Review



primary antibodies for bcl6  (Santa Cruz Biotechnology)


Bioz Verified Symbol Santa Cruz Biotechnology is a verified supplier  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 94
      Buy from Supplier

    Structured Review

    Santa Cruz Biotechnology primary antibodies for bcl6
    Hepatic <t>BCL6</t> is predicted to co-regulate transcription with FXR. ( A ) Top 20 high-confidence causal transcription factors predicted by IMAGE analysis of RNA-seq and H3K27ac datasets from Bcl6 fl/fl and Bcl6 LKO livers. N = 3/group. ( B ) Representative UCSC browser tracks showing hepatic BCL6 and FXR binding at key BA regulatory genes in Bcl6 fl/fl liver.
    Primary Antibodies For Bcl6, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 240 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+antibodies+for+bcl6/Bcl-6+Antibody/pmc12865649-346-0-5
    Average 94 stars, based on 240 article reviews
    primary antibodies for bcl6 - by Bioz Stars, 2026-10
    94/100 stars

    Images

    1) Product Images from "Prevention of Cholestatic Liver Disease Through BCL6-FXR Enterohepatic Crosstalk"

    Article Title: Prevention of Cholestatic Liver Disease Through BCL6-FXR Enterohepatic Crosstalk

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    doi: 10.1016/j.jcmgh.2025.101706

    Hepatic BCL6 is predicted to co-regulate transcription with FXR. ( A ) Top 20 high-confidence causal transcription factors predicted by IMAGE analysis of RNA-seq and H3K27ac datasets from Bcl6 fl/fl and Bcl6 LKO livers. N = 3/group. ( B ) Representative UCSC browser tracks showing hepatic BCL6 and FXR binding at key BA regulatory genes in Bcl6 fl/fl liver.
    Figure Legend Snippet: Hepatic BCL6 is predicted to co-regulate transcription with FXR. ( A ) Top 20 high-confidence causal transcription factors predicted by IMAGE analysis of RNA-seq and H3K27ac datasets from Bcl6 fl/fl and Bcl6 LKO livers. N = 3/group. ( B ) Representative UCSC browser tracks showing hepatic BCL6 and FXR binding at key BA regulatory genes in Bcl6 fl/fl liver.

    Techniques Used: RNA Sequencing, Binding Assay

    Hepatic Bcl6 deletion increases serum cholesterol in males. ( A ) Serum cholesterol and triglycerides from Bcl6 fl/fl and Bcl6 LKO males. N = 8–9/group. ( B ) FPLC quantification of cholesterol and triglycerides from Bcl6 fl/fl and Bcl6 LKO pooled male serum. N = 3–4 animals/pool. ( C ) Liver cholesterol in Bcl6 fl/fl and Bcl6 LKO males. N = 8–9/group. Student’s t -tests were performed in ( A and C ) to compare means. ( D ) Heatmap of Bcl6 fl/fl vs Bcl6 LKO differentially expressed ( P adj < .05, |log 2 FC |> 0) cholesterol synthesis, transport, and sterol-related CYP genes expressed as relative RPKM from RNA-seq performed in Bcl6 fl/fl and Bcl6 LKO male livers. N = 4/group. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.
    Figure Legend Snippet: Hepatic Bcl6 deletion increases serum cholesterol in males. ( A ) Serum cholesterol and triglycerides from Bcl6 fl/fl and Bcl6 LKO males. N = 8–9/group. ( B ) FPLC quantification of cholesterol and triglycerides from Bcl6 fl/fl and Bcl6 LKO pooled male serum. N = 3–4 animals/pool. ( C ) Liver cholesterol in Bcl6 fl/fl and Bcl6 LKO males. N = 8–9/group. Student’s t -tests were performed in ( A and C ) to compare means. ( D ) Heatmap of Bcl6 fl/fl vs Bcl6 LKO differentially expressed ( P adj < .05, |log 2 FC |> 0) cholesterol synthesis, transport, and sterol-related CYP genes expressed as relative RPKM from RNA-seq performed in Bcl6 fl/fl and Bcl6 LKO male livers. N = 4/group. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Techniques Used: RNA Sequencing

    Hepatic Bcl6 deletion increases serum cholesterol in females. ( A ) Serum cholesterol and triglycerides and ( B ) liver cholesterol levels in Bcl6 fl/fl and Bcl6 LKO females. N = 7–9/group. ( C ) Liver qPCR quantifying cholesterol synthesis, transport, and sterol-related CYP genes in Bcl6 fl/fl and Bcl6 LKO females. N = 7–9/group. Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.
    Figure Legend Snippet: Hepatic Bcl6 deletion increases serum cholesterol in females. ( A ) Serum cholesterol and triglycerides and ( B ) liver cholesterol levels in Bcl6 fl/fl and Bcl6 LKO females. N = 7–9/group. ( C ) Liver qPCR quantifying cholesterol synthesis, transport, and sterol-related CYP genes in Bcl6 fl/fl and Bcl6 LKO females. N = 7–9/group. Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Techniques Used:

    Hepatic Bcl6 deletion increases BA synthesis and serum/total levels in males. ( A ) Serum BA levels in Bcl6 fl/fl and Bcl6 LKO males. N = 7–9/group. ( B ) Total BA pool quantification (including liver, gallbladder, and small intestines) in Bcl6 fl/fl and Bcl6 LKO males, expressed as umol per 100 grams of body weight. N = 7–8/group. ( C ) Total fecal BA levels in Bcl6 fl/fl and Bcl6 LKO males. N = 5/group. ( D ) Serum 7a-C4 quantification in Bcl6 fl/fl and Bcl6 LKO males. N = 4–6/group. ( E ) Total ( left ) and individual BA species in serum as proportions of total ( right ), and ( F ) percentages of primary and secondary BAs in overnight-fasted Bcl6 fl/fl and Bcl6 LKO males. N = 8–9/group. ( G ) Serum ALT and bilirubin levels in Bcl6 fl/fl and Bcl6 LKO mice. N = 4/group. ( H ) Representative Picrosirius Red and H&E staining in liver from Bcl6 fl/fl and Bcl6 LKO males. In ( A–E and G ), Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.
    Figure Legend Snippet: Hepatic Bcl6 deletion increases BA synthesis and serum/total levels in males. ( A ) Serum BA levels in Bcl6 fl/fl and Bcl6 LKO males. N = 7–9/group. ( B ) Total BA pool quantification (including liver, gallbladder, and small intestines) in Bcl6 fl/fl and Bcl6 LKO males, expressed as umol per 100 grams of body weight. N = 7–8/group. ( C ) Total fecal BA levels in Bcl6 fl/fl and Bcl6 LKO males. N = 5/group. ( D ) Serum 7a-C4 quantification in Bcl6 fl/fl and Bcl6 LKO males. N = 4–6/group. ( E ) Total ( left ) and individual BA species in serum as proportions of total ( right ), and ( F ) percentages of primary and secondary BAs in overnight-fasted Bcl6 fl/fl and Bcl6 LKO males. N = 8–9/group. ( G ) Serum ALT and bilirubin levels in Bcl6 fl/fl and Bcl6 LKO mice. N = 4/group. ( H ) Representative Picrosirius Red and H&E staining in liver from Bcl6 fl/fl and Bcl6 LKO males. In ( A–E and G ), Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Techniques Used: Staining

    Hepatic Bcl6 deletion increases BA synthesis and serum levels in females. ( A ) Serum BA levels in Bcl6 fl/fl and Bcl6 LKO females. N = 7–9/group. ( B ) Total BA pool quantification (including liver, gallbladder, and small intestines) in Bcl6 fl/fl and Bcl6 LKO females, expressed as umol per 100 grams of body weight. N = 7–11/group. ( C ) Total fecal BA levels in Bcl6 fl/fl and Bcl6 LKO females. N = 5/group. ( D ) Serum 7a-C4 quantification in Bcl6 fl/fl and Bcl6 LKO females. N = 5–6/group. ( E ) Total ( left ) and individual BA species in serum as proportions of total ( right ), and ( F ) percentages of primary and secondary BAs in overnight-fasted Bcl6 fl/fl and Bcl6 LKO females. N = 8/group. In ( A–E ), Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.
    Figure Legend Snippet: Hepatic Bcl6 deletion increases BA synthesis and serum levels in females. ( A ) Serum BA levels in Bcl6 fl/fl and Bcl6 LKO females. N = 7–9/group. ( B ) Total BA pool quantification (including liver, gallbladder, and small intestines) in Bcl6 fl/fl and Bcl6 LKO females, expressed as umol per 100 grams of body weight. N = 7–11/group. ( C ) Total fecal BA levels in Bcl6 fl/fl and Bcl6 LKO females. N = 5/group. ( D ) Serum 7a-C4 quantification in Bcl6 fl/fl and Bcl6 LKO females. N = 5–6/group. ( E ) Total ( left ) and individual BA species in serum as proportions of total ( right ), and ( F ) percentages of primary and secondary BAs in overnight-fasted Bcl6 fl/fl and Bcl6 LKO females. N = 8/group. In ( A–E ), Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Techniques Used:

    Hepatic Bcl6 deletion activates ileal BA signaling while reducing liver sensitivity to FGF15/19 in males. ( A ) KEGG pathway analysis of ileal Bcl6 LKO upregulated genes (log 2 FC > 0, P adj < .05) from RNA-seq performed in Bcl6 fl/fl and Bcl6 LKO male ileum. N = 4/group. ( B ) qPCR of FXR target genes in ileum and ( C ) liver from Bcl6 fl/fl and Bcl6 LKO males. N = 8–9/group. ( D ) Western blot of BA feedback signaling markers from Bcl6 fl/fl and Bcl6 LKO male liver. N = 7/group. ( E ) qPCR of hepatic Cyp7a1 after treatment with FGF19, expressed as % reduction from respective Bcl6 fl/fl or Bcl6 LKO vehicle-treated expression. N = 6/group. In ( B–D ), multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.
    Figure Legend Snippet: Hepatic Bcl6 deletion activates ileal BA signaling while reducing liver sensitivity to FGF15/19 in males. ( A ) KEGG pathway analysis of ileal Bcl6 LKO upregulated genes (log 2 FC > 0, P adj < .05) from RNA-seq performed in Bcl6 fl/fl and Bcl6 LKO male ileum. N = 4/group. ( B ) qPCR of FXR target genes in ileum and ( C ) liver from Bcl6 fl/fl and Bcl6 LKO males. N = 8–9/group. ( D ) Western blot of BA feedback signaling markers from Bcl6 fl/fl and Bcl6 LKO male liver. N = 7/group. ( E ) qPCR of hepatic Cyp7a1 after treatment with FGF19, expressed as % reduction from respective Bcl6 fl/fl or Bcl6 LKO vehicle-treated expression. N = 6/group. In ( B–D ), multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Techniques Used: RNA Sequencing, Western Blot, Expressing

    Hepatic Bcl6 deletion activates hepatic Cyp7a1 in females. ( A ) KEGG pathway analysis of ileal Bcl6 LKO upregulated genes (log 2 FC > 0, P adj < .05) from RNA-seq performed in Bcl6 fl/fl and Bcl6 LKO female ileum. N = 4/group. ( B ) qPCR of FXR target genes in ileum and ( C ) liver from Bcl6 fl/fl and Bcl6 LKO females. N = 7–9/group. ( D ) Western blot of BA feedback signaling markers from Bcl6 fl/fl and Bcl6 LKO female liver. N = 7/group. In ( B–D ), multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.
    Figure Legend Snippet: Hepatic Bcl6 deletion activates hepatic Cyp7a1 in females. ( A ) KEGG pathway analysis of ileal Bcl6 LKO upregulated genes (log 2 FC > 0, P adj < .05) from RNA-seq performed in Bcl6 fl/fl and Bcl6 LKO female ileum. N = 4/group. ( B ) qPCR of FXR target genes in ileum and ( C ) liver from Bcl6 fl/fl and Bcl6 LKO females. N = 7–9/group. ( D ) Western blot of BA feedback signaling markers from Bcl6 fl/fl and Bcl6 LKO female liver. N = 7/group. In ( B–D ), multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Techniques Used: RNA Sequencing, Western Blot

    Dual deletion of Fxr and hepatic Bcl6 causes BA overload and liver damage in males. ( A ) Serum BAs, ( B ) liver BAs, ( C ) serum 7a-C4, ( D ) serum cholesterol, ( E ) serum triglycerides, and ( F ) serum ALT and bilirubin in Fxr KO and Bcl6 LKO Fxr KO males. N = 5–7/group. ( G ) Representative image of serum from Fxr KO and Bcl6 LKO Fxr KO males. ( H ) Liver qPCR of Col1a1 and immune markers in Fxr KO and Bcl6 LKO Fxr KO males. N = 6/group. ( I ) Representative H&E stained (40×) and ( J ) Picrosirius Red stained (40×) images from Fxr KO and Bcl6 LKO Fxr KO male livers. ( K ) Picrosirius Red quantification expressed as % total area in Fxr KO and Bcl6 LKO Fxr KO male livers. Each data point is the average of 3 images/liver. N = 4/group. ( L ) Representative (20×) images of aSMA ( green ) and F4/80 ( red ) immunofluorescence in Fxr KO and Bcl6 LKO Fxr KO male livers. ( M ) aSMA and F4/80 image quantification expressed as % total area in Fxr KO and Bcl6 LKO Fxr KO male liver. Each data point is the average of 4 images/liver. N = 5/group. In ( A–F, H, K and M ) Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.
    Figure Legend Snippet: Dual deletion of Fxr and hepatic Bcl6 causes BA overload and liver damage in males. ( A ) Serum BAs, ( B ) liver BAs, ( C ) serum 7a-C4, ( D ) serum cholesterol, ( E ) serum triglycerides, and ( F ) serum ALT and bilirubin in Fxr KO and Bcl6 LKO Fxr KO males. N = 5–7/group. ( G ) Representative image of serum from Fxr KO and Bcl6 LKO Fxr KO males. ( H ) Liver qPCR of Col1a1 and immune markers in Fxr KO and Bcl6 LKO Fxr KO males. N = 6/group. ( I ) Representative H&E stained (40×) and ( J ) Picrosirius Red stained (40×) images from Fxr KO and Bcl6 LKO Fxr KO male livers. ( K ) Picrosirius Red quantification expressed as % total area in Fxr KO and Bcl6 LKO Fxr KO male livers. Each data point is the average of 3 images/liver. N = 4/group. ( L ) Representative (20×) images of aSMA ( green ) and F4/80 ( red ) immunofluorescence in Fxr KO and Bcl6 LKO Fxr KO male livers. ( M ) aSMA and F4/80 image quantification expressed as % total area in Fxr KO and Bcl6 LKO Fxr KO male liver. Each data point is the average of 4 images/liver. N = 5/group. In ( A–F, H, K and M ) Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Techniques Used: Staining, Immunofluorescence

    Combined loss of Fxr and hepatic Bcl6 upregulates pro-fibrotic genes. ( A ) Venn diagram showing common and unique upregulated genes ( P adj < .05; log 2 FC >0.5) in male Fxr KO , Bcl6 LKO , or Bcl6 LKO Fxr KO livers compared with Bcl6 fl/fl livers. ( B ) Top GO pathways of genes uniquely upregulated in Bcl6 LKO Fxr KO vs Bcl6 fl/fl livers. ( C ) Venn diagram of common and unique downregulated genes ( P adj < .05; log 2 FC <0.5) in male Fxr KO , Bcl6 LKO , or Bcl6 LKO Fxr KO livers compared with Bcl6 fl/fl livers. ( D ) Top GO pathways of genes uniquely downregulated in male Bcl6 LKO Fxr KO vs Bcl6 fl/fl livers. N = 4/group.
    Figure Legend Snippet: Combined loss of Fxr and hepatic Bcl6 upregulates pro-fibrotic genes. ( A ) Venn diagram showing common and unique upregulated genes ( P adj < .05; log 2 FC >0.5) in male Fxr KO , Bcl6 LKO , or Bcl6 LKO Fxr KO livers compared with Bcl6 fl/fl livers. ( B ) Top GO pathways of genes uniquely upregulated in Bcl6 LKO Fxr KO vs Bcl6 fl/fl livers. ( C ) Venn diagram of common and unique downregulated genes ( P adj < .05; log 2 FC <0.5) in male Fxr KO , Bcl6 LKO , or Bcl6 LKO Fxr KO livers compared with Bcl6 fl/fl livers. ( D ) Top GO pathways of genes uniquely downregulated in male Bcl6 LKO Fxr KO vs Bcl6 fl/fl livers. N = 4/group.

    Techniques Used:

    Dual deletion of Fxr and hepatic Bcl6 causes BA overload and liver damage in females. ( A ) Serum BAs, ( B ) liver BAs, ( C ) serum cholesterol, and ( D ) serum triglycerides in Fxr KO and Bcl6 LKO Fxr KO females. N = 6–9/group. ( E ) Representative image of serum from Fxr KO and Bcl6 LKO Fxr KO females. ( F ) Liver qPCR of Col1a1 and immune markers in Fxr KO and Bcl6 LKO Fxr KO females. N = 5–9/group. ( G ) Representative H&E stained (40×) and ( H ) Picrosirius Red stained (40×) images from Fxr KO and Bcl6 LKO Fxr KO female livers. ( I ) Picrosirius Red quantification expressed as % total area in Fxr KO and Bcl6 LKO Fxr KO female liver. Each data point is the average of 3 images/liver. N = 5/group. In ( A–D, F, and I ), Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.
    Figure Legend Snippet: Dual deletion of Fxr and hepatic Bcl6 causes BA overload and liver damage in females. ( A ) Serum BAs, ( B ) liver BAs, ( C ) serum cholesterol, and ( D ) serum triglycerides in Fxr KO and Bcl6 LKO Fxr KO females. N = 6–9/group. ( E ) Representative image of serum from Fxr KO and Bcl6 LKO Fxr KO females. ( F ) Liver qPCR of Col1a1 and immune markers in Fxr KO and Bcl6 LKO Fxr KO females. N = 5–9/group. ( G ) Representative H&E stained (40×) and ( H ) Picrosirius Red stained (40×) images from Fxr KO and Bcl6 LKO Fxr KO female livers. ( I ) Picrosirius Red quantification expressed as % total area in Fxr KO and Bcl6 LKO Fxr KO female liver. Each data point is the average of 3 images/liver. N = 5/group. In ( A–D, F, and I ), Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Techniques Used: Staining

    Dual deletion of Fxr and hepatic Bcl6 in males results in loss of SHP. ( A ) qPCR and ( B ) Western blots of BA regulatory targets in Fxr KO and Bcl6 LKO Fxr KO male livers. N = 4–6/group. ( C ) ( Left ) UCSC browser tracks at the Shp (Nr0b2) locus, showing FXR ( top ) and BCL6 ( bottom ) binding sites in control male livers. Arrows annotate the Shp promoter ( Shp-Pro ) and Shp downstream enhancer ( Shp-DS ) regions. ( Righ t) H3K27ac ChIP qPCR at the Shp-Pro and Shp-DS regions in Fxr KO and Bcl6 LKO Fxr KO male livers, expressed as percent of input chromatin. N = 3/group. Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.
    Figure Legend Snippet: Dual deletion of Fxr and hepatic Bcl6 in males results in loss of SHP. ( A ) qPCR and ( B ) Western blots of BA regulatory targets in Fxr KO and Bcl6 LKO Fxr KO male livers. N = 4–6/group. ( C ) ( Left ) UCSC browser tracks at the Shp (Nr0b2) locus, showing FXR ( top ) and BCL6 ( bottom ) binding sites in control male livers. Arrows annotate the Shp promoter ( Shp-Pro ) and Shp downstream enhancer ( Shp-DS ) regions. ( Righ t) H3K27ac ChIP qPCR at the Shp-Pro and Shp-DS regions in Fxr KO and Bcl6 LKO Fxr KO male livers, expressed as percent of input chromatin. N = 3/group. Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Techniques Used: Western Blot, Binding Assay, Control, ChIP-qPCR

    Dual deletion of Fxr and hepatic Bcl6 in females results in loss of SHP. ( A ) qPCR of BA regulatory targets in Fxr KO and Bcl6 LKO Fxr KO female livers. N = 5–9/group. Multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.
    Figure Legend Snippet: Dual deletion of Fxr and hepatic Bcl6 in females results in loss of SHP. ( A ) qPCR of BA regulatory targets in Fxr KO and Bcl6 LKO Fxr KO female livers. N = 5–9/group. Multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Techniques Used:

    SHP is required for BCL6-FXR co-suppression of CYP7A1 and BAs in males. ( A ) Serum, ( B ) liver total BAs, ( C ) liver western blot of GFP, SHP, CYP7A1, and COL1A1, and ( D ) liver qPCR of Bcl6, Shp, Gfp , Cyp7a1, and immune marker genes in Fxr KO and Bcl6 LKO Fxr KO males treated with AAV-TBG-GFP or AAV-TBG-SHP for 4 weeks. N = 3–6/group. Two-way ANOVA with Holm-Sidak’s post-hoc testing was performed to compare effects of AAV-treatment, genotype, and their interaction on means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.
    Figure Legend Snippet: SHP is required for BCL6-FXR co-suppression of CYP7A1 and BAs in males. ( A ) Serum, ( B ) liver total BAs, ( C ) liver western blot of GFP, SHP, CYP7A1, and COL1A1, and ( D ) liver qPCR of Bcl6, Shp, Gfp , Cyp7a1, and immune marker genes in Fxr KO and Bcl6 LKO Fxr KO males treated with AAV-TBG-GFP or AAV-TBG-SHP for 4 weeks. N = 3–6/group. Two-way ANOVA with Holm-Sidak’s post-hoc testing was performed to compare effects of AAV-treatment, genotype, and their interaction on means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Techniques Used: Western Blot, Marker

    Hepatic Fxr is not required for FXR-BCL6 co-regulation of BAs. ( A ) Serum total BAs, ( B ) liver total BAs, ( C ) liver qPCR of Bcl6, Fxr, Shp, and Cyp7a1 , and ( D ) ileal qPCR of Fxr, Shp, and Fgf15 in Bcl6 fl/fl Fxr fl/fl , Fxr KO , Bcl6 LKO Fxr KO , and Bcl6 LKO Fxr LKO males. N = 4–8/group. One-way ANOVA with Holm-Sidak’s post-hoc testing was performed to compare means. Data are represented as mean ±SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.
    Figure Legend Snippet: Hepatic Fxr is not required for FXR-BCL6 co-regulation of BAs. ( A ) Serum total BAs, ( B ) liver total BAs, ( C ) liver qPCR of Bcl6, Fxr, Shp, and Cyp7a1 , and ( D ) ileal qPCR of Fxr, Shp, and Fgf15 in Bcl6 fl/fl Fxr fl/fl , Fxr KO , Bcl6 LKO Fxr KO , and Bcl6 LKO Fxr LKO males. N = 4–8/group. One-way ANOVA with Holm-Sidak’s post-hoc testing was performed to compare means. Data are represented as mean ±SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Techniques Used:

    Model for BCL6 and FXR co-regulation of BAs. ( Top ) In control ( Bcl6 fl/fl ) mice, BCL6 restrains hepatic and circulating cholesterol while enhancing NTCP and FGFR4 expression. In tandem, FXR activates SHP via enterohepatic and direct liver signaling to suppress CYP7A1 and BA production. ( Bottom left ) Loss of hepatic Bcl6 reduces the BA transporter NTCP and FGFR4 while it increases cholesterol and CYP7A1-directed BA synthesis and circulating levels. ( Bottom right ) Combined loss of hepatic Bcl6 and whole body Fxr unmasks co-dependent regulation of Shp by BCL6 and FXR. Shp levels are strongly reduced, whereas CYP7A1 is reciprocally increased. BA synthesis and levels become severely elevated, leading to cholestasis.
    Figure Legend Snippet: Model for BCL6 and FXR co-regulation of BAs. ( Top ) In control ( Bcl6 fl/fl ) mice, BCL6 restrains hepatic and circulating cholesterol while enhancing NTCP and FGFR4 expression. In tandem, FXR activates SHP via enterohepatic and direct liver signaling to suppress CYP7A1 and BA production. ( Bottom left ) Loss of hepatic Bcl6 reduces the BA transporter NTCP and FGFR4 while it increases cholesterol and CYP7A1-directed BA synthesis and circulating levels. ( Bottom right ) Combined loss of hepatic Bcl6 and whole body Fxr unmasks co-dependent regulation of Shp by BCL6 and FXR. Shp levels are strongly reduced, whereas CYP7A1 is reciprocally increased. BA synthesis and levels become severely elevated, leading to cholestasis.

    Techniques Used: Control, Expressing

    Related Articles

    Incubation:

    Article Title: Prevention of cholestatic liver disease through BCL6-FXR enterohepatic crosstalk.
    Article Snippet: .. Primary antibodies for BCL6 (sc-7388, Santa Cruz) at 1:200, FXR (E4B8P, Cell Signaling) at 1:1000, FGFR4 (D3B12, Cell Signaling) at 1:1000, NTCP (ab131084, Abcam) at 1:1000, pERK1/2 (#9101, Cell Signaling) at 1:1000, ERK1/2 (#137F5, Cell Signaling) at 1:1000, CYP7A1 (18054-1-AP, ProteinTech) at 1:1000, GFP (#G10362, Invitrogen) at 1:1000, SHP (PA5-102494, Thermo Fisher) at 1:1000, CYP8B1 (Abcam, ab191910), or COL1A1 (Cell Signaling, #E8I9Z) were added and incubated overnight at 4 degrees. .. Secondary antibodies (Jackson ImmunoResearch) were added for 1.5 hours.

    Article Title: Prevention of Cholestatic Liver Disease Through BCL6-FXR Enterohepatic Crosstalk
    Article Snippet: .. Primary antibodies for BCL6 (sc-7388, Santa Cruz) at 1:200, FXR (E4B8P, Cell Signaling) at 1:1000, FGFR4 (D3B12, Cell Signaling) at 1:1000, NTCP (ab131084, Abcam) at 1:1000, pERK1/2 (#9101, Cell Signaling) at 1:1000, ERK1/2 (#137F5, Cell Signaling) at 1:1000, CYP7A1 (18054-1-AP, ProteinTech) at 1:1000, GFP (# G10362 , Invitrogen) at 1:1000, SHP (PA5-102494, Thermo Fisher) at 1:1000, CYP8B1 (Abcam, ab191910), or COL1A1 (Cell Signaling, #E8I9Z) were added and incubated overnight at 4 degrees. .. Secondary antibodies (Jackson ImmunoResearch) were added for 1.5 hours.



    Similar Products

    primary antibodies for bcl6  (Santa Cruz Biotechnology)
    94
    Santa Cruz Biotechnology primary antibodies for bcl6
    Hepatic <t>BCL6</t> is predicted to co-regulate transcription with FXR. ( A ) Top 20 high-confidence causal transcription factors predicted by IMAGE analysis of RNA-seq and H3K27ac datasets from Bcl6 fl/fl and Bcl6 LKO livers. N = 3/group. ( B ) Representative UCSC browser tracks showing hepatic BCL6 and FXR binding at key BA regulatory genes in Bcl6 fl/fl liver.
    Primary Antibodies For Bcl6, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+antibodies+for+bcl6/Bcl-6+Antibody/pmc12865649-346-0-5
    Average 94 stars, based on 1 article reviews
    primary antibodies for bcl6 - by Bioz Stars, 2026-10
    94/100 stars
    		  Buy from Supplier
    primary anti human antibodies  (Cell Signaling Technology Inc)
    95
    Cell Signaling Technology Inc primary anti human antibodies
    Hepatic <t>BCL6</t> is predicted to co-regulate transcription with FXR. ( A ) Top 20 high-confidence causal transcription factors predicted by IMAGE analysis of RNA-seq and H3K27ac datasets from Bcl6 fl/fl and Bcl6 LKO livers. N = 3/group. ( B ) Representative UCSC browser tracks showing hepatic BCL6 and FXR binding at key BA regulatory genes in Bcl6 fl/fl liver.
    Primary Anti Human Antibodies, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+antibodies+for+bcl6/BCL6+Antibody/pm41381571-297-0-24
    Average 95 stars, based on 1 article reviews
    primary anti human antibodies - by Bioz Stars, 2026-10
    95/100 stars
    		  Buy from Supplier
    primary anti human antibodies  (Proteintech)
    93
    Proteintech primary anti human antibodies
    Hepatic <t>BCL6</t> is predicted to co-regulate transcription with FXR. ( A ) Top 20 high-confidence causal transcription factors predicted by IMAGE analysis of RNA-seq and H3K27ac datasets from Bcl6 fl/fl and Bcl6 LKO livers. N = 3/group. ( B ) Representative UCSC browser tracks showing hepatic BCL6 and FXR binding at key BA regulatory genes in Bcl6 fl/fl liver.
    Primary Anti Human Antibodies, supplied by Proteintech, 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/product/primary+antibodies+for+bcl6/BCL6+Antibody/pm41381571-297-0-11
    Average 93 stars, based on 1 article reviews
    primary anti human antibodies - by Bioz Stars, 2026-10
    93/100 stars
    		  Buy from Supplier
    primary antibody  (Cell Signaling Technology Inc)
    93
    Cell Signaling Technology Inc primary antibody
    Hepatic <t>BCL6</t> is predicted to co-regulate transcription with FXR. ( A ) Top 20 high-confidence causal transcription factors predicted by IMAGE analysis of RNA-seq and H3K27ac datasets from Bcl6 fl/fl and Bcl6 LKO livers. N = 3/group. ( B ) Representative UCSC browser tracks showing hepatic BCL6 and FXR binding at key BA regulatory genes in Bcl6 fl/fl liver.
    Primary Antibody, supplied by Cell Signaling Technology Inc, 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/product/primary+antibodies+for+bcl6/BCL6+XP+Rabbit+mAb/us12310975-2419-0-5
    Average 93 stars, based on 1 article reviews
    primary antibody - by Bioz Stars, 2026-10
    93/100 stars
    		  Buy from Supplier
    primary antibody against bcl6  (Cell Marque)
    90
    Cell Marque primary antibody against bcl6
    Hepatic <t>BCL6</t> is predicted to co-regulate transcription with FXR. ( A ) Top 20 high-confidence causal transcription factors predicted by IMAGE analysis of RNA-seq and H3K27ac datasets from Bcl6 fl/fl and Bcl6 LKO livers. N = 3/group. ( B ) Representative UCSC browser tracks showing hepatic BCL6 and FXR binding at key BA regulatory genes in Bcl6 fl/fl liver.
    Primary Antibody Against Bcl6, supplied by Cell Marque, 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/product/primary+antibodies+for+bcl6/bcl6+antibody/pmc11793761-56-0-6
    Average 90 stars, based on 1 article reviews
    primary antibody against bcl6 - by Bioz Stars, 2026-10
    90/100 stars
    		  Buy from Supplier
    primary antibody bcl6 rb ab cst-14895  (Cell Signaling Technology Inc)
    90
    Cell Signaling Technology Inc primary antibody bcl6 rb ab cst-14895
    Hepatic <t>BCL6</t> is predicted to co-regulate transcription with FXR. ( A ) Top 20 high-confidence causal transcription factors predicted by IMAGE analysis of RNA-seq and H3K27ac datasets from Bcl6 fl/fl and Bcl6 LKO livers. N = 3/group. ( B ) Representative UCSC browser tracks showing hepatic BCL6 and FXR binding at key BA regulatory genes in Bcl6 fl/fl liver.
    Primary Antibody Bcl6 Rb Ab Cst 14895, supplied by Cell Signaling Technology Inc, 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/product/primary+antibodies+for+bcl6/anti+bcl6/us11986532-2169-0-5
    Average 90 stars, based on 1 article reviews
    primary antibody bcl6 rb ab cst-14895 - by Bioz Stars, 2026-10
    90/100 stars
    		  Buy from Supplier
    bcl6 primary antibody  (Santa Cruz Biotechnology)
    94
    Santa Cruz Biotechnology bcl6 primary antibody
    Hepatic <t>BCL6</t> is predicted to co-regulate transcription with FXR. ( A ) Top 20 high-confidence causal transcription factors predicted by IMAGE analysis of RNA-seq and H3K27ac datasets from Bcl6 fl/fl and Bcl6 LKO livers. N = 3/group. ( B ) Representative UCSC browser tracks showing hepatic BCL6 and FXR binding at key BA regulatory genes in Bcl6 fl/fl liver.
    Bcl6 Primary Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/primary+antibodies+for+bcl6/Bcl-6/us10234465-428-22-25
    Average 94 stars, based on 1 article reviews
    bcl6 primary antibody - by Bioz Stars, 2026-10
    94/100 stars
    		  Buy from Supplier
    primary antibodies rabbit anti bcl6  (Cell Signaling Technology Inc)
    93
    Cell Signaling Technology Inc primary antibodies rabbit anti bcl6
    Figure 1: Co-culture with BMSC or HOB reduces <t>BCL6</t> in ALL cells. A. BCL6 protein in REH and Nalm-27 ALL cells when co-cultured with BMSC or HOB cells relative to media (M) controls as shown by western blot analysis. B. Flow cytometry analysis of REH and Nalm-27 ALL cell BCL6 protein levels when removed from the PD population compared to cells in media alone as shown by median florescence intensity (MFI). C. MFI of Patient 1 (P1) and Patient 2 (P2) when in physical contact with BMSC or HOB compared to those in media alone (ND = not detected). D. Confocal microscopy images of REH and Nalm-27 for BCL6 (yellow) and DAPI (Blue) in cells cultured in media alone compare to those recovered from the PD population of BMSC or HOB co-culture. E. P1 and P2 BCL6 confocal staining of media alone cells relative to those in contact with BMSC or HOB. Scale bar = 10µm.
    Primary Antibodies Rabbit Anti Bcl6, supplied by Cell Signaling Technology Inc, 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/product/primary+antibodies+for+bcl6/BCL6+XP+Rabbit+mAb/pm27015556-136-15-5
    Average 93 stars, based on 1 article reviews
    primary antibodies rabbit anti bcl6 - by Bioz Stars, 2026-10
    93/100 stars
    		  Buy from Supplier

    Image Search Results


    Hepatic BCL6 is predicted to co-regulate transcription with FXR. ( A ) Top 20 high-confidence causal transcription factors predicted by IMAGE analysis of RNA-seq and H3K27ac datasets from Bcl6 fl/fl and Bcl6 LKO livers. N = 3/group. ( B ) Representative UCSC browser tracks showing hepatic BCL6 and FXR binding at key BA regulatory genes in Bcl6 fl/fl liver.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Prevention of Cholestatic Liver Disease Through BCL6-FXR Enterohepatic Crosstalk

    doi: 10.1016/j.jcmgh.2025.101706

    Figure Lengend Snippet: Hepatic BCL6 is predicted to co-regulate transcription with FXR. ( A ) Top 20 high-confidence causal transcription factors predicted by IMAGE analysis of RNA-seq and H3K27ac datasets from Bcl6 fl/fl and Bcl6 LKO livers. N = 3/group. ( B ) Representative UCSC browser tracks showing hepatic BCL6 and FXR binding at key BA regulatory genes in Bcl6 fl/fl liver.

    Article Snippet: Primary antibodies for BCL6 (sc-7388, Santa Cruz) at 1:200, FXR (E4B8P, Cell Signaling) at 1:1000, FGFR4 (D3B12, Cell Signaling) at 1:1000, NTCP (ab131084, Abcam) at 1:1000, pERK1/2 (#9101, Cell Signaling) at 1:1000, ERK1/2 (#137F5, Cell Signaling) at 1:1000, CYP7A1 (18054-1-AP, ProteinTech) at 1:1000, GFP (# G10362 , Invitrogen) at 1:1000, SHP (PA5-102494, Thermo Fisher) at 1:1000, CYP8B1 (Abcam, ab191910), or COL1A1 (Cell Signaling, #E8I9Z) were added and incubated overnight at 4 degrees.

    Techniques: RNA Sequencing, Binding Assay

    Hepatic Bcl6 deletion increases serum cholesterol in males. ( A ) Serum cholesterol and triglycerides from Bcl6 fl/fl and Bcl6 LKO males. N = 8–9/group. ( B ) FPLC quantification of cholesterol and triglycerides from Bcl6 fl/fl and Bcl6 LKO pooled male serum. N = 3–4 animals/pool. ( C ) Liver cholesterol in Bcl6 fl/fl and Bcl6 LKO males. N = 8–9/group. Student’s t -tests were performed in ( A and C ) to compare means. ( D ) Heatmap of Bcl6 fl/fl vs Bcl6 LKO differentially expressed ( P adj < .05, |log 2 FC |> 0) cholesterol synthesis, transport, and sterol-related CYP genes expressed as relative RPKM from RNA-seq performed in Bcl6 fl/fl and Bcl6 LKO male livers. N = 4/group. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Prevention of Cholestatic Liver Disease Through BCL6-FXR Enterohepatic Crosstalk

    doi: 10.1016/j.jcmgh.2025.101706

    Figure Lengend Snippet: Hepatic Bcl6 deletion increases serum cholesterol in males. ( A ) Serum cholesterol and triglycerides from Bcl6 fl/fl and Bcl6 LKO males. N = 8–9/group. ( B ) FPLC quantification of cholesterol and triglycerides from Bcl6 fl/fl and Bcl6 LKO pooled male serum. N = 3–4 animals/pool. ( C ) Liver cholesterol in Bcl6 fl/fl and Bcl6 LKO males. N = 8–9/group. Student’s t -tests were performed in ( A and C ) to compare means. ( D ) Heatmap of Bcl6 fl/fl vs Bcl6 LKO differentially expressed ( P adj < .05, |log 2 FC |> 0) cholesterol synthesis, transport, and sterol-related CYP genes expressed as relative RPKM from RNA-seq performed in Bcl6 fl/fl and Bcl6 LKO male livers. N = 4/group. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Article Snippet: Primary antibodies for BCL6 (sc-7388, Santa Cruz) at 1:200, FXR (E4B8P, Cell Signaling) at 1:1000, FGFR4 (D3B12, Cell Signaling) at 1:1000, NTCP (ab131084, Abcam) at 1:1000, pERK1/2 (#9101, Cell Signaling) at 1:1000, ERK1/2 (#137F5, Cell Signaling) at 1:1000, CYP7A1 (18054-1-AP, ProteinTech) at 1:1000, GFP (# G10362 , Invitrogen) at 1:1000, SHP (PA5-102494, Thermo Fisher) at 1:1000, CYP8B1 (Abcam, ab191910), or COL1A1 (Cell Signaling, #E8I9Z) were added and incubated overnight at 4 degrees.

    Techniques: RNA Sequencing

    Hepatic Bcl6 deletion increases serum cholesterol in females. ( A ) Serum cholesterol and triglycerides and ( B ) liver cholesterol levels in Bcl6 fl/fl and Bcl6 LKO females. N = 7–9/group. ( C ) Liver qPCR quantifying cholesterol synthesis, transport, and sterol-related CYP genes in Bcl6 fl/fl and Bcl6 LKO females. N = 7–9/group. Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Prevention of Cholestatic Liver Disease Through BCL6-FXR Enterohepatic Crosstalk

    doi: 10.1016/j.jcmgh.2025.101706

    Figure Lengend Snippet: Hepatic Bcl6 deletion increases serum cholesterol in females. ( A ) Serum cholesterol and triglycerides and ( B ) liver cholesterol levels in Bcl6 fl/fl and Bcl6 LKO females. N = 7–9/group. ( C ) Liver qPCR quantifying cholesterol synthesis, transport, and sterol-related CYP genes in Bcl6 fl/fl and Bcl6 LKO females. N = 7–9/group. Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Article Snippet: Primary antibodies for BCL6 (sc-7388, Santa Cruz) at 1:200, FXR (E4B8P, Cell Signaling) at 1:1000, FGFR4 (D3B12, Cell Signaling) at 1:1000, NTCP (ab131084, Abcam) at 1:1000, pERK1/2 (#9101, Cell Signaling) at 1:1000, ERK1/2 (#137F5, Cell Signaling) at 1:1000, CYP7A1 (18054-1-AP, ProteinTech) at 1:1000, GFP (# G10362 , Invitrogen) at 1:1000, SHP (PA5-102494, Thermo Fisher) at 1:1000, CYP8B1 (Abcam, ab191910), or COL1A1 (Cell Signaling, #E8I9Z) were added and incubated overnight at 4 degrees.

    Techniques:

    Hepatic Bcl6 deletion increases BA synthesis and serum/total levels in males. ( A ) Serum BA levels in Bcl6 fl/fl and Bcl6 LKO males. N = 7–9/group. ( B ) Total BA pool quantification (including liver, gallbladder, and small intestines) in Bcl6 fl/fl and Bcl6 LKO males, expressed as umol per 100 grams of body weight. N = 7–8/group. ( C ) Total fecal BA levels in Bcl6 fl/fl and Bcl6 LKO males. N = 5/group. ( D ) Serum 7a-C4 quantification in Bcl6 fl/fl and Bcl6 LKO males. N = 4–6/group. ( E ) Total ( left ) and individual BA species in serum as proportions of total ( right ), and ( F ) percentages of primary and secondary BAs in overnight-fasted Bcl6 fl/fl and Bcl6 LKO males. N = 8–9/group. ( G ) Serum ALT and bilirubin levels in Bcl6 fl/fl and Bcl6 LKO mice. N = 4/group. ( H ) Representative Picrosirius Red and H&E staining in liver from Bcl6 fl/fl and Bcl6 LKO males. In ( A–E and G ), Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Prevention of Cholestatic Liver Disease Through BCL6-FXR Enterohepatic Crosstalk

    doi: 10.1016/j.jcmgh.2025.101706

    Figure Lengend Snippet: Hepatic Bcl6 deletion increases BA synthesis and serum/total levels in males. ( A ) Serum BA levels in Bcl6 fl/fl and Bcl6 LKO males. N = 7–9/group. ( B ) Total BA pool quantification (including liver, gallbladder, and small intestines) in Bcl6 fl/fl and Bcl6 LKO males, expressed as umol per 100 grams of body weight. N = 7–8/group. ( C ) Total fecal BA levels in Bcl6 fl/fl and Bcl6 LKO males. N = 5/group. ( D ) Serum 7a-C4 quantification in Bcl6 fl/fl and Bcl6 LKO males. N = 4–6/group. ( E ) Total ( left ) and individual BA species in serum as proportions of total ( right ), and ( F ) percentages of primary and secondary BAs in overnight-fasted Bcl6 fl/fl and Bcl6 LKO males. N = 8–9/group. ( G ) Serum ALT and bilirubin levels in Bcl6 fl/fl and Bcl6 LKO mice. N = 4/group. ( H ) Representative Picrosirius Red and H&E staining in liver from Bcl6 fl/fl and Bcl6 LKO males. In ( A–E and G ), Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Article Snippet: Primary antibodies for BCL6 (sc-7388, Santa Cruz) at 1:200, FXR (E4B8P, Cell Signaling) at 1:1000, FGFR4 (D3B12, Cell Signaling) at 1:1000, NTCP (ab131084, Abcam) at 1:1000, pERK1/2 (#9101, Cell Signaling) at 1:1000, ERK1/2 (#137F5, Cell Signaling) at 1:1000, CYP7A1 (18054-1-AP, ProteinTech) at 1:1000, GFP (# G10362 , Invitrogen) at 1:1000, SHP (PA5-102494, Thermo Fisher) at 1:1000, CYP8B1 (Abcam, ab191910), or COL1A1 (Cell Signaling, #E8I9Z) were added and incubated overnight at 4 degrees.

    Techniques: Staining

    Hepatic Bcl6 deletion increases BA synthesis and serum levels in females. ( A ) Serum BA levels in Bcl6 fl/fl and Bcl6 LKO females. N = 7–9/group. ( B ) Total BA pool quantification (including liver, gallbladder, and small intestines) in Bcl6 fl/fl and Bcl6 LKO females, expressed as umol per 100 grams of body weight. N = 7–11/group. ( C ) Total fecal BA levels in Bcl6 fl/fl and Bcl6 LKO females. N = 5/group. ( D ) Serum 7a-C4 quantification in Bcl6 fl/fl and Bcl6 LKO females. N = 5–6/group. ( E ) Total ( left ) and individual BA species in serum as proportions of total ( right ), and ( F ) percentages of primary and secondary BAs in overnight-fasted Bcl6 fl/fl and Bcl6 LKO females. N = 8/group. In ( A–E ), Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Prevention of Cholestatic Liver Disease Through BCL6-FXR Enterohepatic Crosstalk

    doi: 10.1016/j.jcmgh.2025.101706

    Figure Lengend Snippet: Hepatic Bcl6 deletion increases BA synthesis and serum levels in females. ( A ) Serum BA levels in Bcl6 fl/fl and Bcl6 LKO females. N = 7–9/group. ( B ) Total BA pool quantification (including liver, gallbladder, and small intestines) in Bcl6 fl/fl and Bcl6 LKO females, expressed as umol per 100 grams of body weight. N = 7–11/group. ( C ) Total fecal BA levels in Bcl6 fl/fl and Bcl6 LKO females. N = 5/group. ( D ) Serum 7a-C4 quantification in Bcl6 fl/fl and Bcl6 LKO females. N = 5–6/group. ( E ) Total ( left ) and individual BA species in serum as proportions of total ( right ), and ( F ) percentages of primary and secondary BAs in overnight-fasted Bcl6 fl/fl and Bcl6 LKO females. N = 8/group. In ( A–E ), Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Article Snippet: Primary antibodies for BCL6 (sc-7388, Santa Cruz) at 1:200, FXR (E4B8P, Cell Signaling) at 1:1000, FGFR4 (D3B12, Cell Signaling) at 1:1000, NTCP (ab131084, Abcam) at 1:1000, pERK1/2 (#9101, Cell Signaling) at 1:1000, ERK1/2 (#137F5, Cell Signaling) at 1:1000, CYP7A1 (18054-1-AP, ProteinTech) at 1:1000, GFP (# G10362 , Invitrogen) at 1:1000, SHP (PA5-102494, Thermo Fisher) at 1:1000, CYP8B1 (Abcam, ab191910), or COL1A1 (Cell Signaling, #E8I9Z) were added and incubated overnight at 4 degrees.

    Techniques:

    Hepatic Bcl6 deletion activates ileal BA signaling while reducing liver sensitivity to FGF15/19 in males. ( A ) KEGG pathway analysis of ileal Bcl6 LKO upregulated genes (log 2 FC > 0, P adj < .05) from RNA-seq performed in Bcl6 fl/fl and Bcl6 LKO male ileum. N = 4/group. ( B ) qPCR of FXR target genes in ileum and ( C ) liver from Bcl6 fl/fl and Bcl6 LKO males. N = 8–9/group. ( D ) Western blot of BA feedback signaling markers from Bcl6 fl/fl and Bcl6 LKO male liver. N = 7/group. ( E ) qPCR of hepatic Cyp7a1 after treatment with FGF19, expressed as % reduction from respective Bcl6 fl/fl or Bcl6 LKO vehicle-treated expression. N = 6/group. In ( B–D ), multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Prevention of Cholestatic Liver Disease Through BCL6-FXR Enterohepatic Crosstalk

    doi: 10.1016/j.jcmgh.2025.101706

    Figure Lengend Snippet: Hepatic Bcl6 deletion activates ileal BA signaling while reducing liver sensitivity to FGF15/19 in males. ( A ) KEGG pathway analysis of ileal Bcl6 LKO upregulated genes (log 2 FC > 0, P adj < .05) from RNA-seq performed in Bcl6 fl/fl and Bcl6 LKO male ileum. N = 4/group. ( B ) qPCR of FXR target genes in ileum and ( C ) liver from Bcl6 fl/fl and Bcl6 LKO males. N = 8–9/group. ( D ) Western blot of BA feedback signaling markers from Bcl6 fl/fl and Bcl6 LKO male liver. N = 7/group. ( E ) qPCR of hepatic Cyp7a1 after treatment with FGF19, expressed as % reduction from respective Bcl6 fl/fl or Bcl6 LKO vehicle-treated expression. N = 6/group. In ( B–D ), multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Article Snippet: Primary antibodies for BCL6 (sc-7388, Santa Cruz) at 1:200, FXR (E4B8P, Cell Signaling) at 1:1000, FGFR4 (D3B12, Cell Signaling) at 1:1000, NTCP (ab131084, Abcam) at 1:1000, pERK1/2 (#9101, Cell Signaling) at 1:1000, ERK1/2 (#137F5, Cell Signaling) at 1:1000, CYP7A1 (18054-1-AP, ProteinTech) at 1:1000, GFP (# G10362 , Invitrogen) at 1:1000, SHP (PA5-102494, Thermo Fisher) at 1:1000, CYP8B1 (Abcam, ab191910), or COL1A1 (Cell Signaling, #E8I9Z) were added and incubated overnight at 4 degrees.

    Techniques: RNA Sequencing, Western Blot, Expressing

    Hepatic Bcl6 deletion activates hepatic Cyp7a1 in females. ( A ) KEGG pathway analysis of ileal Bcl6 LKO upregulated genes (log 2 FC > 0, P adj < .05) from RNA-seq performed in Bcl6 fl/fl and Bcl6 LKO female ileum. N = 4/group. ( B ) qPCR of FXR target genes in ileum and ( C ) liver from Bcl6 fl/fl and Bcl6 LKO females. N = 7–9/group. ( D ) Western blot of BA feedback signaling markers from Bcl6 fl/fl and Bcl6 LKO female liver. N = 7/group. In ( B–D ), multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Prevention of Cholestatic Liver Disease Through BCL6-FXR Enterohepatic Crosstalk

    doi: 10.1016/j.jcmgh.2025.101706

    Figure Lengend Snippet: Hepatic Bcl6 deletion activates hepatic Cyp7a1 in females. ( A ) KEGG pathway analysis of ileal Bcl6 LKO upregulated genes (log 2 FC > 0, P adj < .05) from RNA-seq performed in Bcl6 fl/fl and Bcl6 LKO female ileum. N = 4/group. ( B ) qPCR of FXR target genes in ileum and ( C ) liver from Bcl6 fl/fl and Bcl6 LKO females. N = 7–9/group. ( D ) Western blot of BA feedback signaling markers from Bcl6 fl/fl and Bcl6 LKO female liver. N = 7/group. In ( B–D ), multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Article Snippet: Primary antibodies for BCL6 (sc-7388, Santa Cruz) at 1:200, FXR (E4B8P, Cell Signaling) at 1:1000, FGFR4 (D3B12, Cell Signaling) at 1:1000, NTCP (ab131084, Abcam) at 1:1000, pERK1/2 (#9101, Cell Signaling) at 1:1000, ERK1/2 (#137F5, Cell Signaling) at 1:1000, CYP7A1 (18054-1-AP, ProteinTech) at 1:1000, GFP (# G10362 , Invitrogen) at 1:1000, SHP (PA5-102494, Thermo Fisher) at 1:1000, CYP8B1 (Abcam, ab191910), or COL1A1 (Cell Signaling, #E8I9Z) were added and incubated overnight at 4 degrees.

    Techniques: RNA Sequencing, Western Blot

    Dual deletion of Fxr and hepatic Bcl6 causes BA overload and liver damage in males. ( A ) Serum BAs, ( B ) liver BAs, ( C ) serum 7a-C4, ( D ) serum cholesterol, ( E ) serum triglycerides, and ( F ) serum ALT and bilirubin in Fxr KO and Bcl6 LKO Fxr KO males. N = 5–7/group. ( G ) Representative image of serum from Fxr KO and Bcl6 LKO Fxr KO males. ( H ) Liver qPCR of Col1a1 and immune markers in Fxr KO and Bcl6 LKO Fxr KO males. N = 6/group. ( I ) Representative H&E stained (40×) and ( J ) Picrosirius Red stained (40×) images from Fxr KO and Bcl6 LKO Fxr KO male livers. ( K ) Picrosirius Red quantification expressed as % total area in Fxr KO and Bcl6 LKO Fxr KO male livers. Each data point is the average of 3 images/liver. N = 4/group. ( L ) Representative (20×) images of aSMA ( green ) and F4/80 ( red ) immunofluorescence in Fxr KO and Bcl6 LKO Fxr KO male livers. ( M ) aSMA and F4/80 image quantification expressed as % total area in Fxr KO and Bcl6 LKO Fxr KO male liver. Each data point is the average of 4 images/liver. N = 5/group. In ( A–F, H, K and M ) Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Prevention of Cholestatic Liver Disease Through BCL6-FXR Enterohepatic Crosstalk

    doi: 10.1016/j.jcmgh.2025.101706

    Figure Lengend Snippet: Dual deletion of Fxr and hepatic Bcl6 causes BA overload and liver damage in males. ( A ) Serum BAs, ( B ) liver BAs, ( C ) serum 7a-C4, ( D ) serum cholesterol, ( E ) serum triglycerides, and ( F ) serum ALT and bilirubin in Fxr KO and Bcl6 LKO Fxr KO males. N = 5–7/group. ( G ) Representative image of serum from Fxr KO and Bcl6 LKO Fxr KO males. ( H ) Liver qPCR of Col1a1 and immune markers in Fxr KO and Bcl6 LKO Fxr KO males. N = 6/group. ( I ) Representative H&E stained (40×) and ( J ) Picrosirius Red stained (40×) images from Fxr KO and Bcl6 LKO Fxr KO male livers. ( K ) Picrosirius Red quantification expressed as % total area in Fxr KO and Bcl6 LKO Fxr KO male livers. Each data point is the average of 3 images/liver. N = 4/group. ( L ) Representative (20×) images of aSMA ( green ) and F4/80 ( red ) immunofluorescence in Fxr KO and Bcl6 LKO Fxr KO male livers. ( M ) aSMA and F4/80 image quantification expressed as % total area in Fxr KO and Bcl6 LKO Fxr KO male liver. Each data point is the average of 4 images/liver. N = 5/group. In ( A–F, H, K and M ) Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Article Snippet: Primary antibodies for BCL6 (sc-7388, Santa Cruz) at 1:200, FXR (E4B8P, Cell Signaling) at 1:1000, FGFR4 (D3B12, Cell Signaling) at 1:1000, NTCP (ab131084, Abcam) at 1:1000, pERK1/2 (#9101, Cell Signaling) at 1:1000, ERK1/2 (#137F5, Cell Signaling) at 1:1000, CYP7A1 (18054-1-AP, ProteinTech) at 1:1000, GFP (# G10362 , Invitrogen) at 1:1000, SHP (PA5-102494, Thermo Fisher) at 1:1000, CYP8B1 (Abcam, ab191910), or COL1A1 (Cell Signaling, #E8I9Z) were added and incubated overnight at 4 degrees.

    Techniques: Staining, Immunofluorescence

    Combined loss of Fxr and hepatic Bcl6 upregulates pro-fibrotic genes. ( A ) Venn diagram showing common and unique upregulated genes ( P adj < .05; log 2 FC >0.5) in male Fxr KO , Bcl6 LKO , or Bcl6 LKO Fxr KO livers compared with Bcl6 fl/fl livers. ( B ) Top GO pathways of genes uniquely upregulated in Bcl6 LKO Fxr KO vs Bcl6 fl/fl livers. ( C ) Venn diagram of common and unique downregulated genes ( P adj < .05; log 2 FC <0.5) in male Fxr KO , Bcl6 LKO , or Bcl6 LKO Fxr KO livers compared with Bcl6 fl/fl livers. ( D ) Top GO pathways of genes uniquely downregulated in male Bcl6 LKO Fxr KO vs Bcl6 fl/fl livers. N = 4/group.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Prevention of Cholestatic Liver Disease Through BCL6-FXR Enterohepatic Crosstalk

    doi: 10.1016/j.jcmgh.2025.101706

    Figure Lengend Snippet: Combined loss of Fxr and hepatic Bcl6 upregulates pro-fibrotic genes. ( A ) Venn diagram showing common and unique upregulated genes ( P adj < .05; log 2 FC >0.5) in male Fxr KO , Bcl6 LKO , or Bcl6 LKO Fxr KO livers compared with Bcl6 fl/fl livers. ( B ) Top GO pathways of genes uniquely upregulated in Bcl6 LKO Fxr KO vs Bcl6 fl/fl livers. ( C ) Venn diagram of common and unique downregulated genes ( P adj < .05; log 2 FC <0.5) in male Fxr KO , Bcl6 LKO , or Bcl6 LKO Fxr KO livers compared with Bcl6 fl/fl livers. ( D ) Top GO pathways of genes uniquely downregulated in male Bcl6 LKO Fxr KO vs Bcl6 fl/fl livers. N = 4/group.

    Article Snippet: Primary antibodies for BCL6 (sc-7388, Santa Cruz) at 1:200, FXR (E4B8P, Cell Signaling) at 1:1000, FGFR4 (D3B12, Cell Signaling) at 1:1000, NTCP (ab131084, Abcam) at 1:1000, pERK1/2 (#9101, Cell Signaling) at 1:1000, ERK1/2 (#137F5, Cell Signaling) at 1:1000, CYP7A1 (18054-1-AP, ProteinTech) at 1:1000, GFP (# G10362 , Invitrogen) at 1:1000, SHP (PA5-102494, Thermo Fisher) at 1:1000, CYP8B1 (Abcam, ab191910), or COL1A1 (Cell Signaling, #E8I9Z) were added and incubated overnight at 4 degrees.

    Techniques:

    Dual deletion of Fxr and hepatic Bcl6 causes BA overload and liver damage in females. ( A ) Serum BAs, ( B ) liver BAs, ( C ) serum cholesterol, and ( D ) serum triglycerides in Fxr KO and Bcl6 LKO Fxr KO females. N = 6–9/group. ( E ) Representative image of serum from Fxr KO and Bcl6 LKO Fxr KO females. ( F ) Liver qPCR of Col1a1 and immune markers in Fxr KO and Bcl6 LKO Fxr KO females. N = 5–9/group. ( G ) Representative H&E stained (40×) and ( H ) Picrosirius Red stained (40×) images from Fxr KO and Bcl6 LKO Fxr KO female livers. ( I ) Picrosirius Red quantification expressed as % total area in Fxr KO and Bcl6 LKO Fxr KO female liver. Each data point is the average of 3 images/liver. N = 5/group. In ( A–D, F, and I ), Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Prevention of Cholestatic Liver Disease Through BCL6-FXR Enterohepatic Crosstalk

    doi: 10.1016/j.jcmgh.2025.101706

    Figure Lengend Snippet: Dual deletion of Fxr and hepatic Bcl6 causes BA overload and liver damage in females. ( A ) Serum BAs, ( B ) liver BAs, ( C ) serum cholesterol, and ( D ) serum triglycerides in Fxr KO and Bcl6 LKO Fxr KO females. N = 6–9/group. ( E ) Representative image of serum from Fxr KO and Bcl6 LKO Fxr KO females. ( F ) Liver qPCR of Col1a1 and immune markers in Fxr KO and Bcl6 LKO Fxr KO females. N = 5–9/group. ( G ) Representative H&E stained (40×) and ( H ) Picrosirius Red stained (40×) images from Fxr KO and Bcl6 LKO Fxr KO female livers. ( I ) Picrosirius Red quantification expressed as % total area in Fxr KO and Bcl6 LKO Fxr KO female liver. Each data point is the average of 3 images/liver. N = 5/group. In ( A–D, F, and I ), Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Article Snippet: Primary antibodies for BCL6 (sc-7388, Santa Cruz) at 1:200, FXR (E4B8P, Cell Signaling) at 1:1000, FGFR4 (D3B12, Cell Signaling) at 1:1000, NTCP (ab131084, Abcam) at 1:1000, pERK1/2 (#9101, Cell Signaling) at 1:1000, ERK1/2 (#137F5, Cell Signaling) at 1:1000, CYP7A1 (18054-1-AP, ProteinTech) at 1:1000, GFP (# G10362 , Invitrogen) at 1:1000, SHP (PA5-102494, Thermo Fisher) at 1:1000, CYP8B1 (Abcam, ab191910), or COL1A1 (Cell Signaling, #E8I9Z) were added and incubated overnight at 4 degrees.

    Techniques: Staining

    Dual deletion of Fxr and hepatic Bcl6 in males results in loss of SHP. ( A ) qPCR and ( B ) Western blots of BA regulatory targets in Fxr KO and Bcl6 LKO Fxr KO male livers. N = 4–6/group. ( C ) ( Left ) UCSC browser tracks at the Shp (Nr0b2) locus, showing FXR ( top ) and BCL6 ( bottom ) binding sites in control male livers. Arrows annotate the Shp promoter ( Shp-Pro ) and Shp downstream enhancer ( Shp-DS ) regions. ( Righ t) H3K27ac ChIP qPCR at the Shp-Pro and Shp-DS regions in Fxr KO and Bcl6 LKO Fxr KO male livers, expressed as percent of input chromatin. N = 3/group. Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Prevention of Cholestatic Liver Disease Through BCL6-FXR Enterohepatic Crosstalk

    doi: 10.1016/j.jcmgh.2025.101706

    Figure Lengend Snippet: Dual deletion of Fxr and hepatic Bcl6 in males results in loss of SHP. ( A ) qPCR and ( B ) Western blots of BA regulatory targets in Fxr KO and Bcl6 LKO Fxr KO male livers. N = 4–6/group. ( C ) ( Left ) UCSC browser tracks at the Shp (Nr0b2) locus, showing FXR ( top ) and BCL6 ( bottom ) binding sites in control male livers. Arrows annotate the Shp promoter ( Shp-Pro ) and Shp downstream enhancer ( Shp-DS ) regions. ( Righ t) H3K27ac ChIP qPCR at the Shp-Pro and Shp-DS regions in Fxr KO and Bcl6 LKO Fxr KO male livers, expressed as percent of input chromatin. N = 3/group. Student’s t -tests or multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Article Snippet: Primary antibodies for BCL6 (sc-7388, Santa Cruz) at 1:200, FXR (E4B8P, Cell Signaling) at 1:1000, FGFR4 (D3B12, Cell Signaling) at 1:1000, NTCP (ab131084, Abcam) at 1:1000, pERK1/2 (#9101, Cell Signaling) at 1:1000, ERK1/2 (#137F5, Cell Signaling) at 1:1000, CYP7A1 (18054-1-AP, ProteinTech) at 1:1000, GFP (# G10362 , Invitrogen) at 1:1000, SHP (PA5-102494, Thermo Fisher) at 1:1000, CYP8B1 (Abcam, ab191910), or COL1A1 (Cell Signaling, #E8I9Z) were added and incubated overnight at 4 degrees.

    Techniques: Western Blot, Binding Assay, Control, ChIP-qPCR

    Dual deletion of Fxr and hepatic Bcl6 in females results in loss of SHP. ( A ) qPCR of BA regulatory targets in Fxr KO and Bcl6 LKO Fxr KO female livers. N = 5–9/group. Multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Prevention of Cholestatic Liver Disease Through BCL6-FXR Enterohepatic Crosstalk

    doi: 10.1016/j.jcmgh.2025.101706

    Figure Lengend Snippet: Dual deletion of Fxr and hepatic Bcl6 in females results in loss of SHP. ( A ) qPCR of BA regulatory targets in Fxr KO and Bcl6 LKO Fxr KO female livers. N = 5–9/group. Multiple Student’s t -tests were performed to compare means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Article Snippet: Primary antibodies for BCL6 (sc-7388, Santa Cruz) at 1:200, FXR (E4B8P, Cell Signaling) at 1:1000, FGFR4 (D3B12, Cell Signaling) at 1:1000, NTCP (ab131084, Abcam) at 1:1000, pERK1/2 (#9101, Cell Signaling) at 1:1000, ERK1/2 (#137F5, Cell Signaling) at 1:1000, CYP7A1 (18054-1-AP, ProteinTech) at 1:1000, GFP (# G10362 , Invitrogen) at 1:1000, SHP (PA5-102494, Thermo Fisher) at 1:1000, CYP8B1 (Abcam, ab191910), or COL1A1 (Cell Signaling, #E8I9Z) were added and incubated overnight at 4 degrees.

    Techniques:

    SHP is required for BCL6-FXR co-suppression of CYP7A1 and BAs in males. ( A ) Serum, ( B ) liver total BAs, ( C ) liver western blot of GFP, SHP, CYP7A1, and COL1A1, and ( D ) liver qPCR of Bcl6, Shp, Gfp , Cyp7a1, and immune marker genes in Fxr KO and Bcl6 LKO Fxr KO males treated with AAV-TBG-GFP or AAV-TBG-SHP for 4 weeks. N = 3–6/group. Two-way ANOVA with Holm-Sidak’s post-hoc testing was performed to compare effects of AAV-treatment, genotype, and their interaction on means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Prevention of Cholestatic Liver Disease Through BCL6-FXR Enterohepatic Crosstalk

    doi: 10.1016/j.jcmgh.2025.101706

    Figure Lengend Snippet: SHP is required for BCL6-FXR co-suppression of CYP7A1 and BAs in males. ( A ) Serum, ( B ) liver total BAs, ( C ) liver western blot of GFP, SHP, CYP7A1, and COL1A1, and ( D ) liver qPCR of Bcl6, Shp, Gfp , Cyp7a1, and immune marker genes in Fxr KO and Bcl6 LKO Fxr KO males treated with AAV-TBG-GFP or AAV-TBG-SHP for 4 weeks. N = 3–6/group. Two-way ANOVA with Holm-Sidak’s post-hoc testing was performed to compare effects of AAV-treatment, genotype, and their interaction on means. Data are represented as mean ± SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Article Snippet: Primary antibodies for BCL6 (sc-7388, Santa Cruz) at 1:200, FXR (E4B8P, Cell Signaling) at 1:1000, FGFR4 (D3B12, Cell Signaling) at 1:1000, NTCP (ab131084, Abcam) at 1:1000, pERK1/2 (#9101, Cell Signaling) at 1:1000, ERK1/2 (#137F5, Cell Signaling) at 1:1000, CYP7A1 (18054-1-AP, ProteinTech) at 1:1000, GFP (# G10362 , Invitrogen) at 1:1000, SHP (PA5-102494, Thermo Fisher) at 1:1000, CYP8B1 (Abcam, ab191910), or COL1A1 (Cell Signaling, #E8I9Z) were added and incubated overnight at 4 degrees.

    Techniques: Western Blot, Marker

    Hepatic Fxr is not required for FXR-BCL6 co-regulation of BAs. ( A ) Serum total BAs, ( B ) liver total BAs, ( C ) liver qPCR of Bcl6, Fxr, Shp, and Cyp7a1 , and ( D ) ileal qPCR of Fxr, Shp, and Fgf15 in Bcl6 fl/fl Fxr fl/fl , Fxr KO , Bcl6 LKO Fxr KO , and Bcl6 LKO Fxr LKO males. N = 4–8/group. One-way ANOVA with Holm-Sidak’s post-hoc testing was performed to compare means. Data are represented as mean ±SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Prevention of Cholestatic Liver Disease Through BCL6-FXR Enterohepatic Crosstalk

    doi: 10.1016/j.jcmgh.2025.101706

    Figure Lengend Snippet: Hepatic Fxr is not required for FXR-BCL6 co-regulation of BAs. ( A ) Serum total BAs, ( B ) liver total BAs, ( C ) liver qPCR of Bcl6, Fxr, Shp, and Cyp7a1 , and ( D ) ileal qPCR of Fxr, Shp, and Fgf15 in Bcl6 fl/fl Fxr fl/fl , Fxr KO , Bcl6 LKO Fxr KO , and Bcl6 LKO Fxr LKO males. N = 4–8/group. One-way ANOVA with Holm-Sidak’s post-hoc testing was performed to compare means. Data are represented as mean ±SEM. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001.

    Article Snippet: Primary antibodies for BCL6 (sc-7388, Santa Cruz) at 1:200, FXR (E4B8P, Cell Signaling) at 1:1000, FGFR4 (D3B12, Cell Signaling) at 1:1000, NTCP (ab131084, Abcam) at 1:1000, pERK1/2 (#9101, Cell Signaling) at 1:1000, ERK1/2 (#137F5, Cell Signaling) at 1:1000, CYP7A1 (18054-1-AP, ProteinTech) at 1:1000, GFP (# G10362 , Invitrogen) at 1:1000, SHP (PA5-102494, Thermo Fisher) at 1:1000, CYP8B1 (Abcam, ab191910), or COL1A1 (Cell Signaling, #E8I9Z) were added and incubated overnight at 4 degrees.

    Techniques:

    Model for BCL6 and FXR co-regulation of BAs. ( Top ) In control ( Bcl6 fl/fl ) mice, BCL6 restrains hepatic and circulating cholesterol while enhancing NTCP and FGFR4 expression. In tandem, FXR activates SHP via enterohepatic and direct liver signaling to suppress CYP7A1 and BA production. ( Bottom left ) Loss of hepatic Bcl6 reduces the BA transporter NTCP and FGFR4 while it increases cholesterol and CYP7A1-directed BA synthesis and circulating levels. ( Bottom right ) Combined loss of hepatic Bcl6 and whole body Fxr unmasks co-dependent regulation of Shp by BCL6 and FXR. Shp levels are strongly reduced, whereas CYP7A1 is reciprocally increased. BA synthesis and levels become severely elevated, leading to cholestasis.

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    Article Title: Prevention of Cholestatic Liver Disease Through BCL6-FXR Enterohepatic Crosstalk

    doi: 10.1016/j.jcmgh.2025.101706

    Figure Lengend Snippet: Model for BCL6 and FXR co-regulation of BAs. ( Top ) In control ( Bcl6 fl/fl ) mice, BCL6 restrains hepatic and circulating cholesterol while enhancing NTCP and FGFR4 expression. In tandem, FXR activates SHP via enterohepatic and direct liver signaling to suppress CYP7A1 and BA production. ( Bottom left ) Loss of hepatic Bcl6 reduces the BA transporter NTCP and FGFR4 while it increases cholesterol and CYP7A1-directed BA synthesis and circulating levels. ( Bottom right ) Combined loss of hepatic Bcl6 and whole body Fxr unmasks co-dependent regulation of Shp by BCL6 and FXR. Shp levels are strongly reduced, whereas CYP7A1 is reciprocally increased. BA synthesis and levels become severely elevated, leading to cholestasis.

    Article Snippet: Primary antibodies for BCL6 (sc-7388, Santa Cruz) at 1:200, FXR (E4B8P, Cell Signaling) at 1:1000, FGFR4 (D3B12, Cell Signaling) at 1:1000, NTCP (ab131084, Abcam) at 1:1000, pERK1/2 (#9101, Cell Signaling) at 1:1000, ERK1/2 (#137F5, Cell Signaling) at 1:1000, CYP7A1 (18054-1-AP, ProteinTech) at 1:1000, GFP (# G10362 , Invitrogen) at 1:1000, SHP (PA5-102494, Thermo Fisher) at 1:1000, CYP8B1 (Abcam, ab191910), or COL1A1 (Cell Signaling, #E8I9Z) were added and incubated overnight at 4 degrees.

    Techniques: Control, Expressing

    Figure 1: Co-culture with BMSC or HOB reduces BCL6 in ALL cells. A. BCL6 protein in REH and Nalm-27 ALL cells when co-cultured with BMSC or HOB cells relative to media (M) controls as shown by western blot analysis. B. Flow cytometry analysis of REH and Nalm-27 ALL cell BCL6 protein levels when removed from the PD population compared to cells in media alone as shown by median florescence intensity (MFI). C. MFI of Patient 1 (P1) and Patient 2 (P2) when in physical contact with BMSC or HOB compared to those in media alone (ND = not detected). D. Confocal microscopy images of REH and Nalm-27 for BCL6 (yellow) and DAPI (Blue) in cells cultured in media alone compare to those recovered from the PD population of BMSC or HOB co-culture. E. P1 and P2 BCL6 confocal staining of media alone cells relative to those in contact with BMSC or HOB. Scale bar = 10µm.

    Journal: Oncotarget

    Article Title: BCL6 modulation of acute lymphoblastic leukemia response to chemotherapy.

    doi: 10.18632/oncotarget.8273

    Figure Lengend Snippet: Figure 1: Co-culture with BMSC or HOB reduces BCL6 in ALL cells. A. BCL6 protein in REH and Nalm-27 ALL cells when co-cultured with BMSC or HOB cells relative to media (M) controls as shown by western blot analysis. B. Flow cytometry analysis of REH and Nalm-27 ALL cell BCL6 protein levels when removed from the PD population compared to cells in media alone as shown by median florescence intensity (MFI). C. MFI of Patient 1 (P1) and Patient 2 (P2) when in physical contact with BMSC or HOB compared to those in media alone (ND = not detected). D. Confocal microscopy images of REH and Nalm-27 for BCL6 (yellow) and DAPI (Blue) in cells cultured in media alone compare to those recovered from the PD population of BMSC or HOB co-culture. E. P1 and P2 BCL6 confocal staining of media alone cells relative to those in contact with BMSC or HOB. Scale bar = 10µm.

    Article Snippet: ALL cells were stained using Cell Signaling Technology’s recommended protocol for intracellular BCL6 staining using primary antibodies rabbit anti-BCL6 (Cat # 14895) (1:300) or Rabbit (DA1E) mAb IgG XP isotype control (Cat # 3900).

    Techniques: Co-Culture Assay, Cell Culture, Western Blot, Flow Cytometry, Confocal Microscopy, Staining

    Figure 2: Modulation of BCL6 alters cell cycle progression and proliferation of ALL cells. A.- B. Cell density and viability of REH, Sup-B15, and Nalm-27 following exposure to the small molecule BCL6 inhibitor 79-6 (125µM) relative to DMSO controls as shown by trypan blue exclusion cell counts. C. Proliferation index of 79-6 treatment of REH, Sup-B15 and Nalm-27 ALL cells compared to DMSO controls using a CSFE cell retention dye flow cytometry analysis. D. Propidium iodide (PI) DNA staining for cell cycle assessment of REH, Sup-B15 and Nalm-27 treated with 79-6 compared to DMSO controls. E. Cell density of shRNA knockdown of BCL6 (KD1 and KD3) (left panel) and BCL6 overexpression (BCL6 OX) (right panel) of REH cells over time compared to vector controls as evaluated by trypan blue exclusion counts. F. Cell cycle analysis of BCL6 knockdown (left panel) and BCL6 overexpression (right panel) in REH cells using PI staining. (* = p < 0.05 for 79-6 treated cells or knockdown/overexpression cells compared to DMSO or vector controls, respectively).

    Journal: Oncotarget

    Article Title: BCL6 modulation of acute lymphoblastic leukemia response to chemotherapy.

    doi: 10.18632/oncotarget.8273

    Figure Lengend Snippet: Figure 2: Modulation of BCL6 alters cell cycle progression and proliferation of ALL cells. A.- B. Cell density and viability of REH, Sup-B15, and Nalm-27 following exposure to the small molecule BCL6 inhibitor 79-6 (125µM) relative to DMSO controls as shown by trypan blue exclusion cell counts. C. Proliferation index of 79-6 treatment of REH, Sup-B15 and Nalm-27 ALL cells compared to DMSO controls using a CSFE cell retention dye flow cytometry analysis. D. Propidium iodide (PI) DNA staining for cell cycle assessment of REH, Sup-B15 and Nalm-27 treated with 79-6 compared to DMSO controls. E. Cell density of shRNA knockdown of BCL6 (KD1 and KD3) (left panel) and BCL6 overexpression (BCL6 OX) (right panel) of REH cells over time compared to vector controls as evaluated by trypan blue exclusion counts. F. Cell cycle analysis of BCL6 knockdown (left panel) and BCL6 overexpression (right panel) in REH cells using PI staining. (* = p < 0.05 for 79-6 treated cells or knockdown/overexpression cells compared to DMSO or vector controls, respectively).

    Article Snippet: ALL cells were stained using Cell Signaling Technology’s recommended protocol for intracellular BCL6 staining using primary antibodies rabbit anti-BCL6 (Cat # 14895) (1:300) or Rabbit (DA1E) mAb IgG XP isotype control (Cat # 3900).

    Techniques: Flow Cytometry, Staining, shRNA, Knockdown, Over Expression, Plasmid Preparation, Cell Cycle Assay

    Figure 3: BCL6 modulates the cell cycle regulating protein cyclin D3. A. Western blot analysis of protein abundance of BCL6 and cyclin D3 in REH and Nalm-27 cells in media alone compared to PD cells recovered from BMSC or HOB co-culture. B. Comparison of REH BCL6 knockdown and overexpression to vector controls for BCL6 and cyclin D3 protein levels by western blot. C. Protein analysis by western blot of cyclin D3 in REH and Nalm-27 cells when exposed to 79-6.

    Journal: Oncotarget

    Article Title: BCL6 modulation of acute lymphoblastic leukemia response to chemotherapy.

    doi: 10.18632/oncotarget.8273

    Figure Lengend Snippet: Figure 3: BCL6 modulates the cell cycle regulating protein cyclin D3. A. Western blot analysis of protein abundance of BCL6 and cyclin D3 in REH and Nalm-27 cells in media alone compared to PD cells recovered from BMSC or HOB co-culture. B. Comparison of REH BCL6 knockdown and overexpression to vector controls for BCL6 and cyclin D3 protein levels by western blot. C. Protein analysis by western blot of cyclin D3 in REH and Nalm-27 cells when exposed to 79-6.

    Article Snippet: ALL cells were stained using Cell Signaling Technology’s recommended protocol for intracellular BCL6 staining using primary antibodies rabbit anti-BCL6 (Cat # 14895) (1:300) or Rabbit (DA1E) mAb IgG XP isotype control (Cat # 3900).

    Techniques: Western Blot, Quantitative Proteomics, Co-Culture Assay, Comparison, Knockdown, Over Expression, Plasmid Preparation

    Figure 4: Forced expression of BCL6 sensitizes PD ALL cells to chemotherapy exposure. A. Viability comparison of REH vector control, BCL6 overexpression, or BCL6 overexpression cells pre-treated with 79-6 (125µM) following exposure to three chemotherapy drugs (Ara-C [1 µM], MTX [50 µM], VCR [25 µM]). (* = p < 0.05 BCL6 OX to vector control and # = p < 0.05 BCL6 OX to BCL6 + 79-6). B. REH and Nalm-27 BCL6 protein dose response to MG132 and caffeine as shown by western blot. C. Western blot analysis to determine BCL6 protein abundance of REH and Nalm-27 cells when exposed to MG132 or caffeine when recovered from media alone, and the PD population of BMSC or HOB co-culture. D. REH and Nalm-27 cell viability following exposure to Ara-C alone or when pre-treated with MG132 or caffeine 6 hours prior to Ara-C exposure to compare cells in media alone to those recovered from the PD population of BMSC or HOB co-culture. (# = p < 0.05 PD ALL cells from BMSC/HOB relative to media and * = p < 0.05 Ara-C + MG132/ Ara-C + caffeine relative to Ara-C only treatment).

    Journal: Oncotarget

    Article Title: BCL6 modulation of acute lymphoblastic leukemia response to chemotherapy.

    doi: 10.18632/oncotarget.8273

    Figure Lengend Snippet: Figure 4: Forced expression of BCL6 sensitizes PD ALL cells to chemotherapy exposure. A. Viability comparison of REH vector control, BCL6 overexpression, or BCL6 overexpression cells pre-treated with 79-6 (125µM) following exposure to three chemotherapy drugs (Ara-C [1 µM], MTX [50 µM], VCR [25 µM]). (* = p < 0.05 BCL6 OX to vector control and # = p < 0.05 BCL6 OX to BCL6 + 79-6). B. REH and Nalm-27 BCL6 protein dose response to MG132 and caffeine as shown by western blot. C. Western blot analysis to determine BCL6 protein abundance of REH and Nalm-27 cells when exposed to MG132 or caffeine when recovered from media alone, and the PD population of BMSC or HOB co-culture. D. REH and Nalm-27 cell viability following exposure to Ara-C alone or when pre-treated with MG132 or caffeine 6 hours prior to Ara-C exposure to compare cells in media alone to those recovered from the PD population of BMSC or HOB co-culture. (# = p < 0.05 PD ALL cells from BMSC/HOB relative to media and * = p < 0.05 Ara-C + MG132/ Ara-C + caffeine relative to Ara-C only treatment).

    Article Snippet: ALL cells were stained using Cell Signaling Technology’s recommended protocol for intracellular BCL6 staining using primary antibodies rabbit anti-BCL6 (Cat # 14895) (1:300) or Rabbit (DA1E) mAb IgG XP isotype control (Cat # 3900).

    Techniques: Expressing, Comparison, Plasmid Preparation, Control, Over Expression, Western Blot, Quantitative Proteomics, Co-Culture Assay

    Figure 5: In vivo sensitivity to Ara-C is increased by BCL6 overexpression or pre-treatment with caffeine. A. Schematic of NSG mouse experiment to determine GFP+ ALL burden in the femurs of NSG mice. B. Box plot representation of median percentage of GFP+ REH ALL cells relative to total mononuclear cells recovered from femurs of NOD-SCID Gamma (NSG) mice infected with REH vector control (n = 5) or REH BCL6 overexpression (n = 4) ALL cells following three consecutive days of Ara-C treatment. C. Schematic of NSG mouse experiment to determine event free survival of mice pre-treated with BCL6 modulating drugs MG-132 or caffeine. D. Event free survival of NSG mice following treatment with Ara-C (n = 5), MG-132 + Ara-C (n = 6), or caffeine + Ara-C (n = 6) (* = p < 0.05 Ara-C relative to caffeine+ Ara-C).

    Journal: Oncotarget

    Article Title: BCL6 modulation of acute lymphoblastic leukemia response to chemotherapy.

    doi: 10.18632/oncotarget.8273

    Figure Lengend Snippet: Figure 5: In vivo sensitivity to Ara-C is increased by BCL6 overexpression or pre-treatment with caffeine. A. Schematic of NSG mouse experiment to determine GFP+ ALL burden in the femurs of NSG mice. B. Box plot representation of median percentage of GFP+ REH ALL cells relative to total mononuclear cells recovered from femurs of NOD-SCID Gamma (NSG) mice infected with REH vector control (n = 5) or REH BCL6 overexpression (n = 4) ALL cells following three consecutive days of Ara-C treatment. C. Schematic of NSG mouse experiment to determine event free survival of mice pre-treated with BCL6 modulating drugs MG-132 or caffeine. D. Event free survival of NSG mice following treatment with Ara-C (n = 5), MG-132 + Ara-C (n = 6), or caffeine + Ara-C (n = 6) (* = p < 0.05 Ara-C relative to caffeine+ Ara-C).

    Article Snippet: ALL cells were stained using Cell Signaling Technology’s recommended protocol for intracellular BCL6 staining using primary antibodies rabbit anti-BCL6 (Cat # 14895) (1:300) or Rabbit (DA1E) mAb IgG XP isotype control (Cat # 3900).

    Techniques: In Vivo, Over Expression, Infection, Plasmid Preparation, Control