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Ahr inhibitor ch223191

Manufactured by Merck Group

AhR inhibitor CH223191 is a chemical compound used in laboratory research. It functions as an antagonist of the aryl hydrocarbon receptor (AhR), a transcription factor involved in the regulation of gene expression. This product is intended for use in experimental settings to study the role of AhR in various biological processes.

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4 protocols using ahr inhibitor ch223191

1

Measurement of AhR Ligands in Human Serum

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HEK293 cells were grown in DMEM supplemented with 10% FBS and transfected with Fugene-HD Transfection Reagent (Roche), reporter constructs (pAhR-Luc/pTK-Renilla or pGud-Luc/pTK Renilla) as well transcription factor expression constructs (pStat1, pIrf9) as indicated. In some experiments, transfected cells were exposed to 500 IU/ml of mIFN-β (Bio X cell) or AhR inhibitor CH223191 (Sigma). For the measurement of AhR ligands in human serum, 15.000 HEK293 cells were plated in 96 well plates 24 h before transfection with pGud-Luc and pTK-Renilla. After 24 h transfected cells were incubated with DMEM supplemented with 10% of patient serum. Luciferase activity was analyzed 24 h later using Dual Luciferase Reporter System (Promega) and normalized to Renilla luciferase activity.
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2

Measurement of AhR Ligands in Human Serum

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HEK293 cells were grown in DMEM supplemented with 10% FBS and transfected with Fugene-HD Transfection Reagent (Roche), reporter constructs (pAhR-Luc/pTK-Renilla or pGud-Luc/pTK Renilla) as well transcription factor expression constructs (pStat1, pIrf9) as indicated. In some experiments, transfected cells were exposed to 500 IU/ml of mIFN-β (Bio X cell) or AhR inhibitor CH223191 (Sigma). For the measurement of AhR ligands in human serum, 15.000 HEK293 cells were plated in 96 well plates 24 h before transfection with pGud-Luc and pTK-Renilla. After 24 h transfected cells were incubated with DMEM supplemented with 10% of patient serum. Luciferase activity was analyzed 24 h later using Dual Luciferase Reporter System (Promega) and normalized to Renilla luciferase activity.
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3

Modulating Th Cell Differentiation with Glucose and Ahr Inhibitor

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CD4+ T cells were isolated from spleens using anti-mouse CD4-magnetic beads (BD Biosciences). CD4+ T cells were cultured with CBir1 peptides (ThermoFisher Scientific) and irradiated splenic antigen-presenting cells (APCs) or were activated with 5 μg/ml plate-bound anti-mouse-CD3 (Bio X Cell) and 2 μg/ml soluble anti-mouse CD28 (Bio X Cell). Cells were treated with different concentrations of D-glucose (Fisher chemical) in RMPI 1640 medium in the presence or absence of 3 μM Ahr inhibitor CH223191 (Sigma) and cultured under neutral (without exogenous cytokines), Th1 (10 ng/mL IL-12), Th17 (2 ng/mL TGFβ, 50 ng/mL IL6, 10 ug/ml anti-IFNγ mAb, 5 ug/ml anti-IL-4 mAb), or Treg (2 ng/mL TGFβ) polarization conditions. All recombinant antibodies were obtained from Biolegend.
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4

Dioxin Exposure and AhR Modulation

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2,3,7,8-Tetrachlorodibenzodioxin (TCDD, Sigma), AHR inhibitor CH223191 (Sigma) and induction reagents were dissolved in DMSO. In dose titration, TCDD is added to a final concentration of 0.1, 1, 2, or 10 nM as indicated. In other experiments, TCDD is added to a final concentration of 2 nM based on a previous study32 (link). The AHR inhibitor CH223191 is added to a final concentration of 1 uM. For control experiments, equivalent volume of DMSO is added. The final DMSO concentration in both the control and experimental groups were kept at 0.1% to minimize the impact on cell growth.
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