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Ahr inhibitor ch223191

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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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Lab products found in correlation

Mifn β, by BioXCell (2 mentions) Dual luciferase reporter system, by Promega (2 mentions) D glucose, by Thermo Fisher Scientific (1 mentions) Anti mouse cd4 magnetic beads, by BD (1 mentions) Tgf β, by Merck Group (1 mentions)

Close spelling variants of this product

CH223191

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.
Rothhammer V., Mascanfroni I.D., Bunse L., Takenaka M.C., Kenison J.E., Mayo L., Chao C.C., Patel B., Yan R., Blain M., Alvarez J.I., Kébir H., Anandasabapathy N., Izquierdo G., Jung S., Obholzer N., Pochet N., Clish C.B., Prinz M., Prat A., Antel J, & Quintana F.J. (2016). Type I interferons and microbial metabolites of tryptophan modulate astrocyte activity and CNS inflammation via the aryl hydrocarbon receptor. Nature medicine, 22(6), 586-597.
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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.
Rothhammer V., Mascanfroni I.D., Bunse L., Takenaka M.C., Kenison J.E., Mayo L., Chao C.C., Patel B., Yan R., Blain M., Alvarez J.I., Kébir H., Anandasabapathy N., Izquierdo G., Jung S., Obholzer N., Pochet N., Clish C.B., Prinz M., Prat A., Antel J, & Quintana F.J. (2016). Type I interferons and microbial metabolites of tryptophan modulate astrocyte activity and CNS inflammation via the aryl hydrocarbon receptor. Nature medicine, 22(6), 586-597.
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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.
Yu Y., Yang W., Yu T., Zhao X., Zhou Z., Yu Y., Xiong L., Yang H., Bilotta A.J., Yao S., Golovko G., Plasencia A., Quintana F.J., Zhou L., Li Y, & Cong Y. (2022). Glucose promotes regulatory T cell differentiation to maintain intestinal homeostasis. iScience, 25(9), 105004.
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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.
Fu H., Wang L., Wang J., Bennett B.D., Li J.L., Zhao B, & Hu G. (2018). Dioxin and AHR impairs mesoderm gene expression and cardiac differentiation in human embryonic stem cells. The Science of the total environment, 651(Pt 1), 1038-1046.
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