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SUR1 interacted with PARP1 to suppress DNA damage repair and induce apoptosis of bronchial <t>epithelial</t> cells (A) Co-immunoprecipitation and western blot analyses of HEK293T cells transfected with FLAG-SUR1 plasmids (left) or human bronchial epithlial <t>(HBE)</t> cells (right). (B) Immunofluorescence staining of HBE cells. Scale bars, 25 μm. (C) Homologous recombination reporter assay in U2OS-DRGFP cells transfected with SUR1 siRNA, followed by flow cytometry analysis. (D) Western blot analysis of HBE cells transfected with SUR1 siRNAs with or without 20 ng/mL TNF-α or 50 μg/mL LPS treatment for 1 h. (E) ROS levels in HBE cells with SUR1 knockdown, treated with or without TNF-α 20 ng/mL for 3 h. (F) Apoptosis assay by flow cytometry in HBE cells transfected with SUR1 siRNAs and treated with TNF-α. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. Co-localization in (B) was assessed using Pearson’s correlation coefficient. Data in (C–F) were analyzed using two-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.
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SUR1 interacted with PARP1 to suppress DNA damage repair and induce apoptosis of bronchial <t>epithelial</t> cells (A) Co-immunoprecipitation and western blot analyses of HEK293T cells transfected with FLAG-SUR1 plasmids (left) or human bronchial epithlial <t>(HBE)</t> cells (right). (B) Immunofluorescence staining of HBE cells. Scale bars, 25 μm. (C) Homologous recombination reporter assay in U2OS-DRGFP cells transfected with SUR1 siRNA, followed by flow cytometry analysis. (D) Western blot analysis of HBE cells transfected with SUR1 siRNAs with or without 20 ng/mL TNF-α or 50 μg/mL LPS treatment for 1 h. (E) ROS levels in HBE cells with SUR1 knockdown, treated with or without TNF-α 20 ng/mL for 3 h. (F) Apoptosis assay by flow cytometry in HBE cells transfected with SUR1 siRNAs and treated with TNF-α. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. Co-localization in (B) was assessed using Pearson’s correlation coefficient. Data in (C–F) were analyzed using two-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.
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Image Search Results


SUR1 interacted with PARP1 to suppress DNA damage repair and induce apoptosis of bronchial epithelial cells (A) Co-immunoprecipitation and western blot analyses of HEK293T cells transfected with FLAG-SUR1 plasmids (left) or human bronchial epithlial (HBE) cells (right). (B) Immunofluorescence staining of HBE cells. Scale bars, 25 μm. (C) Homologous recombination reporter assay in U2OS-DRGFP cells transfected with SUR1 siRNA, followed by flow cytometry analysis. (D) Western blot analysis of HBE cells transfected with SUR1 siRNAs with or without 20 ng/mL TNF-α or 50 μg/mL LPS treatment for 1 h. (E) ROS levels in HBE cells with SUR1 knockdown, treated with or without TNF-α 20 ng/mL for 3 h. (F) Apoptosis assay by flow cytometry in HBE cells transfected with SUR1 siRNAs and treated with TNF-α. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. Co-localization in (B) was assessed using Pearson’s correlation coefficient. Data in (C–F) were analyzed using two-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.

Journal: iScience

Article Title: Sulfonylurea receptor 1 deficiency alleviates acute lung injury by activating PARP1 in epithelial cells

doi: 10.1016/j.isci.2026.117627

Figure Lengend Snippet: SUR1 interacted with PARP1 to suppress DNA damage repair and induce apoptosis of bronchial epithelial cells (A) Co-immunoprecipitation and western blot analyses of HEK293T cells transfected with FLAG-SUR1 plasmids (left) or human bronchial epithlial (HBE) cells (right). (B) Immunofluorescence staining of HBE cells. Scale bars, 25 μm. (C) Homologous recombination reporter assay in U2OS-DRGFP cells transfected with SUR1 siRNA, followed by flow cytometry analysis. (D) Western blot analysis of HBE cells transfected with SUR1 siRNAs with or without 20 ng/mL TNF-α or 50 μg/mL LPS treatment for 1 h. (E) ROS levels in HBE cells with SUR1 knockdown, treated with or without TNF-α 20 ng/mL for 3 h. (F) Apoptosis assay by flow cytometry in HBE cells transfected with SUR1 siRNAs and treated with TNF-α. Data are presented as mean ± SD ( n = 3). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001. Co-localization in (B) was assessed using Pearson’s correlation coefficient. Data in (C–F) were analyzed using two-way ANOVA followed by Tukey’s multiple-comparisons test. Representative images are shown.

Article Snippet: Human bronchial epithelial cell line HBE , American Type Culture Collection , N/A.

Techniques: Co-Immunoprecipitation Assay, Western Blot, Transfection, Immunofluorescence, Staining, Homologous Recombination, Reporter Assay, Flow Cytometry, Analysis, Knockdown, Apoptosis Assay

Journal: iScience

Article Title: Sulfonylurea receptor 1 deficiency alleviates acute lung injury by activating PARP1 in epithelial cells

doi: 10.1016/j.isci.2026.117627

Figure Lengend Snippet:

Article Snippet: Human bronchial epithelial cell line HBE , American Type Culture Collection , N/A.

Techniques: Cell-Signaling, Recombinant, Transfection, Caspase-3 Activity Assay, Protein Extraction, Knock-Out, Sequencing, Control, Plasmid Preparation, Software, Analysis