mouse psd95 monoclonal antibody  (Cell Signaling Technology Inc)

Journal: bioRxiv

Article Title: Neuronal PARIS-STAT3 axis drives tau pathology and glial activation in Alzheimer’s disease

doi: 10.64898/2025.12.06.692741

Figure Lengend Snippet: a , Immunoblot analysis of PARIS, pSer202/pThr205-tau (AT8), pThr181-tau (AT270), pSer396-tau, total tau, and β-actin in entorhinal cortex samples from 10-month-old mice. The location of PARIS is indicated by arrows. b–e , Quantification of total tau, AT8, AT270, and pSer396-tau levels from a . Data are mean ± SEM (PS19, n = 8; PS19; Paris -/- , n = 5). Statistical significance was assessed by two-tailed t -test. f , Immunoblot analysis of PARIS, pSer202/pThr205-tau (AT8), pThr181-tau (AT270), pSer396-tau, total tau, and β-actin in frontal cortex samples from 10-month-old mice. The location of PARIS is indicated by arrows. g–j , Quantification of total tau, AT8, AT270, and pSer396-tau levels from f . Data are mean ± SEM (PS19, n = 8; PS19; Paris -/- , n = 5). Statistical significance was assessed by two-tailed t -test. k , Representative immunofluorescence images of SYNAPSIN I (green), PSD95 (red), and DAPI (blue) in the hippocampus of 10-month-old mice. Scale bar, 50 µm. l , m , Quantification of SYNAPSIN I–positive area and PSD95–positive area from k . Data are mean ± SEM (WT, n = 29; PS19, n = 31; PS19; Paris -/- , n = 29; images from 5–8 sections per mouse and 5 mice per group). Statistical significance was assessed by one-way ANOVA followed by Tukey’s post hoc test. Comparisons with P ≤ 0.05 are marked on the graph.

Article Snippet: Primary antibodies and working dilutions used were as follows: rabbit polyclonal anti-Synapsin I antibody (Millipore Sigma, AB1543, 1:1000); mouse monoclonal anti-PSD95 antibody (Novus Biologicals, NB300-556, 1:1000); mouse monoclonal anti-STAT3 antibody (Cell Signaling, 9139, 1:1,000); rabbit monoclonal phospho-STAT3 (Tyr705) antibody (Cell Signaling, Cat# 9145, 1:1,000); mouse monoclonal anti-glial fibrillary acidic protein (GFAP) antibody (Millipore Sigma, G3893, 1:2,000); rabbit polyclonal anti-Iba1 antibody (FUJIFILM Wako Pure Chemical Corporation, 019-19741, 1:1,000); rabbit polyclonal anti-complement C3 antibody (Invitrogen, PA5-21349, 1:1,000); rat monoclonal anti-CD16/CD32 antibody (Invitrogen, 14-0161-82, 1:1,000); mouse monoclonal anti-β-Amyloid antibody (6E10) (BioLegend, 803001, 1:1,000).

Techniques: Western Blot, Two Tailed Test, Immunofluorescence

Journal: bioRxiv

Article Title: Neuronal PARIS-STAT3 axis drives tau pathology and glial activation in Alzheimer’s disease

doi: 10.64898/2025.12.06.692741

Figure Lengend Snippet: a , Percentage of time in the novel arm, total distance traveled, and arm entries in the first Y-maze test. Data are mean ± SEM (Control, n = 9; CamK-PARIS, n = 9; CamK-PARIS (+Napabucasin), n = 10). Group differences were assessed by one-way ANOVA followed by Tukey’s post hoc test. b , Mean speed during Barnes maze training. Data are mean ± SEM (Control, n = 9; CamK-PARIS, n = 8; CamK-PARIS (+Napabucasin), n = 8). Group differences were assessed by one-way ANOVA followed by Tukey’s post hoc test. c , Representative immunofluorescence images of SYNAPSIN I (green), PSD95 (red), and DAPI (blue) in the hippocampus of mice. Scale bar, 50 µm. d , e , Quantification of SYNAPSIN I–positive area and PSD95–positive area from c . Data are mean ± SEM (Control, n = 33; CamK-PARIS, n = 32; CamK-PARIS (+Napabucasin), n = 31; images from 5–8 sections per mouse and 5 mice per group). Statistical significance was assessed by one-way ANOVA followed by Tukey’s post hoc test. Comparisons with P ≤ 0.05 are marked on the graph. f , Representative co-immunostaining images of GFAP (red), C3 (green), and DAPI (blue) in the hippocampus of control and CamK-PARIS mice. Scale bar, 50 µm. g–i , Quantification of GFAP and relative C3 fluorescence from f . Data are mean ± SEM (Control, n = 38; CamK-PARIS, n = 47; CamK-PARIS (+Napabucasin), n = 51; images from 7–12 sections per mouse and 5 mice per group). Statistical significance was assessed by one-way ANOVA followed by Tukey’s post hoc test. j , Representative co-immunostaining images of IBA1 (green), CD16/CD32 (red), and DAPI (blue) in the hippocampus of control and CamK-PARIS mice. Scale bar, 50 µm. k , l , Quantification of IBA1 and relative CD16/CD32 fluorescence from j . Data are mean ± SEM (Control, n = 43; CamK-PARIS, n = 45; CamK-PARIS (+Napabucasin), n = 50; images from 7–10 sections per mouse and 5 mice per group). Statistical significance was assessed by one-way ANOVA followed by Tukey’s post hoc test. Comparisons with P ≤ 0.05 are marked on the graph.

Article Snippet: Primary antibodies and working dilutions used were as follows: rabbit polyclonal anti-Synapsin I antibody (Millipore Sigma, AB1543, 1:1000); mouse monoclonal anti-PSD95 antibody (Novus Biologicals, NB300-556, 1:1000); mouse monoclonal anti-STAT3 antibody (Cell Signaling, 9139, 1:1,000); rabbit monoclonal phospho-STAT3 (Tyr705) antibody (Cell Signaling, Cat# 9145, 1:1,000); mouse monoclonal anti-glial fibrillary acidic protein (GFAP) antibody (Millipore Sigma, G3893, 1:2,000); rabbit polyclonal anti-Iba1 antibody (FUJIFILM Wako Pure Chemical Corporation, 019-19741, 1:1,000); rabbit polyclonal anti-complement C3 antibody (Invitrogen, PA5-21349, 1:1,000); rat monoclonal anti-CD16/CD32 antibody (Invitrogen, 14-0161-82, 1:1,000); mouse monoclonal anti-β-Amyloid antibody (6E10) (BioLegend, 803001, 1:1,000).

Techniques: Control, Immunofluorescence, Immunostaining, Fluorescence

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

Journal: iScience

Article Title: Microglia target synaptic sites early during excitatory circuit disassembly in neurodegeneration

doi: 10.1016/j.isci.2025.112201

Figure Lengend Snippet: Microglia-synaptic contacts increase in the IPL after transient IOP elevation (A) Confocal image stacks of an individual microglia (cyan) with engulfed PSD95 (yellow) and CtBP2 (magenta) puncta in control and laser conditions. Below are zoomed in areas of the white bounding box with each signal separated and merged. (B and C) PSD95 puncta density (B) and CtBP2 density (C) in total microglia volume in the OFF and ON sublamina of the IPL. (D and E) PSD95 density (D) and CtBP2 density (E) in individual microglia volume. (F and G) PSD95 (F) and CtBP2 (G) puncta volume was analyzed inside and outside of microglia. (H) Representative images of microglia (cyan) and CD68 (magenta) in control and laser condition. (I) Colocalized volume between microglia and CD68. (J) Representative images of microglia (cyan) and C1q (magenta) in control and laser condition. (K) Colocalized volume between microglia and C1q. Zoomed in insets of the white bounding box is presented in the lower right corner of each image. Bars represent mean ± SEM with black and green bars representing control and laser, respectively. The number of animals (n) is reported in each histogram, with individual values of each male animal represented by “x” and female by “o” markers, respectively. Z-stacks were acquired from the central region of 4 leaflets of each retina and averaged. Statistics: Mann-Whitney U test; ∗ <0.05, ∗∗ <0.01, ∗∗∗ <0.001.

Article Snippet: anti-PSD95 mouse IgG2a monoclonal antibody , Neuromab , Cat# 73-028; RRID: AB_10698024.

Techniques: Control, MANN-WHITNEY

Journal: iScience

Article Title: Microglia target synaptic sites early during excitatory circuit disassembly in neurodegeneration

doi: 10.1016/j.isci.2025.112201

Figure Lengend Snippet: Microglia target synapses on alpha RGCs following IOP elevation (A) Representative image of labeling of a single retinal ganglion cell (blue) with microglia (cyan), PSD95 (yellow), and CtBP2 (magenta), see also Figure S1 . Zoomed-in area with an intact synapse (PSD95 and CtBP2 puncta in apposition), an area with a disassembled synapse (PSD95 with no CtBP2 puncta), and an area of microglia contact with RGC without CtBP2 and PSD95. (B–D) Quantification of the contact between microglia and individual cell dendrites is presented as (B) number of individual contacts, (C) the total volume of contact and (D) the percentage of contact points colocalized with PSD95. (E–G) Colocalization analysis was performed to determine (E) the percentage of PSD95 on the ganglion cell colocalized with microglia; (F) the density of microglia colocalized with intact synapses on an individual ganglion cell; and (G) the density of microglia colocalized with disassembled synapses on an individual ganglion cell. (H) Representative images of labeling of a single RGC with C1q and microglia with zoomed in insets examples of area C1q colocalization to RGC/microglia contact points in control and laser conditions (1–2), and areas of C1q colocalization on RGC without microglia (3). (I) Correlation plot between C1q volume colocalized on RGC dendrites (abscissa) and C1q volume colocalized with RGC dendrites and microglia (ordinata). After performing linear regression analysis with 95% confidence level, R 2 and p value are reported in the chart. Bars represent mean ± SEM with black and green bars representing control and laser conditions respectively. The number of cells (n) is reported in each bar from 6 mice for OFF cells and 3 mice for ON cells (1–6 cells per retina). In all plots, individual values from male animals are represented by “x” and female by “o” markers, respectively. Statistics: Mann-Whitney U test; ∗ <0.05, ∗∗ <0.01, ∗∗∗ <0.001.

Article Snippet: anti-PSD95 mouse IgG2a monoclonal antibody , Neuromab , Cat# 73-028; RRID: AB_10698024.

Techniques: Labeling, Control, MANN-WHITNEY

Journal: iScience

Article Title: Microglia target synaptic sites early during excitatory circuit disassembly in neurodegeneration

doi: 10.1016/j.isci.2025.112201

Figure Lengend Snippet: Microglia depletion partially restores RGC function following IOP elevation (A) Experimental design and timeline of PLX5622 treatment, PERG recording, and laser-induced ocular hypertension. Following PLX5622-induced microglia depletion. (B) The volume of microglia was measured in control (black bar), control with PLX5622 treatment (magenta), laser condition (green), and laser condition animals on PLX5622 treatment (purple). The number of animals (n) is reported in each histogram. (C) Representative maximum intensity projection images of IPL microglia in control and laser conditions with and without PLX5622 treatment. (D) Colocalization analysis of PSD95 on individual ON and OFF alpha ganglion cells is represented as synapse density across the four experimental groups. The number of cells (n) is reported in each histogram from 4 to 7 animals. (E) Representative PERG traces of the four experimental groups. (F and G) Analysis of PERG amplitude (F) P1 and (G) N2 was quantified. Bars represent mean ± SEM. The number of animals (n) is reported in each histogram. In all plots, individual values from male animals are represented by “x” and female by “o” markers, respectively. Statistics: Mann-Whitney U test; ∗ <0.05, ∗∗ <0.01, ∗∗∗ <0.001, ∗∗∗∗ <0.0001.

Article Snippet: anti-PSD95 mouse IgG2a monoclonal antibody , Neuromab , Cat# 73-028; RRID: AB_10698024.

Techniques: Control, MANN-WHITNEY

Journal: iScience

Article Title: Microglia target synaptic sites early during excitatory circuit disassembly in neurodegeneration

doi: 10.1016/j.isci.2025.112201

Figure Lengend Snippet:

Article Snippet: anti-PSD95 mouse IgG2a monoclonal antibody , Neuromab , Cat# 73-028; RRID: AB_10698024.

Techniques: Imaging, Recombinant, Software