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anti sod2 monoclonal rabbit antibody  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc anti sod2 monoclonal rabbit antibody
    Anti Sod2 Monoclonal Rabbit Antibody, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 153 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/anti sod2 monoclonal rabbit antibody/product/Cell Signaling Technology Inc
    Average 95 stars, based on 153 article reviews
    anti sod2 monoclonal rabbit antibody - by Bioz Stars, 2026-02
    95/100 stars

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    Cell Signaling Technology Inc rabbit monoclonal anti sod2 antibody
    Measurement of anti-oxidative marker, pro-inflammatory modulator and synaptic marker in primary neuron by Western blot. Prenatally e-cig exposed offspring demonstrated significantly reduced expression of (A) NRF2 ( p < 0.05), (B) NQO1 ( p < 0.05), (C) <t>SOD2</t> ( p < 0.05), and increased expression of (E) NF-κ B ( p < 0.05) in primary neuron compared to control. However, no significant difference was found in (D) HO-1 expression. Reduced expression of (F) presynaptic marker, synaptophysin ( p < 0.01) and (G) postsynaptic marker, PSD95 ( p < 0.05) have been observed in prenatally e-cig exposed primary neuron compared to control; Biological replicates, n = 3. Data were normalized to β-Actin. C, Control, T, Treatment.
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    Primary and secondary antibodies used for fluorescence immunocytochemistry.

    Journal: International Journal of Pharmaceutics: X

    Article Title: Olive mill wastewater: From by-product to smart antioxidant material

    doi: 10.1016/j.ijpx.2024.100301

    Figure Lengend Snippet: Primary and secondary antibodies used for fluorescence immunocytochemistry.

    Article Snippet: , SOD2 , Rabbit monoclonal anti-SOD2 (Cell Signaling Technology, Danvers, MA, USA) , 1:200.

    Techniques: Fluorescence, Immunocytochemistry

    Measurement of anti-oxidative marker, pro-inflammatory modulator and synaptic marker in primary neuron by Western blot. Prenatally e-cig exposed offspring demonstrated significantly reduced expression of (A) NRF2 ( p < 0.05), (B) NQO1 ( p < 0.05), (C) SOD2 ( p < 0.05), and increased expression of (E) NF-κ B ( p < 0.05) in primary neuron compared to control. However, no significant difference was found in (D) HO-1 expression. Reduced expression of (F) presynaptic marker, synaptophysin ( p < 0.01) and (G) postsynaptic marker, PSD95 ( p < 0.05) have been observed in prenatally e-cig exposed primary neuron compared to control; Biological replicates, n = 3. Data were normalized to β-Actin. C, Control, T, Treatment.

    Journal: Frontiers in Pharmacology

    Article Title: Impact of in-utero electronic cigarette exposure on neonatal neuroinflammation, oxidative stress and mitochondrial function

    doi: 10.3389/fphar.2023.1227145

    Figure Lengend Snippet: Measurement of anti-oxidative marker, pro-inflammatory modulator and synaptic marker in primary neuron by Western blot. Prenatally e-cig exposed offspring demonstrated significantly reduced expression of (A) NRF2 ( p < 0.05), (B) NQO1 ( p < 0.05), (C) SOD2 ( p < 0.05), and increased expression of (E) NF-κ B ( p < 0.05) in primary neuron compared to control. However, no significant difference was found in (D) HO-1 expression. Reduced expression of (F) presynaptic marker, synaptophysin ( p < 0.01) and (G) postsynaptic marker, PSD95 ( p < 0.05) have been observed in prenatally e-cig exposed primary neuron compared to control; Biological replicates, n = 3. Data were normalized to β-Actin. C, Control, T, Treatment.

    Article Snippet: Membranes were incubated with rabbit polyclonal anti-NRF2 antibody (1: 2000, Invitrogen; Cat# 12721), mouse monoclonal anti-NQO1 antibody (1: 1000, Santa Cruz; Cat# SC-376023), rabbit monoclonal anti-SOD2 antibody (1: 2000, Cell Signaling; Cat# D3X8F), rabbit monoclonal anti-HO1 antibody (1:1000, Cell Signaling; Cat# E6Z5G), rabbit monoclonal anti- NF-κB antibody (1:1000, Cell Signaling; Cat# D14E12), rabbit monoclonal anti-Synaptophysin antibody (1: 1000, Cell Signaling; Cat# D8F6H), Rabbit monoclonal anti-PSD95 antibody (1: 1000, Cell Signaling; Cat# D27E11), Rabbit monoclonal antibody anti-Enolase-2 (1:2000, Cell Signaling; Cat# 9536) and mouse monoclonal anti-beta-actin (β-actin) antibody (1: 10000 MilliporeSigma; Cat# A5441) in TBST with 5% bovine serum albumin at 4°C overnight.

    Techniques: Marker, Western Blot, Expressing, Control

    Measurement of anti-oxidative marker and pro-inflammatory modulator in postnatal brain at PD7 and PD90 by Western blot. Prenatally e-cig exposed offspring demonstrated significantly reduced expression of (A) NRF2 ( p < 0.05), (B) NQO1 ( p < 0.05), (D) HO1 ( p < 0.05), and increased expression of (E) NF-κ B ( p < 0.05) in postnatal brain at PD7 compared to control; n = 4. However, no significant difference was found in (C) SOD2 expression at PD7 between prenatally e-cig exposed offspring and control offspring. At PD90, no significant difference was found in expression of (F) NRF2, (G) NQO1, (I) HO1, (J) NF-κB; n = 4. However, prenatally e-cig exposed both male and female offspring demonstrated significantly reduced expression of (H) SOD2 compared to control; n = 4. Data were normalized to β-Actin. C , Control; T, Treatment; CM, Control Male; TM, Treatment Male; CF, Control Female; TF, Treatment Female.

    Journal: Frontiers in Pharmacology

    Article Title: Impact of in-utero electronic cigarette exposure on neonatal neuroinflammation, oxidative stress and mitochondrial function

    doi: 10.3389/fphar.2023.1227145

    Figure Lengend Snippet: Measurement of anti-oxidative marker and pro-inflammatory modulator in postnatal brain at PD7 and PD90 by Western blot. Prenatally e-cig exposed offspring demonstrated significantly reduced expression of (A) NRF2 ( p < 0.05), (B) NQO1 ( p < 0.05), (D) HO1 ( p < 0.05), and increased expression of (E) NF-κ B ( p < 0.05) in postnatal brain at PD7 compared to control; n = 4. However, no significant difference was found in (C) SOD2 expression at PD7 between prenatally e-cig exposed offspring and control offspring. At PD90, no significant difference was found in expression of (F) NRF2, (G) NQO1, (I) HO1, (J) NF-κB; n = 4. However, prenatally e-cig exposed both male and female offspring demonstrated significantly reduced expression of (H) SOD2 compared to control; n = 4. Data were normalized to β-Actin. C , Control; T, Treatment; CM, Control Male; TM, Treatment Male; CF, Control Female; TF, Treatment Female.

    Article Snippet: Membranes were incubated with rabbit polyclonal anti-NRF2 antibody (1: 2000, Invitrogen; Cat# 12721), mouse monoclonal anti-NQO1 antibody (1: 1000, Santa Cruz; Cat# SC-376023), rabbit monoclonal anti-SOD2 antibody (1: 2000, Cell Signaling; Cat# D3X8F), rabbit monoclonal anti-HO1 antibody (1:1000, Cell Signaling; Cat# E6Z5G), rabbit monoclonal anti- NF-κB antibody (1:1000, Cell Signaling; Cat# D14E12), rabbit monoclonal anti-Synaptophysin antibody (1: 1000, Cell Signaling; Cat# D8F6H), Rabbit monoclonal anti-PSD95 antibody (1: 1000, Cell Signaling; Cat# D27E11), Rabbit monoclonal antibody anti-Enolase-2 (1:2000, Cell Signaling; Cat# 9536) and mouse monoclonal anti-beta-actin (β-actin) antibody (1: 10000 MilliporeSigma; Cat# A5441) in TBST with 5% bovine serum albumin at 4°C overnight.

    Techniques: Marker, Western Blot, Expressing, Control