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rabbit polyclonal anti nrf2  (Proteintech)


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    Structured Review

    Proteintech rabbit polyclonal anti nrf2
    Rabbit Polyclonal Anti Nrf2, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 2093 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/rabbit+polyclonal+anti+nrf2/NRF2%2C+NFE2L2+Antibody/pmc13011206-161-29-34
    Average 96 stars, based on 2093 article reviews
    rabbit polyclonal anti nrf2 - by Bioz Stars, 2026-09
    96/100 stars

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    Related Articles

    Incubation:

    Article Title: NRF2 deficiency impairs proliferation and survival of chicken primordial germ cells via oxidative stress, mitochondrial dysfunction and apoptosis
    Article Snippet: .. The membranes were blocked with TBS containing 0.1% Tween 20 and 5% non-fat milk for 2 h at room temperature, followed by overnight incubation at 4°C with primary antibodies: rabbit polyclonal anti-NRF2 (1:2000, 16396-1-AP, Proteintech, Wuhan, China), rabbit polyclonal anti-LC3B (1:1000, NB100-2220, Novus Biologicals, Littleton, CO, USA), and rabbit polyclonal anti-GAPDH (1:1000, 10494-1-AP, Proteintech, Wuhan, China), which was used as the internal loading control for normalization. ..

    Article Title: Nrf2-and p53-inducible REDD2/DDiT4L/Rtp801L confers pancreatic β-cell dysfunction, leading to glucose intolerance in high-fat diet-fed mice
    Article Snippet: TUNEL staining was performed using DeadEnd Fluorometric TUNEL system kit (Promega). .. To analyze the expressions of p53 and Nrf2, the sliced pancreas sections from paraffin block were incubated with mouse monoclonal anti-insulin (D6C4cc) and rabbit polyclonal anti-Nrf2 (16396-1-AP, Proteintech, RRID: AB_2782956 ) or rabbit polyclonal anti-phospho-p53 (Ser15) (#9284, Cell Signaling Technology, RRID: AB_331464 ), followed by incubation with goat anti-mouse IgG (H + L) Cross-Adsorbed Secondary Antibody (Alexa Fluor 488) and goat anti-rabbit IgG (H + L) Cross-Adsorbed Secondary Antibody (Alexa Fluor 555) along with DAPI. .. The tissue sections were observed using a model BZ-X810 HS All-in-one Fluorescence Microscope (Keyence).

    Article Title: NRF2 deficiency impairs proliferation and survival of chicken primordial germ cells via oxidative stress, mitochondrial dysfunction and apoptosis.
    Article Snippet: .. The membranes were blocked with TBS containing 0.1% Tween 20 and 5% non-fat milk for 2 h at room temperature, followed by overnight incubation at 4◦C with primary antibodies: rabbit polyclonal anti-NRF2 (1:2000, 16396-1-AP, Proteintech, Wuhan, China), rabbit polyclonal anti-LC3B (1:1000, NB100-2220, Novus Biologicals, Littleton, CO, USA), and rabbit polyclonal anti-GAPDH (1:1000, 10494-1-AP, Proteintech, Wuhan, China), which was used as the internal loading control for normalization. ..

    Article Title: Nrf2- and p53-inducible REDD2/DDiT4L/Rtp801L confers pancreatic β-cell dysfunction, leading to glucose intolerance in high-fat diet-fed mice.
    Article Snippet: TUNEL staining was performed using DeadEnd Fluorometric TUNEL system kit (Promega). .. To analyze the expressions of p53 and Nrf2, the sliced pancreas sections from paraffin block were incubated with mouse monoclonal anti-insulin (D6C4cc) and rabbit polyclonal anti-Nrf2 (16396-1-AP, Proteintech, RRID:AB_2782956) or rabbit polyclonal anti-phospho-p53 (Ser15) (#9284, Cell Signaling Technology, RRID:AB_331464), followed by incubation with goat anti-mouse IgG (H+L) CrossAdsorbed Secondary Antibody (Alexa Fluor 488) and goat anti-rabbit IgG (H+L) CrossAdsorbed Secondary Antibody (Alexa Fluor 555) along with DAPI. .. The tissue sections were observed using a model BZ-X810 HS All-in-one Fluorescence Microscope Jo urn al Pr e-p roo f (Keyence, Osaka, Japan).

    Article Title: MitoQ alleviates H 2 O 2 -induced mitochondrial dysfunction in keratinocytes through the Nrf2/PINK1 pathway.
    Article Snippet: Oxidative stress plays a critical role in the pathogenesis of vitiligo by damaging keratinocytes, which disrupts their biological functions and influences the progression of the disease.. MitoQ, a mitochondria-specific antioxidant, has the potential to prevent disorders associated with oxidative stress and to exert protective effects specifically on mitochondria.. This study investigated the protective effects of MitoQ against oxidative stress in keratinocytes.

    Control:

    Article Title: NRF2 deficiency impairs proliferation and survival of chicken primordial germ cells via oxidative stress, mitochondrial dysfunction and apoptosis
    Article Snippet: .. The membranes were blocked with TBS containing 0.1% Tween 20 and 5% non-fat milk for 2 h at room temperature, followed by overnight incubation at 4°C with primary antibodies: rabbit polyclonal anti-NRF2 (1:2000, 16396-1-AP, Proteintech, Wuhan, China), rabbit polyclonal anti-LC3B (1:1000, NB100-2220, Novus Biologicals, Littleton, CO, USA), and rabbit polyclonal anti-GAPDH (1:1000, 10494-1-AP, Proteintech, Wuhan, China), which was used as the internal loading control for normalization. ..

    Article Title: NRF2 deficiency impairs proliferation and survival of chicken primordial germ cells via oxidative stress, mitochondrial dysfunction and apoptosis.
    Article Snippet: .. The membranes were blocked with TBS containing 0.1% Tween 20 and 5% non-fat milk for 2 h at room temperature, followed by overnight incubation at 4◦C with primary antibodies: rabbit polyclonal anti-NRF2 (1:2000, 16396-1-AP, Proteintech, Wuhan, China), rabbit polyclonal anti-LC3B (1:1000, NB100-2220, Novus Biologicals, Littleton, CO, USA), and rabbit polyclonal anti-GAPDH (1:1000, 10494-1-AP, Proteintech, Wuhan, China), which was used as the internal loading control for normalization. ..

    Blocking Assay:

    Article Title: Nrf2-and p53-inducible REDD2/DDiT4L/Rtp801L confers pancreatic β-cell dysfunction, leading to glucose intolerance in high-fat diet-fed mice
    Article Snippet: TUNEL staining was performed using DeadEnd Fluorometric TUNEL system kit (Promega). .. To analyze the expressions of p53 and Nrf2, the sliced pancreas sections from paraffin block were incubated with mouse monoclonal anti-insulin (D6C4cc) and rabbit polyclonal anti-Nrf2 (16396-1-AP, Proteintech, RRID: AB_2782956 ) or rabbit polyclonal anti-phospho-p53 (Ser15) (#9284, Cell Signaling Technology, RRID: AB_331464 ), followed by incubation with goat anti-mouse IgG (H + L) Cross-Adsorbed Secondary Antibody (Alexa Fluor 488) and goat anti-rabbit IgG (H + L) Cross-Adsorbed Secondary Antibody (Alexa Fluor 555) along with DAPI. .. The tissue sections were observed using a model BZ-X810 HS All-in-one Fluorescence Microscope (Keyence).

    Article Title: Nrf2- and p53-inducible REDD2/DDiT4L/Rtp801L confers pancreatic β-cell dysfunction, leading to glucose intolerance in high-fat diet-fed mice.
    Article Snippet: TUNEL staining was performed using DeadEnd Fluorometric TUNEL system kit (Promega). .. To analyze the expressions of p53 and Nrf2, the sliced pancreas sections from paraffin block were incubated with mouse monoclonal anti-insulin (D6C4cc) and rabbit polyclonal anti-Nrf2 (16396-1-AP, Proteintech, RRID:AB_2782956) or rabbit polyclonal anti-phospho-p53 (Ser15) (#9284, Cell Signaling Technology, RRID:AB_331464), followed by incubation with goat anti-mouse IgG (H+L) CrossAdsorbed Secondary Antibody (Alexa Fluor 488) and goat anti-rabbit IgG (H+L) CrossAdsorbed Secondary Antibody (Alexa Fluor 555) along with DAPI. .. The tissue sections were observed using a model BZ-X810 HS All-in-one Fluorescence Microscope Jo urn al Pr e-p roo f (Keyence, Osaka, Japan).

    Article Title: MitoQ alleviates H 2 O 2 -induced mitochondrial dysfunction in keratinocytes through the Nrf2/PINK1 pathway.
    Article Snippet: Oxidative stress plays a critical role in the pathogenesis of vitiligo by damaging keratinocytes, which disrupts their biological functions and influences the progression of the disease.. MitoQ, a mitochondria-specific antioxidant, has the potential to prevent disorders associated with oxidative stress and to exert protective effects specifically on mitochondria.. This study investigated the protective effects of MitoQ against oxidative stress in keratinocytes.

    Western Blot:

    Article Title: Ivacaftor attenuates gentamicin-induced ototoxicity through the CFTR-Nrf2-HO1/NQO1 pathway
    Article Snippet: Total protein was extracted with RIPA lysis buffer (CW2333, CWBIO, CN) with 1x Protease Inhibitor Cocktail (CW2000, CWBIO, CN). .. The primary antibodies used for western blot were as follows: mouse monoclonal anti-CFTR (66928-1-Ig, Proteintech, CN), Rabbit polyclonal anti-Nrf2 (16396-1-AP, Proteintech, CN), rabbit polyclonal anti-HO1 (ab52947, Abcam, USA), NQO1 (ab80588, Abcam, USA), SOD2 (66474-1-Ig, Proteintech, CN), and Keap1 (10503-2-AP, Proteintech, CN), anti-Cleaved Caspase 3 (25128-1-AP, Proteintech, CN), anti-beta actin (66009-1-Ig, Proteintech, CN), anti-Laminb1 (66095-1-Ig, Proteintech, CN), anti-GAPDH (10494-1-AP, Proteintech, CN). ..

    other:

    Article Title: Endothelial cell Nrf2 controls neuroinflammation following a systemic insult
    Article Snippet: Rabbit polyclonal anti-Nrf2 , Proteintech , Cat16396-1-AP; RRID: AB_2782956.



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    Ivacaftor reduces lipid peroxidation and protects CFBE cells from erastin-induced ferroptosis. A-B. The bar graphs show the ratio FITC-A/PE-A mean fluorescence intensity (oxidized/reduced) C11-BODIPY. Error bars are mean ± SD. A. CFBE cells manifest higher levels of lipid hydroperoxides compared to 16HBE after 24h in a 12-well plate. Paired Student's t -test (∗p < 0.05). B. CFBE cells were treated 24, 48, or 72h with elexacaftor (VX-445), tezacaftor (VX-661), lumacaftor (VX-809) or ivacaftor (VX-770) at the indicated concentrations. Vehicle DMSO was included as negative control, while RTA-408 as positive control. Data are expressed as fold change to DMSO. Ivacaftor reduces lipid hydroperoxides level in CFBE cells already after 24h of treatment. Ordinary one-way ANOVA multiple comparison vs. DMSO with Dunnett's correction (∗∗p < 0.01; ∗∗∗p < 0.001). C -D. The bar graphs show resazurin-based cell viability of CFBE cells, expressed as percentage relative to vehicle DMSO. Cells were treated with erastin (Era) alone or in combination (blue dots). Ordinary one-way ANOVA multiple comparison vs. Era with Dunnett's correction (∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001). C. VX-770 protects CFBE cells from Era-induced ferroptosis already at 24h and this effect persists over the 72h treatment. The <t>Nrf2</t> activator RTA-408 does not protect from Era like vehicle DMSO, while ferroptosis inhibitor Fer-1 was included as a positive control. D. At 24h VX-770's protective ability in CFBE cells is maintained also when combined with CFTR correctors and in the triple-combination VX-770, VX-445 and VX-661 (ETI).
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    Ivacaftor reduces lipid peroxidation and protects CFBE cells from erastin-induced ferroptosis. A-B. The bar graphs show the ratio FITC-A/PE-A mean fluorescence intensity (oxidized/reduced) C11-BODIPY. Error bars are mean ± SD. A. CFBE cells manifest higher levels of lipid hydroperoxides compared to 16HBE after 24h in a 12-well plate. Paired Student's t -test (∗p < 0.05). B. CFBE cells were treated 24, 48, or 72h with elexacaftor (VX-445), tezacaftor (VX-661), lumacaftor (VX-809) or ivacaftor (VX-770) at the indicated concentrations. Vehicle DMSO was included as negative control, while RTA-408 as positive control. Data are expressed as fold change to DMSO. Ivacaftor reduces lipid hydroperoxides level in CFBE cells already after 24h of treatment. Ordinary one-way ANOVA multiple comparison vs. DMSO with Dunnett's correction (∗∗p < 0.01; ∗∗∗p < 0.001). C -D. The bar graphs show resazurin-based cell viability of CFBE cells, expressed as percentage relative to vehicle DMSO. Cells were treated with erastin (Era) alone or in combination (blue dots). Ordinary one-way ANOVA multiple comparison vs. Era with Dunnett's correction (∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001). C. VX-770 protects CFBE cells from Era-induced ferroptosis already at 24h and this effect persists over the 72h treatment. The <t>Nrf2</t> activator RTA-408 does not protect from Era like vehicle DMSO, while ferroptosis inhibitor Fer-1 was included as a positive control. D. At 24h VX-770's protective ability in CFBE cells is maintained also when combined with CFTR correctors and in the triple-combination VX-770, VX-445 and VX-661 (ETI).
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    Effect of trans‐fatty acids on <t>Sirt1/Ppargc1a/Nfe2l2</t> pathway of rat blood vessels. (A) Western blotting results of Silent information regulator 1 (Sirt1), Peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (Ppargc1a), and nuclear factor erythroid 2‐related factor 2 (Nfe2l2). (B−D) Semi‐quantitative analyses of protein expression. Results are shown as mean ± SD ( n = 6). * p < 0.05 by contrast with ND group; # p < 0.05 by contrast with LTD group. ND, normal diet; LTD, 1% trans‐fatty acids diet; HTD, 4% trans‐fatty acids diet.
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    Effect of trans‐fatty acids on <t>Sirt1/Ppargc1a/Nfe2l2</t> pathway of rat blood vessels. (A) Western blotting results of Silent information regulator 1 (Sirt1), Peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (Ppargc1a), and nuclear factor erythroid 2‐related factor 2 (Nfe2l2). (B−D) Semi‐quantitative analyses of protein expression. Results are shown as mean ± SD ( n = 6). * p < 0.05 by contrast with ND group; # p < 0.05 by contrast with LTD group. ND, normal diet; LTD, 1% trans‐fatty acids diet; HTD, 4% trans‐fatty acids diet.
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    Image Search Results


    Ivacaftor reduces lipid peroxidation and protects CFBE cells from erastin-induced ferroptosis. A-B. The bar graphs show the ratio FITC-A/PE-A mean fluorescence intensity (oxidized/reduced) C11-BODIPY. Error bars are mean ± SD. A. CFBE cells manifest higher levels of lipid hydroperoxides compared to 16HBE after 24h in a 12-well plate. Paired Student's t -test (∗p < 0.05). B. CFBE cells were treated 24, 48, or 72h with elexacaftor (VX-445), tezacaftor (VX-661), lumacaftor (VX-809) or ivacaftor (VX-770) at the indicated concentrations. Vehicle DMSO was included as negative control, while RTA-408 as positive control. Data are expressed as fold change to DMSO. Ivacaftor reduces lipid hydroperoxides level in CFBE cells already after 24h of treatment. Ordinary one-way ANOVA multiple comparison vs. DMSO with Dunnett's correction (∗∗p < 0.01; ∗∗∗p < 0.001). C -D. The bar graphs show resazurin-based cell viability of CFBE cells, expressed as percentage relative to vehicle DMSO. Cells were treated with erastin (Era) alone or in combination (blue dots). Ordinary one-way ANOVA multiple comparison vs. Era with Dunnett's correction (∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001). C. VX-770 protects CFBE cells from Era-induced ferroptosis already at 24h and this effect persists over the 72h treatment. The Nrf2 activator RTA-408 does not protect from Era like vehicle DMSO, while ferroptosis inhibitor Fer-1 was included as a positive control. D. At 24h VX-770's protective ability in CFBE cells is maintained also when combined with CFTR correctors and in the triple-combination VX-770, VX-445 and VX-661 (ETI).

    Journal: Redox Biology

    Article Title: Beyond CFTR: Ivacaftor's role in restoring cellular redox balance and preventing ferroptosis

    doi: 10.1016/j.redox.2025.103944

    Figure Lengend Snippet: Ivacaftor reduces lipid peroxidation and protects CFBE cells from erastin-induced ferroptosis. A-B. The bar graphs show the ratio FITC-A/PE-A mean fluorescence intensity (oxidized/reduced) C11-BODIPY. Error bars are mean ± SD. A. CFBE cells manifest higher levels of lipid hydroperoxides compared to 16HBE after 24h in a 12-well plate. Paired Student's t -test (∗p < 0.05). B. CFBE cells were treated 24, 48, or 72h with elexacaftor (VX-445), tezacaftor (VX-661), lumacaftor (VX-809) or ivacaftor (VX-770) at the indicated concentrations. Vehicle DMSO was included as negative control, while RTA-408 as positive control. Data are expressed as fold change to DMSO. Ivacaftor reduces lipid hydroperoxides level in CFBE cells already after 24h of treatment. Ordinary one-way ANOVA multiple comparison vs. DMSO with Dunnett's correction (∗∗p < 0.01; ∗∗∗p < 0.001). C -D. The bar graphs show resazurin-based cell viability of CFBE cells, expressed as percentage relative to vehicle DMSO. Cells were treated with erastin (Era) alone or in combination (blue dots). Ordinary one-way ANOVA multiple comparison vs. Era with Dunnett's correction (∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001). C. VX-770 protects CFBE cells from Era-induced ferroptosis already at 24h and this effect persists over the 72h treatment. The Nrf2 activator RTA-408 does not protect from Era like vehicle DMSO, while ferroptosis inhibitor Fer-1 was included as a positive control. D. At 24h VX-770's protective ability in CFBE cells is maintained also when combined with CFTR correctors and in the triple-combination VX-770, VX-445 and VX-661 (ETI).

    Article Snippet: Rabbit anti-xCT polyclonal antibody 1:1000 (26864-1-AP, Proteintech) Rabbit anti-Nrf2 polyclonal antibody 1:1000 (16396-1-AP, Proteintech) , Goat anti-rabbit IgG HRP conjugate, 1:5000 (NEF812001EA, Perkin Elmer).

    Techniques: Fluorescence, Negative Control, Positive Control, Comparison

    Ivacaftor modulates the Nrf2-based antioxidant response in CFBE cells. A. Representative Western blot analysis of Nrf2 protein. CFBE cells display a decreased level of Nrf2 compared to 16HBE cells. Values in the bar graph represent normalized integrated density of Western blot, expressed as fold change to 16HBE. Error bars are mean ± SD. Unpaired Student's t -test (∗∗p < 0.01). Representative Western blot of Nrf2 (B) or xCT (C) proteins in CFBE cells treated 24, 48, or 72h with ivacaftor (VX-770) 10 μM. Vehicle DMSO was used as control. Filled dots correspond to addition of the compound/vehicle. Values in the bar graphs represent normalized integrated density of Western blot and are expressed as fold change to DMSO. Error bars are mean ± SD. Unpaired Student's t -test (∗p < 0.05; ∗∗∗p < 0.001). VX-770 significantly increases Nrf2 level at 24h (B) and xCT at 48h (C) . D. 72-h treatment with VX-770 10 μM significantly increases total glutathione (tGSH) in CFBE cells. RTA-408 was included as positive control. tGSH was measured with Tietze assay and normalized to total intracellular proteins. Each point represents an independent biological replicate. Error bars are mean ± SD. Ordinary one-way ANOVA multiple comparison vs. DMSO with Dunnett's correction (∗p < 0.05; ∗∗p < 0.01). E. Similarly to the Nrf2 activator RTA-408 included as positive control, VX-770 10 μM increases the normalized relative luciferase activity in CFBE cells transiently transfected with the pGL3-8xARE-luciferase Nrf2 reporter plasmid. Each point represents an independent biological replicate and is expressed as fold change to DMSO. Error bars are mean ± SD. Ordinary one-way ANOVA multiple comparison vs. DMSO with Dunnett's correction (∗p < 0.05; ∗∗p < 0.01).

    Journal: Redox Biology

    Article Title: Beyond CFTR: Ivacaftor's role in restoring cellular redox balance and preventing ferroptosis

    doi: 10.1016/j.redox.2025.103944

    Figure Lengend Snippet: Ivacaftor modulates the Nrf2-based antioxidant response in CFBE cells. A. Representative Western blot analysis of Nrf2 protein. CFBE cells display a decreased level of Nrf2 compared to 16HBE cells. Values in the bar graph represent normalized integrated density of Western blot, expressed as fold change to 16HBE. Error bars are mean ± SD. Unpaired Student's t -test (∗∗p < 0.01). Representative Western blot of Nrf2 (B) or xCT (C) proteins in CFBE cells treated 24, 48, or 72h with ivacaftor (VX-770) 10 μM. Vehicle DMSO was used as control. Filled dots correspond to addition of the compound/vehicle. Values in the bar graphs represent normalized integrated density of Western blot and are expressed as fold change to DMSO. Error bars are mean ± SD. Unpaired Student's t -test (∗p < 0.05; ∗∗∗p < 0.001). VX-770 significantly increases Nrf2 level at 24h (B) and xCT at 48h (C) . D. 72-h treatment with VX-770 10 μM significantly increases total glutathione (tGSH) in CFBE cells. RTA-408 was included as positive control. tGSH was measured with Tietze assay and normalized to total intracellular proteins. Each point represents an independent biological replicate. Error bars are mean ± SD. Ordinary one-way ANOVA multiple comparison vs. DMSO with Dunnett's correction (∗p < 0.05; ∗∗p < 0.01). E. Similarly to the Nrf2 activator RTA-408 included as positive control, VX-770 10 μM increases the normalized relative luciferase activity in CFBE cells transiently transfected with the pGL3-8xARE-luciferase Nrf2 reporter plasmid. Each point represents an independent biological replicate and is expressed as fold change to DMSO. Error bars are mean ± SD. Ordinary one-way ANOVA multiple comparison vs. DMSO with Dunnett's correction (∗p < 0.05; ∗∗p < 0.01).

    Article Snippet: Rabbit anti-xCT polyclonal antibody 1:1000 (26864-1-AP, Proteintech) Rabbit anti-Nrf2 polyclonal antibody 1:1000 (16396-1-AP, Proteintech) , Goat anti-rabbit IgG HRP conjugate, 1:5000 (NEF812001EA, Perkin Elmer).

    Techniques: Western Blot, Control, Positive Control, Comparison, Luciferase, Activity Assay, Transfection, Plasmid Preparation

    Ivacaftor's regulates FSP1 protein level but does not base its anti-ferroptotic activity on it. A. Representative Western blot of FSP1 protein in CFBE cells treated 24, 48, or 72h with ivacaftor (VX-770) 10 μM. Vehicle DMSO was used as control. Filled dots correspond to addition of the compound/vehicle. Values in the bar graphs represent normalized integrated density of Western blot and are expressed as fold change to DMSO. Error bars are mean ± SD. Unpaired Student's t -test (∗p < 0.05). VX-770 significantly increases FSP1 level at 24h. Western blot validation of the CRISPR-Cas9-generated CFBE Nrf2 KO (B) and FSP1 KO (C) cells, compared to the non-target control (N.T.) CFBE cell line. D. Resazurin-based cell viability assay of N.T., Nrf2 KO and FSP1 KO CFBE cells treated 24h with the ferroptosis inducer erastin. Concentrations of erastin varied in a range between 0 and 10 μM. VX-770 5 μM efficiently protected each cell line from erastin-induced ferroptosis, thus suggesting that VX-770's activity does not depend on Nrf2 and FSP1. Each point represents the mean ± SD of at least three independent biological replicates.

    Journal: Redox Biology

    Article Title: Beyond CFTR: Ivacaftor's role in restoring cellular redox balance and preventing ferroptosis

    doi: 10.1016/j.redox.2025.103944

    Figure Lengend Snippet: Ivacaftor's regulates FSP1 protein level but does not base its anti-ferroptotic activity on it. A. Representative Western blot of FSP1 protein in CFBE cells treated 24, 48, or 72h with ivacaftor (VX-770) 10 μM. Vehicle DMSO was used as control. Filled dots correspond to addition of the compound/vehicle. Values in the bar graphs represent normalized integrated density of Western blot and are expressed as fold change to DMSO. Error bars are mean ± SD. Unpaired Student's t -test (∗p < 0.05). VX-770 significantly increases FSP1 level at 24h. Western blot validation of the CRISPR-Cas9-generated CFBE Nrf2 KO (B) and FSP1 KO (C) cells, compared to the non-target control (N.T.) CFBE cell line. D. Resazurin-based cell viability assay of N.T., Nrf2 KO and FSP1 KO CFBE cells treated 24h with the ferroptosis inducer erastin. Concentrations of erastin varied in a range between 0 and 10 μM. VX-770 5 μM efficiently protected each cell line from erastin-induced ferroptosis, thus suggesting that VX-770's activity does not depend on Nrf2 and FSP1. Each point represents the mean ± SD of at least three independent biological replicates.

    Article Snippet: Rabbit anti-xCT polyclonal antibody 1:1000 (26864-1-AP, Proteintech) Rabbit anti-Nrf2 polyclonal antibody 1:1000 (16396-1-AP, Proteintech) , Goat anti-rabbit IgG HRP conjugate, 1:5000 (NEF812001EA, Perkin Elmer).

    Techniques: Activity Assay, Western Blot, Control, Biomarker Discovery, CRISPR, Generated, Viability Assay

    Effect of trans‐fatty acids on Sirt1/Ppargc1a/Nfe2l2 pathway of rat blood vessels. (A) Western blotting results of Silent information regulator 1 (Sirt1), Peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (Ppargc1a), and nuclear factor erythroid 2‐related factor 2 (Nfe2l2). (B−D) Semi‐quantitative analyses of protein expression. Results are shown as mean ± SD ( n = 6). * p < 0.05 by contrast with ND group; # p < 0.05 by contrast with LTD group. ND, normal diet; LTD, 1% trans‐fatty acids diet; HTD, 4% trans‐fatty acids diet.

    Journal: Food Science & Nutrition

    Article Title: Trans‐Fatty Acids ( TFA ) Induced Vascular Injury Through the Regulation of the Sirt1‐Ppargc1a‐Nfe2l2 Signaling Pathway in Male Rats

    doi: 10.1002/fsn3.70975

    Figure Lengend Snippet: Effect of trans‐fatty acids on Sirt1/Ppargc1a/Nfe2l2 pathway of rat blood vessels. (A) Western blotting results of Silent information regulator 1 (Sirt1), Peroxisome proliferator‐activated receptor gamma coactivator 1‐alpha (Ppargc1a), and nuclear factor erythroid 2‐related factor 2 (Nfe2l2). (B−D) Semi‐quantitative analyses of protein expression. Results are shown as mean ± SD ( n = 6). * p < 0.05 by contrast with ND group; # p < 0.05 by contrast with LTD group. ND, normal diet; LTD, 1% trans‐fatty acids diet; HTD, 4% trans‐fatty acids diet.

    Article Snippet: The following primary antibodies were employed in the study: anti‐rabbit Bcl2 (Signalway Antibody, China), anti‐rabbit Bax (Cell Signaling Technology, USA), anti‐rabbit Ppargc1a (Affinity, China), anti‐rabbit Casp3 (GeneTex, USA), anti‐rabbit Cleaved Casp3 (Arigo Biolaboratories, China), anti‐rabbit Nfe2l2 (Medical & Biological Laboratories, China), anti‐rabbit Sirt1 (OriGene, USA), and anti‐rabbit β‐actin (Abcam, China).

    Techniques: Western Blot, Expressing