antibody against nrf 2  (Proteintech)

Journal: MedComm

Article Title: Slc7a11‐Mediated Cystine/Glutamate Antiport Reprograms Macrophage Polarization and Ameliorates Atherosclerosis

doi: 10.1002/mco2.70646

Figure Lengend Snippet: Slc7a11 expression is enhanced in the macrophages of atherosclerotic lesions. (A) Pathway enrichment analysis of RNA‐sequencing data from foamy and nonfoamy macrophages isolated from atherosclerotic intima. (B) Heatmap presenting differentially expressed genes in cellular response to oxidative stress, ferroptosis, glutathione metabolic process, and amino acid transmembrane transport pathways. (C) Real‐time PCR analysis of Slc7a11 mRNA level in bone marrow‐derived macrophage (BMDMs) treated with oxidized low‐density lipoprotein (oxLDL, 50 or 100 µg/mL) for 0, 6, 12, and 24 h ( n = 3 biological replicates per group). (D and E) Western blot analysis of Slc7a11 protein expression level in BMDMs treated with oxLDL (100 µg/mL) for 0, 12, 24, and 36 h ( n = 3 biological replicates per group). (F and G) Western blot analysis of Slc7a11 protein expression level in BMDMs treated with 0, 50, 100, and 200 µg/mL oxLDL for 24 h ( n = 3 biological replicates per group). (H) Quantification of flow cytometric analysis for Slc7a11 expression in BMDMs treated with oxLDL (100 or 200 µg/mL) for 36 and 48 h, respectively. (I) Slc7a11 mRNA expression level in BMDMs treated with 50 µg/mL oxLDL for 24 h in the presence or absence of Nrf2‐inhibitor Nrf‐In‐1 (2 µM) ( n = 3 biological replicates per group). (J) Representative images of immunofluorescence staining for Slc7a11 (red), Mac‐3 (macrophage marker, green), and 4′,6‐diamidino‐2‐phenylindole (DAPI, cell nuclei, blue) in the atherosclerotic plaques from ApoE –/– mice fed a western diet for 16 weeks. Images are representative of n = 3 independent experiments. Scale bar, 50 µm. Student's t ‐test was used to compare the two groups. One‐way ANOVA test was used to compare multiple groups. * p < 0.05, ** p < 0.01, *** p < 0.001. The molecular weight (in kDa) was indicated to the right of each band.

Article Snippet: For the experiment of Nrf2 inhibitor, the BMDMs were treated with 50 μg/mL oxLDL for 24 h in the presence of 2 μM Nrf2‐inhibitor Nrf‐IN‐1 (TargetMol; Cat. No. 1610022‐76‐8, China).

Techniques: Expressing, RNA Sequencing, Isolation, Real-time Polymerase Chain Reaction, Derivative Assay, Western Blot, Immunofluorescence, Staining, Marker, Molecular Weight

Journal: iScience

Article Title: USP1 promotes hepatocellular carcinoma progression by modulating mitophagy via stabilizing MCM3 to regulate the Keap1-Nrf2 axis

doi: 10.1016/j.isci.2026.114927

Figure Lengend Snippet: MCM3 regulates mitophagy by influencing the expression and localization of Nrf-2 (A) WB used to detect the impact of MCM3 knockdown on P62, LC3B II/I, TOMM20, FUNDC1, Parkin, and PINK1 in Huh7 and LM3 cells. (B) WB was used to assess the impact of MCM3 knockdown on Nucleus Nrf2 in Huh7 and LM3 cells. (C) IF was used to evaluate the impact of MCM3 knockdown on Nrf2 in Huh7 and LM3 cells ( n = 3 biologically independent experiments). (D) WB was used to measure the impact of MCM3 knockdown on HMOX-1 and NQO1 expression in Huh7 and LM3 cells, with or without THBQ. (E) WB was performed to detect the impact of MCM3 knockdown on P62, LC3B II/I, TOMM20, FUNDC1, Parkin, and PINK1 in Huh7 and LM3 cells, with or without THBQ. Data are presented as mean ± SD. ∗∗∗∗ p < 0.0001; ∗∗∗ p < 0.001; ∗∗ p < 0.01; ∗ p < 0.05, ns p ≥ 0.05. For (A), (D), and (E), statistical analysis was performed using a one-way ANOVA ( n = 3 biologically independent experiments); For B, statistical analysis was performed using a two-tailed unpaired Student’s t test ( n = 3 biologically independent experiments).

Article Snippet: Following three washes with PBS, the cells were blocked with an immunofluorescence blocking solution (Beyotime) at 37°C for 1 h. Subsequently, the cells were incubated with a primary antibody against Nrf-2 (Proteintech, #16396-1-AP, 1:50 dilution) at 4°C overnight.

Techniques: Expressing, Knockdown, Two Tailed Test

Journal: iScience

Article Title: USP1 promotes hepatocellular carcinoma progression by modulating mitophagy via stabilizing MCM3 to regulate the Keap1-Nrf2 axis

doi: 10.1016/j.isci.2026.114927

Figure Lengend Snippet: MCM3 regulates mitophagy by influencing the expression and localization of Nrf-2 (A) WB used to detect the impact of MCM3 knockdown on P62, LC3B II/I, TOMM20, FUNDC1, Parkin, and PINK1 in Huh7 and LM3 cells. (B) WB was used to assess the impact of MCM3 knockdown on Nucleus Nrf2 in Huh7 and LM3 cells. (C) IF was used to evaluate the impact of MCM3 knockdown on Nrf2 in Huh7 and LM3 cells ( n = 3 biologically independent experiments). (D) WB was used to measure the impact of MCM3 knockdown on HMOX-1 and NQO1 expression in Huh7 and LM3 cells, with or without THBQ. (E) WB was performed to detect the impact of MCM3 knockdown on P62, LC3B II/I, TOMM20, FUNDC1, Parkin, and PINK1 in Huh7 and LM3 cells, with or without THBQ. Data are presented as mean ± SD. ∗∗∗∗ p < 0.0001; ∗∗∗ p < 0.001; ∗∗ p < 0.01; ∗ p < 0.05, ns p ≥ 0.05. For (A), (D), and (E), statistical analysis was performed using a one-way ANOVA ( n = 3 biologically independent experiments); For B, statistical analysis was performed using a two-tailed unpaired Student’s t test ( n = 3 biologically independent experiments).

Article Snippet: Nrf-2 , Proteintech , Cat# 16396-1-AP; RRID: AB_2782956.

Techniques: Expressing, Knockdown, Two Tailed Test