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ahr  (Novus Biologicals)


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    Structured Review

    Novus Biologicals ahr
    Hepatic <t>AHR</t> signalling is restored in adult WD-challenged offspring with perinatal exposure to Ind and I3A, concomitant with reduced fibrogenesis. ( a ) Protein levels by Simple Western analysis for AHR <t>and</t> <t>CYP1A1.</t> Representative images and densitometry quantification are shown. Vinculin was the loading control for AHR and GAPDH for CYP1A1. Data are mean ± SEM, n = 6–9/group (3–5 litters/group). ∗∗p < 0.01, ∗∗∗p < 0.001, and ∗∗∗∗p < 0.0001 vs. WD by one-way ANOVA with Dunnett's test. Hepatic (whole liver) gene expression analysis for de novo lipogenesis genes ( Srebp1c , Fasn , and Acc1 ) and lipid transport ( Cd36 ) ( b ), genes associated with hepatic stellate cell activation and liver fibrosis ( c ), inflammatory genes ( d ), and genes associated with monocyte infiltration ( e ) by qPCR, normalised to Tbp . Data are mean ± SEM, n = 6–9/group (3–5 litters/group). ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, and ∗∗∗∗p < 0.0001 vs. WD by one-way ANOVA with Dunnett's test, except Acta2 , Timp1 , and Ccr2 by Kruskal–Wallis with Dunn's test. ( f ) Gene expression of genes in isolated hepatocytes by qPCR, normalised to Rpl13a . Data are mean ± SEM, n = 9/group (3–6 litters/group). ∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. Gene expression of genes associated with AHR ( Cyp1a2 ) and oxidative defence ( g ) and inflammatory genes ( h ) in MerTK + liver macrophages by qPCR, normalised to Actb . Data are mean ± SEM, n = 6–12/group (3–6 litters/group). ∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. ( i ) Gene expression of genes involved in fibrosis in hepatic stellate cells (HSCs) by qPCR, normalised to Rn18s . Data are mean ± SEM, n = 3–7/group (3 litters/group). ∗p < 0.05 and ∗∗p < 0.01 vs. WD by one-way ANOVA with Dunnett's test.
    Ahr, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ahr+nb100+2289/pmc12799784-88-38-40?v=Novus+Biologicals
    Average 94 stars, based on 15 article reviews
    ahr - by Bioz Stars, 2026-07
    94/100 stars

    Images

    1) Product Images from "Reprogramming offspring liver health: maternal indole supplementation as a preventive strategy against MASLD"

    Article Title: Reprogramming offspring liver health: maternal indole supplementation as a preventive strategy against MASLD

    Journal: eBioMedicine

    doi: 10.1016/j.ebiom.2025.106098

    Hepatic AHR signalling is restored in adult WD-challenged offspring with perinatal exposure to Ind and I3A, concomitant with reduced fibrogenesis. ( a ) Protein levels by Simple Western analysis for AHR and CYP1A1. Representative images and densitometry quantification are shown. Vinculin was the loading control for AHR and GAPDH for CYP1A1. Data are mean ± SEM, n = 6–9/group (3–5 litters/group). ∗∗p < 0.01, ∗∗∗p < 0.001, and ∗∗∗∗p < 0.0001 vs. WD by one-way ANOVA with Dunnett's test. Hepatic (whole liver) gene expression analysis for de novo lipogenesis genes ( Srebp1c , Fasn , and Acc1 ) and lipid transport ( Cd36 ) ( b ), genes associated with hepatic stellate cell activation and liver fibrosis ( c ), inflammatory genes ( d ), and genes associated with monocyte infiltration ( e ) by qPCR, normalised to Tbp . Data are mean ± SEM, n = 6–9/group (3–5 litters/group). ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, and ∗∗∗∗p < 0.0001 vs. WD by one-way ANOVA with Dunnett's test, except Acta2 , Timp1 , and Ccr2 by Kruskal–Wallis with Dunn's test. ( f ) Gene expression of genes in isolated hepatocytes by qPCR, normalised to Rpl13a . Data are mean ± SEM, n = 9/group (3–6 litters/group). ∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. Gene expression of genes associated with AHR ( Cyp1a2 ) and oxidative defence ( g ) and inflammatory genes ( h ) in MerTK + liver macrophages by qPCR, normalised to Actb . Data are mean ± SEM, n = 6–12/group (3–6 litters/group). ∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. ( i ) Gene expression of genes involved in fibrosis in hepatic stellate cells (HSCs) by qPCR, normalised to Rn18s . Data are mean ± SEM, n = 3–7/group (3 litters/group). ∗p < 0.05 and ∗∗p < 0.01 vs. WD by one-way ANOVA with Dunnett's test.
    Figure Legend Snippet: Hepatic AHR signalling is restored in adult WD-challenged offspring with perinatal exposure to Ind and I3A, concomitant with reduced fibrogenesis. ( a ) Protein levels by Simple Western analysis for AHR and CYP1A1. Representative images and densitometry quantification are shown. Vinculin was the loading control for AHR and GAPDH for CYP1A1. Data are mean ± SEM, n = 6–9/group (3–5 litters/group). ∗∗p < 0.01, ∗∗∗p < 0.001, and ∗∗∗∗p < 0.0001 vs. WD by one-way ANOVA with Dunnett's test. Hepatic (whole liver) gene expression analysis for de novo lipogenesis genes ( Srebp1c , Fasn , and Acc1 ) and lipid transport ( Cd36 ) ( b ), genes associated with hepatic stellate cell activation and liver fibrosis ( c ), inflammatory genes ( d ), and genes associated with monocyte infiltration ( e ) by qPCR, normalised to Tbp . Data are mean ± SEM, n = 6–9/group (3–5 litters/group). ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, and ∗∗∗∗p < 0.0001 vs. WD by one-way ANOVA with Dunnett's test, except Acta2 , Timp1 , and Ccr2 by Kruskal–Wallis with Dunn's test. ( f ) Gene expression of genes in isolated hepatocytes by qPCR, normalised to Rpl13a . Data are mean ± SEM, n = 9/group (3–6 litters/group). ∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. Gene expression of genes associated with AHR ( Cyp1a2 ) and oxidative defence ( g ) and inflammatory genes ( h ) in MerTK + liver macrophages by qPCR, normalised to Actb . Data are mean ± SEM, n = 6–12/group (3–6 litters/group). ∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. ( i ) Gene expression of genes involved in fibrosis in hepatic stellate cells (HSCs) by qPCR, normalised to Rn18s . Data are mean ± SEM, n = 3–7/group (3 litters/group). ∗p < 0.05 and ∗∗p < 0.01 vs. WD by one-way ANOVA with Dunnett's test.

    Techniques Used: Simple Western, Control, Gene Expression, Activation Assay, Isolation



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    Hepatic <t>AHR</t> signalling is restored in adult WD-challenged offspring with perinatal exposure to Ind and I3A, concomitant with reduced fibrogenesis. ( a ) Protein levels by Simple Western analysis for AHR <t>and</t> <t>CYP1A1.</t> Representative images and densitometry quantification are shown. Vinculin was the loading control for AHR and GAPDH for CYP1A1. Data are mean ± SEM, n = 6–9/group (3–5 litters/group). ∗∗p < 0.01, ∗∗∗p < 0.001, and ∗∗∗∗p < 0.0001 vs. WD by one-way ANOVA with Dunnett's test. Hepatic (whole liver) gene expression analysis for de novo lipogenesis genes ( Srebp1c , Fasn , and Acc1 ) and lipid transport ( Cd36 ) ( b ), genes associated with hepatic stellate cell activation and liver fibrosis ( c ), inflammatory genes ( d ), and genes associated with monocyte infiltration ( e ) by qPCR, normalised to Tbp . Data are mean ± SEM, n = 6–9/group (3–5 litters/group). ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, and ∗∗∗∗p < 0.0001 vs. WD by one-way ANOVA with Dunnett's test, except Acta2 , Timp1 , and Ccr2 by Kruskal–Wallis with Dunn's test. ( f ) Gene expression of genes in isolated hepatocytes by qPCR, normalised to Rpl13a . Data are mean ± SEM, n = 9/group (3–6 litters/group). ∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. Gene expression of genes associated with AHR ( Cyp1a2 ) and oxidative defence ( g ) and inflammatory genes ( h ) in MerTK + liver macrophages by qPCR, normalised to Actb . Data are mean ± SEM, n = 6–12/group (3–6 litters/group). ∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. ( i ) Gene expression of genes involved in fibrosis in hepatic stellate cells (HSCs) by qPCR, normalised to Rn18s . Data are mean ± SEM, n = 3–7/group (3 litters/group). ∗p < 0.05 and ∗∗p < 0.01 vs. WD by one-way ANOVA with Dunnett's test.
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    Hepatic AHR signalling is restored in adult WD-challenged offspring with perinatal exposure to Ind and I3A, concomitant with reduced fibrogenesis. ( a ) Protein levels by Simple Western analysis for AHR and CYP1A1. Representative images and densitometry quantification are shown. Vinculin was the loading control for AHR and GAPDH for CYP1A1. Data are mean ± SEM, n = 6–9/group (3–5 litters/group). ∗∗p < 0.01, ∗∗∗p < 0.001, and ∗∗∗∗p < 0.0001 vs. WD by one-way ANOVA with Dunnett's test. Hepatic (whole liver) gene expression analysis for de novo lipogenesis genes ( Srebp1c , Fasn , and Acc1 ) and lipid transport ( Cd36 ) ( b ), genes associated with hepatic stellate cell activation and liver fibrosis ( c ), inflammatory genes ( d ), and genes associated with monocyte infiltration ( e ) by qPCR, normalised to Tbp . Data are mean ± SEM, n = 6–9/group (3–5 litters/group). ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, and ∗∗∗∗p < 0.0001 vs. WD by one-way ANOVA with Dunnett's test, except Acta2 , Timp1 , and Ccr2 by Kruskal–Wallis with Dunn's test. ( f ) Gene expression of genes in isolated hepatocytes by qPCR, normalised to Rpl13a . Data are mean ± SEM, n = 9/group (3–6 litters/group). ∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. Gene expression of genes associated with AHR ( Cyp1a2 ) and oxidative defence ( g ) and inflammatory genes ( h ) in MerTK + liver macrophages by qPCR, normalised to Actb . Data are mean ± SEM, n = 6–12/group (3–6 litters/group). ∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. ( i ) Gene expression of genes involved in fibrosis in hepatic stellate cells (HSCs) by qPCR, normalised to Rn18s . Data are mean ± SEM, n = 3–7/group (3 litters/group). ∗p < 0.05 and ∗∗p < 0.01 vs. WD by one-way ANOVA with Dunnett's test.

    Journal: eBioMedicine

    Article Title: Reprogramming offspring liver health: maternal indole supplementation as a preventive strategy against MASLD

    doi: 10.1016/j.ebiom.2025.106098

    Figure Lengend Snippet: Hepatic AHR signalling is restored in adult WD-challenged offspring with perinatal exposure to Ind and I3A, concomitant with reduced fibrogenesis. ( a ) Protein levels by Simple Western analysis for AHR and CYP1A1. Representative images and densitometry quantification are shown. Vinculin was the loading control for AHR and GAPDH for CYP1A1. Data are mean ± SEM, n = 6–9/group (3–5 litters/group). ∗∗p < 0.01, ∗∗∗p < 0.001, and ∗∗∗∗p < 0.0001 vs. WD by one-way ANOVA with Dunnett's test. Hepatic (whole liver) gene expression analysis for de novo lipogenesis genes ( Srebp1c , Fasn , and Acc1 ) and lipid transport ( Cd36 ) ( b ), genes associated with hepatic stellate cell activation and liver fibrosis ( c ), inflammatory genes ( d ), and genes associated with monocyte infiltration ( e ) by qPCR, normalised to Tbp . Data are mean ± SEM, n = 6–9/group (3–5 litters/group). ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, and ∗∗∗∗p < 0.0001 vs. WD by one-way ANOVA with Dunnett's test, except Acta2 , Timp1 , and Ccr2 by Kruskal–Wallis with Dunn's test. ( f ) Gene expression of genes in isolated hepatocytes by qPCR, normalised to Rpl13a . Data are mean ± SEM, n = 9/group (3–6 litters/group). ∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. Gene expression of genes associated with AHR ( Cyp1a2 ) and oxidative defence ( g ) and inflammatory genes ( h ) in MerTK + liver macrophages by qPCR, normalised to Actb . Data are mean ± SEM, n = 6–12/group (3–6 litters/group). ∗p < 0.05 vs. WD by one-way ANOVA with Dunnett's test. ( i ) Gene expression of genes involved in fibrosis in hepatic stellate cells (HSCs) by qPCR, normalised to Rn18s . Data are mean ± SEM, n = 3–7/group (3 litters/group). ∗p < 0.05 and ∗∗p < 0.01 vs. WD by one-way ANOVA with Dunnett's test.

    Article Snippet: Jess assays using 12–230 kDa modules were run according to manufacturer's instructions with 0.2–0.5 mg/mL total protein concentration and primary antibodies AKT (1:50; CST Cat# 9272, RRID: AB_329827 ), phospho-AKT (Ser473; 1:10; CST Cat# 9271, RRID: AB_329825 ), AHR (1:100; Novus Cat# NB100-2289, RRID: AB_10002581 ), CYP1A1 (1:50; Proteintech Cat# 13241-1-AP, RRID: AB_2877928 ), and occludin (1:50; CST Cat# 91131, RRID: AB_2934013 ).

    Techniques: Simple Western, Control, Gene Expression, Activation Assay, Isolation