markers (B). (C) Color-code for data in (E) and (H). (D) Representative images of Synaptophysin and PSD95 immunolabeling with Emerin KD (2 top rows) and Emerin OE in excitatory (2 center rows) and inhibitory neurons (2 bottom rows). (E) Quantification of Synaptophysin and PSD95 puncta and their colocalization with Emerin KD (top row), Emerin OE in excitatory (center row), and inhibitory neurons (bottom row). (F and G) Representative images of Homer1 and Gephyrin with Emerin KD (F) and Emerin OE in excitatory neurons (G). Boxed regions in DAPI images are shown enlarged for Homer1 and Gephyrin. (H) Quantification of Homer1 and Gephyrin puncta with Emerin KD (top row) and Emerin OE in excitatory (center row) and inhibitory neurons (bottom row). (E and H) Quantification of postsynaptic components is highlighted in gray. Punctum counts are normalized to neuron numbers, based on DAPI. n = 12 individual wells from 4 independent culture preparations, Mann-Whitney test. Lines indicate median and 95% CI. (I–N) Spine morphology analysis with Emerin KD. (I) Representative image of a sparsely labeled neuron expressing EGFP. Blue rectangle, a representative secondary dendrite selected for analysis. (J) Representative dendritic stretches from Emerin KD and sham KD neurons. Examples of the four spine types quantified are labeled. (K–N) Counts of all spine types (K), filopodia (L), mushroom (M), and all types excluding filopodia (N). n = 10–11 ~45-mm dendritic stretches, each from one individual neuron. 3 independent culture preparations, Mann-Whitney test. Lines indicate median and 95% CI. Scale bars: 50 μm (D), 100 μm (I), and 10 μm (J). The scale bars in (G) (50 μm) apply to (F).

    Article Snippet: Mouse anti-PSD95 monoclonal primary antibody , Cell signaling #36233 , RRID: AB_2721262.

    Techniques: Immunolabeling, MANN-WHITNEY, Labeling, Expressing

    Acute sleep deprivation caused Ca 2+ overload and impaired synaptic plasticity in the PL of mice with memory impairment. (A) Timeline of tissue collection for measuring Ca 2+ concentration and PSD95 expression. (B) Ca 2+ concentration in the PL was significantly higher in the ASD FC group. (C) PSD95 mRNA level was significantly lower in the ASD FC group. (D) Representative immunoblot images of PSD95. (E) The expression of PSD95 proteins was significantly reduced in sleep deprived mice. (F) Representative immunofluorescence of PSD95 in two groups. (G) Quantitative analysis showed that PSD95 protein expression was significantly decreased. (H) Timeline for dendrite spine density analysis. (I) Schematic diagram showing the dendritic spines of PL neurons. Secondary basal spine dendrites were analyzed. Scale bar: 10 μm (J) Representative dendrites spines of PL neurons from control and sleep-deprived mice. Scale bar: 2 μm. (K) Dendritic spine densities of PL neurons in control and sleep-deprived mice were quantified. n ​= ​12–15 dendrites from 3 mice per group. FC: fear conditioned; ASD: acute sleep deprivation; Mean ±SEM. ∗ p ​< ​0.05, ∗∗ p ​< ​0.01, ∗∗∗∗ p < 0.0001. Scale bar: 40 μm.

    Journal: Cell Insight

    Article Title: The role of TRPV4 in acute sleep deprivation-induced memory impairment: Mechanisms of calcium dysregulation and synaptic plasticity disruption

    doi: 10.1016/j.cellin.2025.100240

    Figure Lengend Snippet: Acute sleep deprivation caused Ca 2+ overload and impaired synaptic plasticity in the PL of mice with memory impairment. (A) Timeline of tissue collection for measuring Ca 2+ concentration and PSD95 expression. (B) Ca 2+ concentration in the PL was significantly higher in the ASD FC group. (C) PSD95 mRNA level was significantly lower in the ASD FC group. (D) Representative immunoblot images of PSD95. (E) The expression of PSD95 proteins was significantly reduced in sleep deprived mice. (F) Representative immunofluorescence of PSD95 in two groups. (G) Quantitative analysis showed that PSD95 protein expression was significantly decreased. (H) Timeline for dendrite spine density analysis. (I) Schematic diagram showing the dendritic spines of PL neurons. Secondary basal spine dendrites were analyzed. Scale bar: 10 μm (J) Representative dendrites spines of PL neurons from control and sleep-deprived mice. Scale bar: 2 μm. (K) Dendritic spine densities of PL neurons in control and sleep-deprived mice were quantified. n ​= ​12–15 dendrites from 3 mice per group. FC: fear conditioned; ASD: acute sleep deprivation; Mean ±SEM. ∗ p ​< ​0.05, ∗∗ p ​< ​0.01, ∗∗∗∗ p < 0.0001. Scale bar: 40 μm.

    Article Snippet: Next, the brain slices were incubated overnight at 4 °C with anti-PSD95 primary antibody (1:1000, Proteintech, 20665-1-AP, RRID: AB_2687961, Wuhan, China).

    Techniques: Concentration Assay, Expressing, Western Blot, Immunofluorescence, Control

    Ca 2+ concentration was reduced, and impaired synaptic plasticity was reversed in the PL following TRPV4-shRNA lentivirus infusion in sleep-deprived mice. (A) Timeline of tissue collection for measuring Ca 2+ concentration and PSD95 expression after TRPV4-shRNA knockdown. (B) TRPV4 knockdown significantly reduced the concentration of Ca 2+ in the PL of sleep-deprived mice. (C) PSD95 mRNA level was significantly increased in the ASD TRPV4-shRNA group. (D) Representative immunoblot images of PSD95 in the two groups. (E) PSD95 protein expression was significantly increased after TRPV4-shRNA infusion compared to scramble virus infusion. (F) Representative immunofluorescence of PSD95 in the two groups. (G) Quantitative analysis showed that PSD95 protein expression was significantly enhanced. (H) Timeline for dendrite spine density analysis in different groups. (I) Schematic diagram showing dendritic spines of PL neurons. Secondary basal spine dendrites were analyzed. Scale bar: 10 μm. (J) Representative dendrites spines of PL neurons from sleep-deprived mice after scramble or TRPV4-shRNA lentivirus infusion. Scale bar: 2 μm. (K) Dendritic spine densities of PL neurons in sleep-deprived mice were quantified after different virus infusions ( n ​= ​12–18 dendrites from 3 mice per group). FC: fear conditioned; ASD: acute sleep deprivation; Mean ±SEM. ∗ p ​< ​0.05, ∗∗ p ​< ​0.01, ∗∗∗ p < 0.001. Scale bar: 40 μm.

    Journal: Cell Insight

    Article Title: The role of TRPV4 in acute sleep deprivation-induced memory impairment: Mechanisms of calcium dysregulation and synaptic plasticity disruption

    doi: 10.1016/j.cellin.2025.100240

    Figure Lengend Snippet: Ca 2+ concentration was reduced, and impaired synaptic plasticity was reversed in the PL following TRPV4-shRNA lentivirus infusion in sleep-deprived mice. (A) Timeline of tissue collection for measuring Ca 2+ concentration and PSD95 expression after TRPV4-shRNA knockdown. (B) TRPV4 knockdown significantly reduced the concentration of Ca 2+ in the PL of sleep-deprived mice. (C) PSD95 mRNA level was significantly increased in the ASD TRPV4-shRNA group. (D) Representative immunoblot images of PSD95 in the two groups. (E) PSD95 protein expression was significantly increased after TRPV4-shRNA infusion compared to scramble virus infusion. (F) Representative immunofluorescence of PSD95 in the two groups. (G) Quantitative analysis showed that PSD95 protein expression was significantly enhanced. (H) Timeline for dendrite spine density analysis in different groups. (I) Schematic diagram showing dendritic spines of PL neurons. Secondary basal spine dendrites were analyzed. Scale bar: 10 μm. (J) Representative dendrites spines of PL neurons from sleep-deprived mice after scramble or TRPV4-shRNA lentivirus infusion. Scale bar: 2 μm. (K) Dendritic spine densities of PL neurons in sleep-deprived mice were quantified after different virus infusions ( n ​= ​12–18 dendrites from 3 mice per group). FC: fear conditioned; ASD: acute sleep deprivation; Mean ±SEM. ∗ p ​< ​0.05, ∗∗ p ​< ​0.01, ∗∗∗ p < 0.001. Scale bar: 40 μm.

    Article Snippet: Next, the brain slices were incubated overnight at 4 °C with anti-PSD95 primary antibody (1:1000, Proteintech, 20665-1-AP, RRID: AB_2687961, Wuhan, China).

    Techniques: Concentration Assay, shRNA, Expressing, Knockdown, Western Blot, Virus, Immunofluorescence