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anti β3 tubulin primary antibody  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc anti β3 tubulin primary antibody
    Fig. 6. DSRM ameliorated oxidative stress-induced neurite injury in N2a cells. (A-C) GOx inhibited N2a cell proliferation and neurite growth in the RA-induced N2a cell differentiation model (magnification 400 × ); (D-E) Immunocytochemistry demonstrated that 10 μM DSRM pre-treatment for 2 h enhanced <t>β3-tubulin</t> expression induced by 7 mU/mL GOx for 12 h in N2a cells (scale bar: 50 μm). N ≥3, **p < 0.01, ****p < 0.0001.
    Anti β3 Tubulin Primary Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 423 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti β3 tubulin primary antibody/product/Cell Signaling Technology Inc
    Average 97 stars, based on 423 article reviews
    anti β3 tubulin primary antibody - by Bioz Stars, 2026-02
    97/100 stars

    Images

    1) Product Images from "Inhibiting the SARM1-NAD + axis reduces oxidative stress-induced damage to retinal and nerve cells."

    Article Title: Inhibiting the SARM1-NAD + axis reduces oxidative stress-induced damage to retinal and nerve cells.

    Journal: International immunopharmacology

    doi: 10.1016/j.intimp.2024.112193

    Fig. 6. DSRM ameliorated oxidative stress-induced neurite injury in N2a cells. (A-C) GOx inhibited N2a cell proliferation and neurite growth in the RA-induced N2a cell differentiation model (magnification 400 × ); (D-E) Immunocytochemistry demonstrated that 10 μM DSRM pre-treatment for 2 h enhanced β3-tubulin expression induced by 7 mU/mL GOx for 12 h in N2a cells (scale bar: 50 μm). N ≥3, **p < 0.01, ****p < 0.0001.
    Figure Legend Snippet: Fig. 6. DSRM ameliorated oxidative stress-induced neurite injury in N2a cells. (A-C) GOx inhibited N2a cell proliferation and neurite growth in the RA-induced N2a cell differentiation model (magnification 400 × ); (D-E) Immunocytochemistry demonstrated that 10 μM DSRM pre-treatment for 2 h enhanced β3-tubulin expression induced by 7 mU/mL GOx for 12 h in N2a cells (scale bar: 50 μm). N ≥3, **p < 0.01, ****p < 0.0001.

    Techniques Used: Cell Differentiation, Immunocytochemistry, Expressing



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    Fig. 6. DSRM ameliorated oxidative stress-induced neurite injury in N2a cells. (A-C) GOx inhibited N2a cell proliferation and neurite growth in the RA-induced N2a cell differentiation model (magnification 400 × ); (D-E) Immunocytochemistry demonstrated that 10 μM DSRM pre-treatment for 2 h enhanced <t>β3-tubulin</t> expression induced by 7 mU/mL GOx for 12 h in N2a cells (scale bar: 50 μm). N ≥3, **p < 0.01, ****p < 0.0001.
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    Cell Signaling Technology Inc mouse anti β3 tubulin primary antibody
    Fig. 1 A3AR expression on cultured rat DRG neurons. Con- focal imaging analysis showing 20X (upper panels) and respec- tive magnification of A3AR-like immunofluorescence (red) on <t>β-III-tubulin</t> (green)-expressing DRG neuronal cultures. Cells nuclei are marked with DAPI (blue)
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    Image Search Results


    Fig. 6. DSRM ameliorated oxidative stress-induced neurite injury in N2a cells. (A-C) GOx inhibited N2a cell proliferation and neurite growth in the RA-induced N2a cell differentiation model (magnification 400 × ); (D-E) Immunocytochemistry demonstrated that 10 μM DSRM pre-treatment for 2 h enhanced β3-tubulin expression induced by 7 mU/mL GOx for 12 h in N2a cells (scale bar: 50 μm). N ≥3, **p < 0.01, ****p < 0.0001.

    Journal: International immunopharmacology

    Article Title: Inhibiting the SARM1-NAD + axis reduces oxidative stress-induced damage to retinal and nerve cells.

    doi: 10.1016/j.intimp.2024.112193

    Figure Lengend Snippet: Fig. 6. DSRM ameliorated oxidative stress-induced neurite injury in N2a cells. (A-C) GOx inhibited N2a cell proliferation and neurite growth in the RA-induced N2a cell differentiation model (magnification 400 × ); (D-E) Immunocytochemistry demonstrated that 10 μM DSRM pre-treatment for 2 h enhanced β3-tubulin expression induced by 7 mU/mL GOx for 12 h in N2a cells (scale bar: 50 μm). N ≥3, **p < 0.01, ****p < 0.0001.

    Article Snippet: After culturing and treating the cells in 24-well plates and fixing and permeabilizing them with methanol at -20 ◦C for 15 min, the cells were then washed 3 times with PBS, and then incubated in containment buffer (5 % donkey serum for containment) for 20 min, and then incubated with anti-GSDMD primary antibody (1:500, Abclonal, Wuhan, China, Cat#A20197), anti-β3-tubulin primary antibody (1:1000, CST, USA, Cat#5568S) was incubated at 4 ◦C overnight.

    Techniques: Cell Differentiation, Immunocytochemistry, Expressing

    Fig. 1 A3AR expression on cultured rat DRG neurons. Con- focal imaging analysis showing 20X (upper panels) and respec- tive magnification of A3AR-like immunofluorescence (red) on β-III-tubulin (green)-expressing DRG neuronal cultures. Cells nuclei are marked with DAPI (blue)

    Journal: Purinergic signalling

    Article Title: Covalently Binding Adenosine A 3 Receptor Agonist ICBM Irreversibly Reduces Voltage-Gated Ca 2+ Currents in Dorsal Root Ganglion Neurons.

    doi: 10.1007/s11302-023-09929-y

    Figure Lengend Snippet: Fig. 1 A3AR expression on cultured rat DRG neurons. Con- focal imaging analysis showing 20X (upper panels) and respec- tive magnification of A3AR-like immunofluorescence (red) on β-III-tubulin (green)-expressing DRG neuronal cultures. Cells nuclei are marked with DAPI (blue)

    Article Snippet: After triply washing with PBS, the neurons were incubated with 10% goat serum (Merck Life Science S.r.l) in PBST (PBST-GS) for 30 min, to block nonspecific antibody binding, and then incubated at ambient temperature for 2.5 h in PBST-GS containing primary rabbit anti-A3R antibody (Alomone Labs, Jerusalem, Israel, diluted 1:100) plus mouse anti-β3-tubulin primary antibody (Cell Signaling Technology, Danvers, MA, USA, diluted 1:400).

    Techniques: Expressing, Cell Culture, Imaging, Immunofluorescence