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nf κb inhibitor imd0354  (Tocris)


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    Tocris nf κb inhibitor imd0354
    Fig. 6. The PM2.5-induced increase in α-SMA was dependent on NF-κB, but not AhR signaling. A and B) Fibroblasts were exposed to repeated treatment of PM2.5 from Beijing (A) or NIST (B) in the presence or absence of 10 µM of the the AhR inhibitor CH223191. Levels of α-SMA and collagen 1a1 were analyzed by immunoblot. Representative immunoblots from two independent experiments from both Beijing and NIST PM2.5 are shown. C) and D) Fibroblasts given repeated treatment of PM2.5 from Beijing (C) or NIST (D) in the presence or absence of 100 nM of the NF-κB inhibitor <t>IMD0354</t> were analyzed for α-SMA or collagen 1a1 expression by immunoblot. Shown are representative blots from two (C) and three (D) independent experiments with densitometric analysis relative to α-tubulin shown below. * P < 0.05, * * P < 0.01.
    Nf κb Inhibitor Imd0354, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 25 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/nf κb inhibitor imd0354/product/Tocris
    Average 93 stars, based on 25 article reviews
    nf κb inhibitor imd0354 - by Bioz Stars, 2026-02
    93/100 stars

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    1) Product Images from "Promotion of myofibroblast differentiation through repeated treatment of fibroblasts to low concentrations of PM 2.5 ."

    Article Title: Promotion of myofibroblast differentiation through repeated treatment of fibroblasts to low concentrations of PM 2.5 .

    Journal: Environmental toxicology and pharmacology

    doi: 10.1016/j.etap.2023.104329

    Fig. 6. The PM2.5-induced increase in α-SMA was dependent on NF-κB, but not AhR signaling. A and B) Fibroblasts were exposed to repeated treatment of PM2.5 from Beijing (A) or NIST (B) in the presence or absence of 10 µM of the the AhR inhibitor CH223191. Levels of α-SMA and collagen 1a1 were analyzed by immunoblot. Representative immunoblots from two independent experiments from both Beijing and NIST PM2.5 are shown. C) and D) Fibroblasts given repeated treatment of PM2.5 from Beijing (C) or NIST (D) in the presence or absence of 100 nM of the NF-κB inhibitor IMD0354 were analyzed for α-SMA or collagen 1a1 expression by immunoblot. Shown are representative blots from two (C) and three (D) independent experiments with densitometric analysis relative to α-tubulin shown below. * P < 0.05, * * P < 0.01.
    Figure Legend Snippet: Fig. 6. The PM2.5-induced increase in α-SMA was dependent on NF-κB, but not AhR signaling. A and B) Fibroblasts were exposed to repeated treatment of PM2.5 from Beijing (A) or NIST (B) in the presence or absence of 10 µM of the the AhR inhibitor CH223191. Levels of α-SMA and collagen 1a1 were analyzed by immunoblot. Representative immunoblots from two independent experiments from both Beijing and NIST PM2.5 are shown. C) and D) Fibroblasts given repeated treatment of PM2.5 from Beijing (C) or NIST (D) in the presence or absence of 100 nM of the NF-κB inhibitor IMD0354 were analyzed for α-SMA or collagen 1a1 expression by immunoblot. Shown are representative blots from two (C) and three (D) independent experiments with densitometric analysis relative to α-tubulin shown below. * P < 0.05, * * P < 0.01.

    Techniques Used: Western Blot, Expressing



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    Tocris nf κb inhibitor imd0354
    Fig. 6. The PM2.5-induced increase in α-SMA was dependent on NF-κB, but not AhR signaling. A and B) Fibroblasts were exposed to repeated treatment of PM2.5 from Beijing (A) or NIST (B) in the presence or absence of 10 µM of the the AhR inhibitor CH223191. Levels of α-SMA and collagen 1a1 were analyzed by immunoblot. Representative immunoblots from two independent experiments from both Beijing and NIST PM2.5 are shown. C) and D) Fibroblasts given repeated treatment of PM2.5 from Beijing (C) or NIST (D) in the presence or absence of 100 nM of the NF-κB inhibitor <t>IMD0354</t> were analyzed for α-SMA or collagen 1a1 expression by immunoblot. Shown are representative blots from two (C) and three (D) independent experiments with densitometric analysis relative to α-tubulin shown below. * P < 0.05, * * P < 0.01.
    Nf κb Inhibitor Imd0354, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/nf κb inhibitor imd0354/product/Tocris
    Average 93 stars, based on 1 article reviews
    nf κb inhibitor imd0354 - by Bioz Stars, 2026-02
    93/100 stars
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    a nuclear factor-kappab (nf-κb) inhibitor (imd0354)  (Millipore)
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    Fig. 6. The PM2.5-induced increase in α-SMA was dependent on NF-κB, but not AhR signaling. A and B) Fibroblasts were exposed to repeated treatment of PM2.5 from Beijing (A) or NIST (B) in the presence or absence of 10 µM of the the AhR inhibitor CH223191. Levels of α-SMA and collagen 1a1 were analyzed by immunoblot. Representative immunoblots from two independent experiments from both Beijing and NIST PM2.5 are shown. C) and D) Fibroblasts given repeated treatment of PM2.5 from Beijing (C) or NIST (D) in the presence or absence of 100 nM of the NF-κB inhibitor <t>IMD0354</t> were analyzed for α-SMA or collagen 1a1 expression by immunoblot. Shown are representative blots from two (C) and three (D) independent experiments with densitometric analysis relative to α-tubulin shown below. * P < 0.05, * * P < 0.01.
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    https://www.bioz.com/result/a nuclear factor-kappab (nf-κb) inhibitor (imd0354)/product/Millipore
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    Image Search Results


    Fig. 6. The PM2.5-induced increase in α-SMA was dependent on NF-κB, but not AhR signaling. A and B) Fibroblasts were exposed to repeated treatment of PM2.5 from Beijing (A) or NIST (B) in the presence or absence of 10 µM of the the AhR inhibitor CH223191. Levels of α-SMA and collagen 1a1 were analyzed by immunoblot. Representative immunoblots from two independent experiments from both Beijing and NIST PM2.5 are shown. C) and D) Fibroblasts given repeated treatment of PM2.5 from Beijing (C) or NIST (D) in the presence or absence of 100 nM of the NF-κB inhibitor IMD0354 were analyzed for α-SMA or collagen 1a1 expression by immunoblot. Shown are representative blots from two (C) and three (D) independent experiments with densitometric analysis relative to α-tubulin shown below. * P < 0.05, * * P < 0.01.

    Journal: Environmental toxicology and pharmacology

    Article Title: Promotion of myofibroblast differentiation through repeated treatment of fibroblasts to low concentrations of PM 2.5 .

    doi: 10.1016/j.etap.2023.104329

    Figure Lengend Snippet: Fig. 6. The PM2.5-induced increase in α-SMA was dependent on NF-κB, but not AhR signaling. A and B) Fibroblasts were exposed to repeated treatment of PM2.5 from Beijing (A) or NIST (B) in the presence or absence of 10 µM of the the AhR inhibitor CH223191. Levels of α-SMA and collagen 1a1 were analyzed by immunoblot. Representative immunoblots from two independent experiments from both Beijing and NIST PM2.5 are shown. C) and D) Fibroblasts given repeated treatment of PM2.5 from Beijing (C) or NIST (D) in the presence or absence of 100 nM of the NF-κB inhibitor IMD0354 were analyzed for α-SMA or collagen 1a1 expression by immunoblot. Shown are representative blots from two (C) and three (D) independent experiments with densitometric analysis relative to α-tubulin shown below. * P < 0.05, * * P < 0.01.

    Article Snippet: In some experiments, the cells were pre-incubated with the AhR antagonist CH223191 (10 μM, Tocris Bioscience, Ellisville, MO) or the NF-κB inhibitor IMD0354 (10 nM, Tocris Bioscience) for 30 min prior to addition of PM2.5.

    Techniques: Western Blot, Expressing