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mln120b  (Millipore)

 
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    Structured Review

    Millipore mln120b
    NF-κB inhibitor significantly inhibited the increase of Bif-1 and autophagy in J774A.1 cells. (A-D) J774A.1 cells were treated with LPS (500 ng/ml) for 6 h in the presence or absence of <t>MLN120B</t> (1 µM), then stimulated with 5 mM ATP for 30 min. Protein expression of (A) Bif-1, p62, LC3-II and LC3-I was investigated using western blotting. The relative protein levels of (B) Bif-1, (C) p62 and (D) LC3-II/I were analyzed using ImageJ (version 1.45; National Institutes of Health). (E) J774A.1 cell monolayers stained with LC3 (green) and DAPI (blue) fluorescence. Representative images from three independent experiments are shown. Scale bar, 10 µm (magnification, ×600). Data are expressed as mean ± SD (n=3). P<0.05 was considered to indicate a statistically significant difference (*P<0.05 vs. Con). LPS/ATP (L/A), LPS/ATP group; Con, control group treated with LPS/ATP; MLN120B, LPS/ATP group treated with MLN120B (1 µM); LPS, lipopolysaccharide; ATP, adenosine triphosphate; IL, interleukin; Bif-1, Bax-interacting factor 1; Con, control; LC, light chain; NF-κB, nuclear factor-κB.
    Mln120b, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mln120b/product/Millipore
    Average 90 stars, based on 1 article reviews
    mln120b - by Bioz Stars, 2026-02
    90/100 stars

    Images

    1) Product Images from "Bif‑1 inhibits activation of inflammasome through autophagy regulatory mechanism"

    Article Title: Bif‑1 inhibits activation of inflammasome through autophagy regulatory mechanism

    Journal: Molecular Medicine Reports

    doi: 10.3892/mmr.2024.13191

    NF-κB inhibitor significantly inhibited the increase of Bif-1 and autophagy in J774A.1 cells. (A-D) J774A.1 cells were treated with LPS (500 ng/ml) for 6 h in the presence or absence of MLN120B (1 µM), then stimulated with 5 mM ATP for 30 min. Protein expression of (A) Bif-1, p62, LC3-II and LC3-I was investigated using western blotting. The relative protein levels of (B) Bif-1, (C) p62 and (D) LC3-II/I were analyzed using ImageJ (version 1.45; National Institutes of Health). (E) J774A.1 cell monolayers stained with LC3 (green) and DAPI (blue) fluorescence. Representative images from three independent experiments are shown. Scale bar, 10 µm (magnification, ×600). Data are expressed as mean ± SD (n=3). P<0.05 was considered to indicate a statistically significant difference (*P<0.05 vs. Con). LPS/ATP (L/A), LPS/ATP group; Con, control group treated with LPS/ATP; MLN120B, LPS/ATP group treated with MLN120B (1 µM); LPS, lipopolysaccharide; ATP, adenosine triphosphate; IL, interleukin; Bif-1, Bax-interacting factor 1; Con, control; LC, light chain; NF-κB, nuclear factor-κB.
    Figure Legend Snippet: NF-κB inhibitor significantly inhibited the increase of Bif-1 and autophagy in J774A.1 cells. (A-D) J774A.1 cells were treated with LPS (500 ng/ml) for 6 h in the presence or absence of MLN120B (1 µM), then stimulated with 5 mM ATP for 30 min. Protein expression of (A) Bif-1, p62, LC3-II and LC3-I was investigated using western blotting. The relative protein levels of (B) Bif-1, (C) p62 and (D) LC3-II/I were analyzed using ImageJ (version 1.45; National Institutes of Health). (E) J774A.1 cell monolayers stained with LC3 (green) and DAPI (blue) fluorescence. Representative images from three independent experiments are shown. Scale bar, 10 µm (magnification, ×600). Data are expressed as mean ± SD (n=3). P<0.05 was considered to indicate a statistically significant difference (*P<0.05 vs. Con). LPS/ATP (L/A), LPS/ATP group; Con, control group treated with LPS/ATP; MLN120B, LPS/ATP group treated with MLN120B (1 µM); LPS, lipopolysaccharide; ATP, adenosine triphosphate; IL, interleukin; Bif-1, Bax-interacting factor 1; Con, control; LC, light chain; NF-κB, nuclear factor-κB.

    Techniques Used: Expressing, Western Blot, Staining, Fluorescence



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    mln120b  (Millipore)
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    Millipore mln120b
    NF-κB inhibitor significantly inhibited the increase of Bif-1 and autophagy in J774A.1 cells. (A-D) J774A.1 cells were treated with LPS (500 ng/ml) for 6 h in the presence or absence of <t>MLN120B</t> (1 µM), then stimulated with 5 mM ATP for 30 min. Protein expression of (A) Bif-1, p62, LC3-II and LC3-I was investigated using western blotting. The relative protein levels of (B) Bif-1, (C) p62 and (D) LC3-II/I were analyzed using ImageJ (version 1.45; National Institutes of Health). (E) J774A.1 cell monolayers stained with LC3 (green) and DAPI (blue) fluorescence. Representative images from three independent experiments are shown. Scale bar, 10 µm (magnification, ×600). Data are expressed as mean ± SD (n=3). P<0.05 was considered to indicate a statistically significant difference (*P<0.05 vs. Con). LPS/ATP (L/A), LPS/ATP group; Con, control group treated with LPS/ATP; MLN120B, LPS/ATP group treated with MLN120B (1 µM); LPS, lipopolysaccharide; ATP, adenosine triphosphate; IL, interleukin; Bif-1, Bax-interacting factor 1; Con, control; LC, light chain; NF-κB, nuclear factor-κB.
    Mln120b, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mln120b/product/Millipore
    Average 90 stars, based on 1 article reviews
    mln120b - by Bioz Stars, 2026-02
    90/100 stars
    		  Buy from Supplier

    Image Search Results


    NF-κB inhibitor significantly inhibited the increase of Bif-1 and autophagy in J774A.1 cells. (A-D) J774A.1 cells were treated with LPS (500 ng/ml) for 6 h in the presence or absence of MLN120B (1 µM), then stimulated with 5 mM ATP for 30 min. Protein expression of (A) Bif-1, p62, LC3-II and LC3-I was investigated using western blotting. The relative protein levels of (B) Bif-1, (C) p62 and (D) LC3-II/I were analyzed using ImageJ (version 1.45; National Institutes of Health). (E) J774A.1 cell monolayers stained with LC3 (green) and DAPI (blue) fluorescence. Representative images from three independent experiments are shown. Scale bar, 10 µm (magnification, ×600). Data are expressed as mean ± SD (n=3). P<0.05 was considered to indicate a statistically significant difference (*P<0.05 vs. Con). LPS/ATP (L/A), LPS/ATP group; Con, control group treated with LPS/ATP; MLN120B, LPS/ATP group treated with MLN120B (1 µM); LPS, lipopolysaccharide; ATP, adenosine triphosphate; IL, interleukin; Bif-1, Bax-interacting factor 1; Con, control; LC, light chain; NF-κB, nuclear factor-κB.

    Journal: Molecular Medicine Reports

    Article Title: Bif‑1 inhibits activation of inflammasome through autophagy regulatory mechanism

    doi: 10.3892/mmr.2024.13191

    Figure Lengend Snippet: NF-κB inhibitor significantly inhibited the increase of Bif-1 and autophagy in J774A.1 cells. (A-D) J774A.1 cells were treated with LPS (500 ng/ml) for 6 h in the presence or absence of MLN120B (1 µM), then stimulated with 5 mM ATP for 30 min. Protein expression of (A) Bif-1, p62, LC3-II and LC3-I was investigated using western blotting. The relative protein levels of (B) Bif-1, (C) p62 and (D) LC3-II/I were analyzed using ImageJ (version 1.45; National Institutes of Health). (E) J774A.1 cell monolayers stained with LC3 (green) and DAPI (blue) fluorescence. Representative images from three independent experiments are shown. Scale bar, 10 µm (magnification, ×600). Data are expressed as mean ± SD (n=3). P<0.05 was considered to indicate a statistically significant difference (*P<0.05 vs. Con). LPS/ATP (L/A), LPS/ATP group; Con, control group treated with LPS/ATP; MLN120B, LPS/ATP group treated with MLN120B (1 µM); LPS, lipopolysaccharide; ATP, adenosine triphosphate; IL, interleukin; Bif-1, Bax-interacting factor 1; Con, control; LC, light chain; NF-κB, nuclear factor-κB.

    Article Snippet: Specifically, the following inhibitors were employed: MLN120B (1 µM; Sigma-Aldrich; Merck KGaA) and MRT68921 (0.25 µM; MedChemExpress).

    Techniques: Expressing, Western Blot, Staining, Fluorescence