rabbit polyclonal antibodies against nox4  (Cell Signaling Technology Inc)

Journal: Journal of Cancer

Article Title: LncRNA C2orf27A Promotes Gastric Cancer by Sponging MiR-610 and Elevating NOX4 Expression

doi: 10.7150/jca.100621

Figure Lengend Snippet: Figure 6. MiR-610 blocks the malignant behavior of GC cells by inhibiting NOX4 expression. (A, B) The data from TCGA-STAD and GTEx indicated that NOX4 expression was significantly higher in GC tissues than that in normal gastric tissues (unpaired and paired samples). (C) The correlation analysis of miR-610 and NOX4 expression in GC tissues based on TCGA-STAD. (D) Bioinformatics analysis using DIANA-microT-CDS showed the putative binding site between miR-610 and NOX4. (E) Luciferase reporter gene assays revealed that miR-610 negatively regulated the luciferase activity of NOX4-WT rather than that of the mutant NOX4-MUT. (F, G) qRT-PCR and western blot were used to detect NOX4 levels after transfecting miR-610 mimics into HGC-27 cells. (H-K) NOX4 overexpression partially offset the functions of miR-610 mimics on proliferation, colony formation, cell cycle progression, and apoptosis of HGC-27 cells. Data are presented as the mean ± SD of three independent experiments. *P < 0.05, **P < 0.01, and ***P <0.001, ns: no significance.

Article Snippet: After blocking with 10% skim milk for an hour at room temperature, the membranes were incubated overnight at 4°C with rabbit polyclonal antibodies against NOX4 (1:2000) and GAPDH (1:6000, Proteintech, China).

Techniques: Expressing, Binding Assay, Luciferase, Activity Assay, Mutagenesis, Quantitative RT-PCR, Western Blot, Over Expression

Journal: Journal of Cancer

Article Title: LncRNA C2orf27A Promotes Gastric Cancer by Sponging MiR-610 and Elevating NOX4 Expression

doi: 10.7150/jca.100621

Figure Lengend Snippet: Figure 7. C2orf27A knockdown exerts antitumor effects in GC cells by downregulating NOX4 expression. (A) Correlation analysis of C2orf27A and NOX4 expression in GC cells based on TCGA-STAD. (B, C) qRT-PCR and western blot detected the levels of NOX4 in HGC-27 and NCI-C87 cells after C2orf27A knockdown. (D-G) NOX4 overexpression partially offset the effects of C2orf27A knockdown on proliferation, colony formation, cell cycle progression and apoptosis of HGC-27 cells. Data are presented as the mean ± SD of three independent experiments. *P < 0.05, and **P < 0.01, ***P <0.001, ns: no significance.

Article Snippet: After blocking with 10% skim milk for an hour at room temperature, the membranes were incubated overnight at 4°C with rabbit polyclonal antibodies against NOX4 (1:2000) and GAPDH (1:6000, Proteintech, China).

Techniques: Knockdown, Expressing, Quantitative RT-PCR, Western Blot, Over Expression

Journal: Diabetes

Article Title: VEGF-A: A Novel Mechanistic Link Between CYP2C-Derived EETs and Nox4 in Diabetic Kidney Disease.

doi: 10.2337/db22-0636

Figure Lengend Snippet: Figure 2—AUDA regulates superoxide production, Nox4 mRNA and protein levels, and NADPH oxidase activity. A: Superoxide generation evaluated using HPLC. B: Relative mRNA levels of Nox4. C: Histogram showing quantitation of Nox4/GAPDH from five different rats in each group. D: NADPH-dependent superoxide generation. All values are the means ± SE. *P < 0.05 vs. control; #P < 0.05 vs. untreated diabetic rats. DHE, dihydroethidium; EOH, 2-hydroxyethidium; RLU, relative light unit.

Article Snippet: Treated cells or homogenates from glomeruli isolated from the renal cortex were prepared, and Western blot analysis was performed as previously described (13,30,32) using rabbit polyclonal antibodies against Nox4 (1:250; Santa Cruz Biotechnology), VEGF-A (1:500; Abcam), and collagen IV (1:1,000; Abcam).

Techniques: Activity Assay, Quantitation Assay, Control

Journal: Diabetes

Article Title: VEGF-A: A Novel Mechanistic Link Between CYP2C-Derived EETs and Nox4 in Diabetic Kidney Disease.

doi: 10.2337/db22-0636

Figure Lengend Snippet: Figure 5—Anti-VEGF and SU5416 regulate superoxide production, Nox4 mRNA and protein levels and NADPH oxidase activity are shown. A: Superoxide generation evaluated using HPLC. B: Relative mRNA levels of Nox4. C: Histogram showing quantitation of Nox4/ GAPDH from five different rats in each group. D: NADPH-dependent superoxide generation. All values are the means ± SE. *P < 0.05 vs. control; #P < 0.05 vs. untreated diabetic rats. DHE, dihydroethidium; EOH, 2-hydroxyethidium; RLU, relative light unit.

Article Snippet: Treated cells or homogenates from glomeruli isolated from the renal cortex were prepared, and Western blot analysis was performed as previously described (13,30,32) using rabbit polyclonal antibodies against Nox4 (1:250; Santa Cruz Biotechnology), VEGF-A (1:500; Abcam), and collagen IV (1:1,000; Abcam).

Techniques: Activity Assay, Quantitation Assay, Control

Journal: Antioxidants

Article Title: Nootkatone Supplementation Attenuates Carbon Tetrachloride Exposure-Induced Nephrotoxicity in Mice

doi: 10.3390/antiox12020370

Figure Lengend Snippet: Immunohistochemical images of NOX4 protein in the kidney tissue. After treatment, the expression of NOX4 protein in the kidney tissues was measured by using an immunohistochemical staining method. The representative images ( on the left ) and semi-quantitative analysis ( on the right ) were shown. ** p < 0.01 and *** p < 0.001. Bar = 50 μm.

Article Snippet: A rabbit polyclonal antibody against NOX4 antibody (1:200; ProteinTech, Chicago, IL, USA) and a goat anti-rabbit IgG (1:200; Santa Cruz, Dallas, TX, USA) were used.

Techniques: Immunohistochemical staining, Expressing, Staining

Journal: Antioxidants

Article Title: Nootkatone Supplementation Attenuates Carbon Tetrachloride Exposure-Induced Nephrotoxicity in Mice

doi: 10.3390/antiox12020370

Figure Lengend Snippet: The effects of NKT pre-treatment on the mRNA expressions of different inflammation pathway genes in murine kidney tissues. After 24 h post CCl 4 treatment, the expressions of NF-κB ( A ), IL-1β ( B ), IL-6 ( C ), TNF-α ( D ), iNOS ( E ), NOX4 ( F ), Nrf2 ( G ), and HO-1 ( H ) transcript levels in the kidney tissues were determined, respectively. Data are presented as mean ± S.D. ( n = 6 in each group). * p < 0.05, ** p < 0.01, and *** p < 0.001.

Article Snippet: A rabbit polyclonal antibody against NOX4 antibody (1:200; ProteinTech, Chicago, IL, USA) and a goat anti-rabbit IgG (1:200; Santa Cruz, Dallas, TX, USA) were used.

Techniques:

Journal: Antioxidants

Article Title: Nootkatone Supplementation Attenuates Carbon Tetrachloride Exposure-Induced Nephrotoxicity in Mice

doi: 10.3390/antiox12020370

Figure Lengend Snippet: Pathways of NKT supplementation protecting against CCl 4 exposure -induced nephrotoxicity. MDA, malondialdehyde; SOD, superoxide dismutase; CAT, catalase; GSH, glutathione; GPX, glutathione peroxidase; Keap1, kelch like ECH associated protein 1; Nrf2, NF-E2-related factor; HO-1, heme oxygenase-1; NOX4, NADPH oxidase 4; NF-κB, nuclear factor-kappaB; iNOS, inducible nitric oxide synthase; IL-1β, interleukin-1β; IL-6, interleukin-6; TNF-α, tumor necrosis factor-α; ARE, antioxidant response element.

Article Snippet: A rabbit polyclonal antibody against NOX4 antibody (1:200; ProteinTech, Chicago, IL, USA) and a goat anti-rabbit IgG (1:200; Santa Cruz, Dallas, TX, USA) were used.

Techniques: