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Proteintech foxm1

<t>FoxM1</t> is highly expressed in fibroblasts of fibrotic lung tissues. (A, B) qPCR (n = 9) and Western blot (n = 6) analysis of the expression of FoxM1 in normal and IPF lung tissues. ∗ P < 0.05. (C) qPCR analysis of the mRNA levels of FoxM1 in the lung tissues from BLM-treated mice. n = 3, ∗ P < 0.05. (D) Western blot analysis of the protein levels of FoxM1, CTHRC1, α-SMA, and Collagen I in the lung tissues from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (E) The Pearson's correlation analysis of COL1A1 expression with FoxM1 expression based on the RNA-seq results of GSE24206 from GEO database. (F) The Pearson's correlation analysis of Ashcroft score with FoxM1 expression in the lung tissues from BLM-treated mice. (G) Representative images of co-immunostaining for α-SMA and FoxM1 in IPF lung tissues. White arrows indicate double-positive cells. (H) Representative images of co-immunostaining for α-SMA and FoxM1 in the lung tissues from BLM-treated mice. White arrows indicate double-positive cells. (I) Western blot analysis of FoxM1 expression in pulmonary fibroblasts isolated from mice subjected to BLM treatment. n = 3, ∗ P < 0.05. (J) Western blot analysis of FoxM1, CTHRC1, α-SMA, and Collagen I expression in pulmonary fibroblasts treated with TGF-β1. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (A, B, I) and one-way ANOVA with Tukey's post-hoc test (C, D, J) were used for statistical analysis.

Foxm1, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 147 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/anti+foxm1/FOXM1+Antibody/pmc12991958-77-5-16
Average 96 stars, based on 147 article reviews

foxm1 - by Bioz Stars, 2026-10

96/100 stars

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1) Product Images from "SIRT3-mediated deacetylation of FoxM1 prevents pulmonary fibrosis via modulating the activation of pulmonary fibroblasts"

Article Title: SIRT3-mediated deacetylation of FoxM1 prevents pulmonary fibrosis via modulating the activation of pulmonary fibroblasts

Journal: Redox Biology

doi: 10.1016/j.redox.2026.104108

FoxM1 is highly expressed in fibroblasts of fibrotic lung tissues. (A, B) qPCR (n = 9) and Western blot (n = 6) analysis of the expression of FoxM1 in normal and IPF lung tissues. ∗ P < 0.05. (C) qPCR analysis of the mRNA levels of FoxM1 in the lung tissues from BLM-treated mice. n = 3, ∗ P < 0.05. (D) Western blot analysis of the protein levels of FoxM1, CTHRC1, α-SMA, and Collagen I in the lung tissues from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (E) The Pearson's correlation analysis of COL1A1 expression with FoxM1 expression based on the RNA-seq results of GSE24206 from GEO database. (F) The Pearson's correlation analysis of Ashcroft score with FoxM1 expression in the lung tissues from BLM-treated mice. (G) Representative images of co-immunostaining for α-SMA and FoxM1 in IPF lung tissues. White arrows indicate double-positive cells. (H) Representative images of co-immunostaining for α-SMA and FoxM1 in the lung tissues from BLM-treated mice. White arrows indicate double-positive cells. (I) Western blot analysis of FoxM1 expression in pulmonary fibroblasts isolated from mice subjected to BLM treatment. n = 3, ∗ P < 0.05. (J) Western blot analysis of FoxM1, CTHRC1, α-SMA, and Collagen I expression in pulmonary fibroblasts treated with TGF-β1. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (A, B, I) and one-way ANOVA with Tukey's post-hoc test (C, D, J) were used for statistical analysis.

Figure Legend Snippet: FoxM1 is highly expressed in fibroblasts of fibrotic lung tissues. (A, B) qPCR (n = 9) and Western blot (n = 6) analysis of the expression of FoxM1 in normal and IPF lung tissues. ∗ P < 0.05. (C) qPCR analysis of the mRNA levels of FoxM1 in the lung tissues from BLM-treated mice. n = 3, ∗ P < 0.05. (D) Western blot analysis of the protein levels of FoxM1, CTHRC1, α-SMA, and Collagen I in the lung tissues from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (E) The Pearson's correlation analysis of COL1A1 expression with FoxM1 expression based on the RNA-seq results of GSE24206 from GEO database. (F) The Pearson's correlation analysis of Ashcroft score with FoxM1 expression in the lung tissues from BLM-treated mice. (G) Representative images of co-immunostaining for α-SMA and FoxM1 in IPF lung tissues. White arrows indicate double-positive cells. (H) Representative images of co-immunostaining for α-SMA and FoxM1 in the lung tissues from BLM-treated mice. White arrows indicate double-positive cells. (I) Western blot analysis of FoxM1 expression in pulmonary fibroblasts isolated from mice subjected to BLM treatment. n = 3, ∗ P < 0.05. (J) Western blot analysis of FoxM1, CTHRC1, α-SMA, and Collagen I expression in pulmonary fibroblasts treated with TGF-β1. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (A, B, I) and one-way ANOVA with Tukey's post-hoc test (C, D, J) were used for statistical analysis.

Techniques Used: Western Blot, Expressing, RNA Sequencing, Immunostaining, Isolation

Enhanced FoxM1 expression is responsible for the resistance of fibroblasts to FasL-mediated apoptosis . (A) Caspase 3 activity analysis in pulmonary fibroblasts isolated from bleomycin (BLM)-treated mice following FasL treatment. (B) Cell viability assessment using the CCK-8 assay in pulmonary fibroblasts isolated from BLM-treated mice after FasL treatment. (C) Caspase 3 activity analysis in TGF-β1-treated pulmonary fibroblasts, along with or without FasL treatment. (D) Cell viability assessment using the CCK-8 assay in TGF-β1-treated pulmonary fibroblasts, along with or without FasL treatment. (E) Western blot analysis of FoxM1 expression in pulmonary fibroblasts transfected with or without LV-FoxM1. (F) Western blot analysis of FoxM1 expression in pulmonary fibroblasts transfected with or without FoxM1 siRNA (si-FoxM1). (G, H) Caspase 3 activity and cell viability assessment in pulmonary fibroblasts transfected with or without LV-FoxM1, following with or without FasL treatment. (I, J) Caspase 3 activity and cell viability assessment in pulmonary fibroblasts transfected with or without si-FoxM1, following with or without FasL treatment. All data (n = 3, ∗ P < 0.05) were presented as the means ± SEM. Paired t -test was used for statistical analysis.

Figure Legend Snippet: Enhanced FoxM1 expression is responsible for the resistance of fibroblasts to FasL-mediated apoptosis . (A) Caspase 3 activity analysis in pulmonary fibroblasts isolated from bleomycin (BLM)-treated mice following FasL treatment. (B) Cell viability assessment using the CCK-8 assay in pulmonary fibroblasts isolated from BLM-treated mice after FasL treatment. (C) Caspase 3 activity analysis in TGF-β1-treated pulmonary fibroblasts, along with or without FasL treatment. (D) Cell viability assessment using the CCK-8 assay in TGF-β1-treated pulmonary fibroblasts, along with or without FasL treatment. (E) Western blot analysis of FoxM1 expression in pulmonary fibroblasts transfected with or without LV-FoxM1. (F) Western blot analysis of FoxM1 expression in pulmonary fibroblasts transfected with or without FoxM1 siRNA (si-FoxM1). (G, H) Caspase 3 activity and cell viability assessment in pulmonary fibroblasts transfected with or without LV-FoxM1, following with or without FasL treatment. (I, J) Caspase 3 activity and cell viability assessment in pulmonary fibroblasts transfected with or without si-FoxM1, following with or without FasL treatment. All data (n = 3, ∗ P < 0.05) were presented as the means ± SEM. Paired t -test was used for statistical analysis.

Techniques Used: Expressing, Activity Assay, Isolation, CCK-8 Assay, Western Blot, Transfection

Impairing nuclear translocation of FoxM1 suppresses fibroblast activation and protects mice from bleomycin-induced pulmonary fibrosis. (A) Western blot analysis was performed to assess the nuclear expression levels of FoxM1 in pulmonary fibroblasts isolated from BLM-treated mice. n = 3, ∗ P < 0.05. (B) Western blot analysis of nuclear FoxM1, CTHRC1, α-SMA, and Collagen I expression in TGF-β1-treated pulmonary fibroblasts accompany with or without RCM-1 treatment. n = 3, ∗ P < 0.05. (C, D) EdU assay for the proliferation of TGF-β1-treated pulmonary fibroblasts accompany with or without RCM-1 treatment. n = 3, ∗ P < 0.05. (E) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from BLM-treated mice injected with or without RCM-1. (F, G) The ashcroft score (n = 6, ∗ P < 0.05.) and hydroxyproline contents (n = 6, ∗ P < 0.05.) in the lung tissues of BLM-treated mice injected with or without RCM-1. (H) The survival of BLM-treated mice injected with or without RCM-1. n = 18. (I) Western blot analysis of FoxM1, CTHRC1, α-SMA, and Collagen I expression in the lung tissues from BLM-treated mice injected with or without RCM-1. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (A) and one-way ANOVA with Tukey's post-hoc test (B, D, F–I) were used for statistical analysis.

Figure Legend Snippet: Impairing nuclear translocation of FoxM1 suppresses fibroblast activation and protects mice from bleomycin-induced pulmonary fibrosis. (A) Western blot analysis was performed to assess the nuclear expression levels of FoxM1 in pulmonary fibroblasts isolated from BLM-treated mice. n = 3, ∗ P < 0.05. (B) Western blot analysis of nuclear FoxM1, CTHRC1, α-SMA, and Collagen I expression in TGF-β1-treated pulmonary fibroblasts accompany with or without RCM-1 treatment. n = 3, ∗ P < 0.05. (C, D) EdU assay for the proliferation of TGF-β1-treated pulmonary fibroblasts accompany with or without RCM-1 treatment. n = 3, ∗ P < 0.05. (E) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from BLM-treated mice injected with or without RCM-1. (F, G) The ashcroft score (n = 6, ∗ P < 0.05.) and hydroxyproline contents (n = 6, ∗ P < 0.05.) in the lung tissues of BLM-treated mice injected with or without RCM-1. (H) The survival of BLM-treated mice injected with or without RCM-1. n = 18. (I) Western blot analysis of FoxM1, CTHRC1, α-SMA, and Collagen I expression in the lung tissues from BLM-treated mice injected with or without RCM-1. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (A) and one-way ANOVA with Tukey's post-hoc test (B, D, F–I) were used for statistical analysis.

Techniques Used: Translocation Assay, Activation Assay, Western Blot, Expressing, Isolation, EdU Assay, Staining, Injection

Acetylation of FoxM1 is required for the activation of pulmonary fibroblasts. (A, B) Western blot analysis of FoxM1 expression in the cytoplasm and nucleus of CHX-treated pulmonary fibroblasts along with or without MG132 treatment at indicated time. n = 3, ∗ P < 0.05. (C) Western blot analysis of FoxM1 expression in CHX-treated pulmonary fibroblasts along with or without TGF-β1 treatment. n = 3, ∗ P < 0.05. (D) Western blot analysis of the acetylation levels of FoxM1 in pulmonary fibroblasts isolated from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (E) Western blot analysis of the acetylation levels of FoxM1 in pulmonary fibroblasts treated with or without TGF-β1. n = 3, ∗ P < 0.05. (F, G) Western blot analysis of FoxM1 acetylation, CTHRC1, α-SMA, and Collagen I expression in pulmonary fibroblasts treated with TSA (50 nM), or NAM (1 mM) for 24 h, or not. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (D, E) and one-way ANOVA with Tukey's post-hoc test (B, C, G) were used for statistical analysis.

Figure Legend Snippet: Acetylation of FoxM1 is required for the activation of pulmonary fibroblasts. (A, B) Western blot analysis of FoxM1 expression in the cytoplasm and nucleus of CHX-treated pulmonary fibroblasts along with or without MG132 treatment at indicated time. n = 3, ∗ P < 0.05. (C) Western blot analysis of FoxM1 expression in CHX-treated pulmonary fibroblasts along with or without TGF-β1 treatment. n = 3, ∗ P < 0.05. (D) Western blot analysis of the acetylation levels of FoxM1 in pulmonary fibroblasts isolated from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (E) Western blot analysis of the acetylation levels of FoxM1 in pulmonary fibroblasts treated with or without TGF-β1. n = 3, ∗ P < 0.05. (F, G) Western blot analysis of FoxM1 acetylation, CTHRC1, α-SMA, and Collagen I expression in pulmonary fibroblasts treated with TSA (50 nM), or NAM (1 mM) for 24 h, or not. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (D, E) and one-way ANOVA with Tukey's post-hoc test (B, C, G) were used for statistical analysis.

Techniques Used: Activation Assay, Western Blot, Expressing, Isolation

Sirt3-dependent deacetylation of FoxM1 regulates the stability of FoxM1. (A) The Pearson's correlation analysis of COL1A1 expression with SIRTs expression based on the RNA-seq results of GSE2052 from GEO database. (B) Western blot analysis of SIRT3 expression in the lung tissues from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (C) Western blot analysis of the acetylation levels of FoxM1 in SIRT3 flox/flox mice intratracheally injected with AAV-Cre. n = 3, ∗ P < 0.05. (D) Western blot analysis was performed to assess the acetylation status of FoxM1 in pulmonary fibroblasts following transfection with Sirt3 siRNA (si-Sirt3). n = 3, ∗ P < 0.05. (E) Western blot analysis of FoxM1 expression in CHX-treated pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (F) Western blot analysis of CTHRC1, α-SMA and Collagen I expression in pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (G) EdU assay for the proliferation of pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (H) Western blot analysis of FoxM1 acetylation, CTHRC1, α-SMA, and Collagen I expression in TGF-β1-treated pulmonary fibroblasts transfected with or without LV-Sirt3. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (B-D, F, G) and one-way ANOVA with Tukey's post-hoc test (E, H) were used for statistical analysis.

Figure Legend Snippet: Sirt3-dependent deacetylation of FoxM1 regulates the stability of FoxM1. (A) The Pearson's correlation analysis of COL1A1 expression with SIRTs expression based on the RNA-seq results of GSE2052 from GEO database. (B) Western blot analysis of SIRT3 expression in the lung tissues from bleomycin (BLM)-treated mice. n = 3, ∗ P < 0.05. (C) Western blot analysis of the acetylation levels of FoxM1 in SIRT3 flox/flox mice intratracheally injected with AAV-Cre. n = 3, ∗ P < 0.05. (D) Western blot analysis was performed to assess the acetylation status of FoxM1 in pulmonary fibroblasts following transfection with Sirt3 siRNA (si-Sirt3). n = 3, ∗ P < 0.05. (E) Western blot analysis of FoxM1 expression in CHX-treated pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (F) Western blot analysis of CTHRC1, α-SMA and Collagen I expression in pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (G) EdU assay for the proliferation of pulmonary fibroblasts transfected with or without si-Sirt3. n = 3, ∗ P < 0.05. (H) Western blot analysis of FoxM1 acetylation, CTHRC1, α-SMA, and Collagen I expression in TGF-β1-treated pulmonary fibroblasts transfected with or without LV-Sirt3. n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. Paired t -test (B-D, F, G) and one-way ANOVA with Tukey's post-hoc test (E, H) were used for statistical analysis.

Techniques Used: Expressing, RNA Sequencing, Western Blot, Injection, Transfection, EdU Assay

Sirt3 knockdown accelerates BLM-induced pulmonary fibrosis via activation pulmonary fibroblasts in vivo. (A) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from SIRT3 flox/flox mice or BLM-treated SIRT3 flox/flox mice that intratracheally injected with or without AAV-Cre. (B, C) The ashcroft score (n = 6, ∗ P < 0.05.) and the hydroxyproline contents (n = 6, ∗ P < 0.05.) in the lung tissues of mice treated as in A. (D) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in the lung tissues from mice treated as in A n = 3, ∗ P < 0.05. (E) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in pulmonary fibroblasts isolated from mice treated as in A n = 3, ∗ P < 0.05. (F, G) EdU assay for the proliferation of pulmonary fibroblasts isolated from mice treated as in A. All data were presented as the means ± SEM. One-way ANOVA with Tukey's post-hoc test was used for statistical analysis.

Figure Legend Snippet: Sirt3 knockdown accelerates BLM-induced pulmonary fibrosis via activation pulmonary fibroblasts in vivo. (A) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from SIRT3 flox/flox mice or BLM-treated SIRT3 flox/flox mice that intratracheally injected with or without AAV-Cre. (B, C) The ashcroft score (n = 6, ∗ P < 0.05.) and the hydroxyproline contents (n = 6, ∗ P < 0.05.) in the lung tissues of mice treated as in A. (D) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in the lung tissues from mice treated as in A n = 3, ∗ P < 0.05. (E) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in pulmonary fibroblasts isolated from mice treated as in A n = 3, ∗ P < 0.05. (F, G) EdU assay for the proliferation of pulmonary fibroblasts isolated from mice treated as in A. All data were presented as the means ± SEM. One-way ANOVA with Tukey's post-hoc test was used for statistical analysis.

Techniques Used: Knockdown, Activation Assay, In Vivo, Staining, Injection, Western Blot, Expressing, Isolation, EdU Assay

Nicotinamide riboside protects mice from bleomycin-induced pulmonary fibrosis via activation of SIRT3. (A) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in TGF-β1-treated pulmonary fibroblasts accompany with or without NR treatment. n = 3, ∗ P < 0.05. (B) Cell viability assessment using the CCK-8 assay in pulmonary fibroblasts treated as in A n = 6, ∗ P < 0.05. (C) The survival of BLM-treated mice oral gavaged with or without NR. n = 18. (D) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from mice treated as in C. (E) The ashcroft score of mice treated as in C n = 6, ∗ P < 0.05. (F) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in the lung tissues from mice treated as in C n = 3, ∗ P < 0.05. (G) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in pulmonary fibroblasts isolated from the lung tissues of mice treated as in C n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. One-way ANOVA with Tukey's post-hoc test was used for statistical analysis.

Figure Legend Snippet: Nicotinamide riboside protects mice from bleomycin-induced pulmonary fibrosis via activation of SIRT3. (A) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in TGF-β1-treated pulmonary fibroblasts accompany with or without NR treatment. n = 3, ∗ P < 0.05. (B) Cell viability assessment using the CCK-8 assay in pulmonary fibroblasts treated as in A n = 6, ∗ P < 0.05. (C) The survival of BLM-treated mice oral gavaged with or without NR. n = 18. (D) Hematoxylin–eosin (H&E) and masson's trichrome staining for the lung tissues from mice treated as in C. (E) The ashcroft score of mice treated as in C n = 6, ∗ P < 0.05. (F) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in the lung tissues from mice treated as in C n = 3, ∗ P < 0.05. (G) Western blot analysis of CTHRC1, SIRT3, FoxM1, α-SMA and Collagen I expression in pulmonary fibroblasts isolated from the lung tissues of mice treated as in C n = 3, ∗ P < 0.05. All data were presented as the means ± SEM. One-way ANOVA with Tukey's post-hoc test was used for statistical analysis.

Techniques Used: Activation Assay, Western Blot, Expressing, CCK-8 Assay, Staining, Isolation

Western Blot:

Article Title: m6A reader IGF2BP2 mediates paclitaxel resistance in esophageal squamous cell carcinoma via FOXM1 mRNA stabilization.
Article Snippet: Esophageal squamous cell carcinoma (ESCC) ranks among the primary contributors to cancer‐related mortality in China.. Resistance to paclitaxel markedly diminishes its thera‐ peutic effectiveness and outcomes.. Anaerobic glycolysis is a pivotal mechanism in cancer progression.

Article Title: Mitochondria-located circRCP regulates redox homeostasis via stabilizing LRPPRC/SLIRP complex to promote bladder urothelial carcinoma tumorigenesis.
Article Snippet: The function of circular RNAs (circRNAs) located within the mitochondria in the pathogenesis of urothelial carcinoma of the bladder (UCB) remains largely unexplored.. This study identified a mitochondria-located circRNA named circRCP from the nuclear genome of UCB cells.. It is frequently upregulated in UCB and serves as an independent prognostic factor.

Article Title: m6A reader IGF2BP2 mediates paclitaxel resistance in esophageal squamous cell carcinoma via FOXM1 mRNA stabilization
Article Snippet: Protein samples (30 μg) were separated by SDS-PAGE on 10% gels (cat. no. PG112; Shanghai EpiZyme Co., Ltd.) and then transferred onto PVDF membranes (cat. no. WGPVDF22; Servicebio Co., Ltd.). .. Subsequently, the membranes were blocked with high-efficiency western blocking reagent (cat. no. GF1815; Shanghai Genefist Co., Ltd.) for 15 min at room temperature and maintained overnight at 4°C with the primary antibodies, including anti-IGF2BP2 (1:2,000; cat. no. 11601-1-AP; Proteintech Group, Inc.), anti-FOXM1 (1:2,000; cat. no. 13147-1-AP; Proteintech Group, Inc.) and anti-GAPDH (1:5,000; cat. no. 10494-1-AP; Proteintech Group, Inc.). .. After rinsing the membrane three times with TBST (cat. no. G2150-1L; Wuhan Servicebio Technology Co., Ltd.), the PVDF membranes were exposed to secondary rabbit antibodies (1:5,000; cat. no. SA00001-2; Proteintech Group, Inc.) for 1 h at ambient temperature.

Blocking Assay:

Immunofluorescence:

Immunohistochemistry:

Control:

Article Title: Enhanced or reversible RNA N6-methyladenosine editing by red/far-red light induction.
Article Snippet: .. GAPDH, FOXM1, SO X2, A CTB, and internal control proteins including Vinculin and GAPDH were probed with the corresponding antiGAPDH antibody (ABclonal, #AC002, 1:10 000 dilution), anti-FOXM1 (Proteintech, #13147-1-AP, 1:5000 dilution), anti-SOX2 (Proteintech, #11064-1-AP, 1:1000 dilution), antiβ-actin (High Dilution) (ABclonal, -#AC026, 1:50 000 dilution), anti-Vinculin (proteintech, #66305-1-Ig, 1:5000 dilution), and corresponding secondary antibodies as described above. m 6 A dot blot RNA was isolated from transfected cells. .. Equal amounts of RNA were dropped on a nylon membrane (Thermo Fisher Scientific) followed by cross-linking under conditions of ultraviolet light at 254 nm, 0.12 J cm –2 .

Dot Blot:

Isolation:

Transfection:

Incubation:

Article Title: The oxidative modification of transcription factor FOXM1 by Peroxiredoxin1 facilitates DNA damage repair and cancer progression
Article Snippet: .. After blocked with 5% FBS, cells were incubated with anti-FOXM1 (Santacruz, sc-271746, 1:250), anti-PRDX1 (Abcam, Ab41906, 1:250), anti-Flag (Proteintech, 20543-1-AP, 1:250) or anti-γH2AX (Abcam, Ab81299, 1:250) overnight at 4°C, and then incubated with cy3 tagged anti-Rabbit IgG (Beyotime, A0521, 1:250) or Alexa Fluor 488 tagged anti-Mouse IgG (Beyotime, A0423, 1:250) for 1 h. Then cells were stained by Antifade Mounting Medium with DAPI (Beyotime, P0131), and observed by confocal microscopy (OLYMPUS). .. The Pearson’s Correlation Coefficient values of the co-localization of two proteins were calculated by Image J software and graphed with GraphPad Prism 10.

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