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mouse anti bcl 6 sc 7388 (Santa Cruz Biotechnology)

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Santa Cruz Biotechnology mouse anti bcl 6 sc 7388
Mouse Anti Bcl 6 Sc 7388, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 239 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/bcl+6/pm41644848-266-4-7?v=Santa+Cruz+Biotechnology
Average 94 stars, based on 239 article reviews

mouse anti bcl 6 sc 7388 - by Bioz Stars, 2026-07

94/100 stars

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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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

Techniques: Control, Expressing

Volcano plots of differentially expressed RNA species in BCL6 KO (two guides averaged over three replicates per guide) EWS502 cells (A) or TC32 cells (B) vs Chr2.2 control cells. GSEA in EWS502 (C) or TC32 (D) BCL6 KO cells shows a positive correlation with a published BCL6 gene signature derived from BCL6 promoter binding data 25 . SOCS2 and CISH transcripts have increased expression by RT-qPCR in BCL6 KO EWS502 cells (E and F) or TC32 cells (G and H) vs control guides. Average expression from three independent cell transductions (performed in technical triplicate) is shown. RT-qPCR data was compared by one-way ANOVA; NS = not significant, **** p < 0.001. All error bars in the figure show mean ± SD. Immunoblotting shows BCL6 KO and corresponding increase in SOCS2 protein levels in EWS502 (I) and TC32 (J) cells. Each lane is from an independent transduction of cells. GAPDH serves as a loading control.

Journal: Journal of the American Chemical Society

Article Title: Rewiring the fusion oncoprotein EWSR1::FLI1 in Ewing sarcoma with bivalent small molecules

doi: 10.1021/jacs.5c05634

Figure Lengend Snippet: Volcano plots of differentially expressed RNA species in BCL6 KO (two guides averaged over three replicates per guide) EWS502 cells (A) or TC32 cells (B) vs Chr2.2 control cells. GSEA in EWS502 (C) or TC32 (D) BCL6 KO cells shows a positive correlation with a published BCL6 gene signature derived from BCL6 promoter binding data 25 . SOCS2 and CISH transcripts have increased expression by RT-qPCR in BCL6 KO EWS502 cells (E and F) or TC32 cells (G and H) vs control guides. Average expression from three independent cell transductions (performed in technical triplicate) is shown. RT-qPCR data was compared by one-way ANOVA; NS = not significant, **** p < 0.001. All error bars in the figure show mean ± SD. Immunoblotting shows BCL6 KO and corresponding increase in SOCS2 protein levels in EWS502 (I) and TC32 (J) cells. Each lane is from an independent transduction of cells. GAPDH serves as a loading control.

Article Snippet: For BCL6 KO experiments, 2 × 10 6 EWS502 or TC32 cells were seeded into 6-well plates in a volume of 1 mL of RPMI media supplemented with 8 or 4 μg/mL of polybrene (Santa Cruz Biotechnology, SC-134220), respectively.

Techniques: Control, Derivative Assay, Binding Assay, Expressing, Quantitative RT-PCR, Western Blot, Transduction

(A) Schematic of EB-TCIP mechanism of action. EB-TCIP induces a ternary complex between FKBP F36V tagged EWSR1::FLI1 and BCL6, which leads to activation of BCL6 target gene transcription. Image made with Biorender. (B) Structures of compounds used in this work. (C) EB-TCIP increases the association of BCL6 with FKBP-E::F in a dose-dependent manner in EWS502 FKBP-E::F cell lysates while NEG-1 (D) does not induce a ternary complex. The association is reversible as excess BI3812 (C) and excess OAP (free acid) (D) abrogate ternary complex formation. GAPDH was probed to confirm that unbound proteins were removed by washing. EB-TCIP dose-dependently increases SOCS2 (E) and CISH (F) expression by RT-qPCR. (G) SOCS2 protein levels dose-dependently increase while BCL6 protein levels dose-dependently decrease after EB-TCIP treatment. EB-TCIP induces higher SOCS2 (H) and CISH (I) transcript levels than chemical inhibition with BI3812 or chemically induced degradation with BI3802 (DEG) . (J) SOCS2 protein levels are highest in EB-TCIP treated cells compared to BI3812 , BI3802 (DEG) , or negative control compounds that do not form ternary complexes. Immunoblotting is representative of three biological replicates and GAPDH serves as a loading control. All experiments were performed in FKBP-E::F expressing EWS502 cells. RT-qPCR experiments show one experiment with technical triplicate that is representative of three biological replicates. Means of SOCS2 and CISH expression were compared using one-way ANOVA with multiple comparisons; NS = not significant, *** p < 0.005, **** p < 0.001. All error bars in the figure indicate mean ± SD. Unless indicated with brackets, significance above each condition indicates comparison of that mean to the mean of DMSO.

Journal: Journal of the American Chemical Society

Article Title: Rewiring the fusion oncoprotein EWSR1::FLI1 in Ewing sarcoma with bivalent small molecules

doi: 10.1021/jacs.5c05634

Figure Lengend Snippet: (A) Schematic of EB-TCIP mechanism of action. EB-TCIP induces a ternary complex between FKBP F36V tagged EWSR1::FLI1 and BCL6, which leads to activation of BCL6 target gene transcription. Image made with Biorender. (B) Structures of compounds used in this work. (C) EB-TCIP increases the association of BCL6 with FKBP-E::F in a dose-dependent manner in EWS502 FKBP-E::F cell lysates while NEG-1 (D) does not induce a ternary complex. The association is reversible as excess BI3812 (C) and excess OAP (free acid) (D) abrogate ternary complex formation. GAPDH was probed to confirm that unbound proteins were removed by washing. EB-TCIP dose-dependently increases SOCS2 (E) and CISH (F) expression by RT-qPCR. (G) SOCS2 protein levels dose-dependently increase while BCL6 protein levels dose-dependently decrease after EB-TCIP treatment. EB-TCIP induces higher SOCS2 (H) and CISH (I) transcript levels than chemical inhibition with BI3812 or chemically induced degradation with BI3802 (DEG) . (J) SOCS2 protein levels are highest in EB-TCIP treated cells compared to BI3812 , BI3802 (DEG) , or negative control compounds that do not form ternary complexes. Immunoblotting is representative of three biological replicates and GAPDH serves as a loading control. All experiments were performed in FKBP-E::F expressing EWS502 cells. RT-qPCR experiments show one experiment with technical triplicate that is representative of three biological replicates. Means of SOCS2 and CISH expression were compared using one-way ANOVA with multiple comparisons; NS = not significant, *** p < 0.005, **** p < 0.001. All error bars in the figure indicate mean ± SD. Unless indicated with brackets, significance above each condition indicates comparison of that mean to the mean of DMSO.

Techniques: Expressing, Activation Assay, Quantitative RT-PCR, Inhibition, Negative Control, Western Blot, Control, Comparison

(A) Time course of SOCS2 and BCL6 protein levels. BCL6 degradation occurs within 1 h for both EB-TCIP and BI3802 (DEG) . EB-TCIP induces SOCS2 expression by 2 h and maintains higher expression levels than BI3812 or BI3802 (DEG) throughout the time course. SOCS2 (B) and CISH (C) transcripts reach a maximum between 2 and 4 h by RT-qPCR. (D) EB-TCIP induced SOCS2 protein expression can be reversed with 25-fold excess OAP (free acid). Co-treatment of 1 µM BI3812 and OAP do not increase SOCS2 protein expression more than 1 µM BI3812 alone. EB-TCIP induced SOCS2 (E) and CISH (F) transcript expression is reversed with excess OAP . BI3812 and OAP must be chemically linked to induce maximum transcript expression. (G) EB-TCIP induces the highest expression of SOCS2 protein in EWS502 FKBP-E::F cells compared to EWS502 parental cells or EWS502 cells expressing FKBP-GFP. Only treatment with EB-TCIP induces more expression of SOCS2 (H) and CISH (I) than BI3812 in EWS502 FKBP-E::F cells. EB-TCIP : BI3812 ratio was calculated by dividing the average expression of each transcript in EB-TCIP treated cells by the average expression of each transcript in BI3812 treated cells. Immunoblotting is representative of three biological replicates. RT-qPCR experiments show one experiment with technical triplicate or quadruplicate that is representative of three biological replicates. The means of SOCS2 and CISH expression were compared using one-way ANOVA with multiple comparisons; NS = not significant, * p < 0.05, ** p < 0.01, *** p < 0.005, **** p < 0.001. All error bars in the figure represent mean ± SD. Unless indicated with brackets, significance above each condition indicates comparison of that mean to the mean of DMSO. In (H) and (I), unless indicated with brackets, the means of BI3812 , EB-TCIP , and NEG-1 were compared to the DMSO sample for the corresponding cell line.

Journal: Journal of the American Chemical Society

Article Title: Rewiring the fusion oncoprotein EWSR1::FLI1 in Ewing sarcoma with bivalent small molecules

doi: 10.1021/jacs.5c05634

Figure Lengend Snippet: (A) Time course of SOCS2 and BCL6 protein levels. BCL6 degradation occurs within 1 h for both EB-TCIP and BI3802 (DEG) . EB-TCIP induces SOCS2 expression by 2 h and maintains higher expression levels than BI3812 or BI3802 (DEG) throughout the time course. SOCS2 (B) and CISH (C) transcripts reach a maximum between 2 and 4 h by RT-qPCR. (D) EB-TCIP induced SOCS2 protein expression can be reversed with 25-fold excess OAP (free acid). Co-treatment of 1 µM BI3812 and OAP do not increase SOCS2 protein expression more than 1 µM BI3812 alone. EB-TCIP induced SOCS2 (E) and CISH (F) transcript expression is reversed with excess OAP . BI3812 and OAP must be chemically linked to induce maximum transcript expression. (G) EB-TCIP induces the highest expression of SOCS2 protein in EWS502 FKBP-E::F cells compared to EWS502 parental cells or EWS502 cells expressing FKBP-GFP. Only treatment with EB-TCIP induces more expression of SOCS2 (H) and CISH (I) than BI3812 in EWS502 FKBP-E::F cells. EB-TCIP : BI3812 ratio was calculated by dividing the average expression of each transcript in EB-TCIP treated cells by the average expression of each transcript in BI3812 treated cells. Immunoblotting is representative of three biological replicates. RT-qPCR experiments show one experiment with technical triplicate or quadruplicate that is representative of three biological replicates. The means of SOCS2 and CISH expression were compared using one-way ANOVA with multiple comparisons; NS = not significant, * p < 0.05, ** p < 0.01, *** p < 0.005, **** p < 0.001. All error bars in the figure represent mean ± SD. Unless indicated with brackets, significance above each condition indicates comparison of that mean to the mean of DMSO. In (H) and (I), unless indicated with brackets, the means of BI3812 , EB-TCIP , and NEG-1 were compared to the DMSO sample for the corresponding cell line.

Techniques: Activity Assay, Expressing, Quantitative RT-PCR, Western Blot, Comparison

Volcano plots portraying log 2 fold changes of gene expression from cells treated with 2.5 µM EB-TCIP versus DMSO at 8 (A) and 24 (B) h with a −log 10 adjusted P-value cut off of 1. EB-TCIP treatment predominantly increases expression of transcripts at both timepoints. Volcano plots portraying log 2 fold changes of cells treated with 2.5 µM EB-TCIP versus 2.5 µM BI3812 (C) or 2.5 µM NEG-1 (D) at 8 hours with a −log 10 P-value cut off of 1.3. EB-TCIP induces higher expression of BCL6 transcripts than BI3812 or NEG-1 at this early timepoint. Dots corresponding to SOCS2, CISH, and CXCL11 are labelled with black borders. (E) Heatmaps of changes in BCL6 target gene expression at 4, 8 and 24 h show that EB-TCIP induces faster and/or higher expression of these select genes. (F) GSEA comparing EB-TCIP treated EWS502 FKBP-E::F cells to BCL6 KO EWS502 parental cells (LFC ≥ 1.65) at 4 (top), 8 (middle) and 24 h (bottom) show significant positive correlation between the two gene sets. RNA-seq data is shown as the average of three independent replicates.

Journal: Journal of the American Chemical Society

Article Title: Rewiring the fusion oncoprotein EWSR1::FLI1 in Ewing sarcoma with bivalent small molecules

doi: 10.1021/jacs.5c05634

Figure Lengend Snippet: Volcano plots portraying log 2 fold changes of gene expression from cells treated with 2.5 µM EB-TCIP versus DMSO at 8 (A) and 24 (B) h with a −log 10 adjusted P-value cut off of 1. EB-TCIP treatment predominantly increases expression of transcripts at both timepoints. Volcano plots portraying log 2 fold changes of cells treated with 2.5 µM EB-TCIP versus 2.5 µM BI3812 (C) or 2.5 µM NEG-1 (D) at 8 hours with a −log 10 P-value cut off of 1.3. EB-TCIP induces higher expression of BCL6 transcripts than BI3812 or NEG-1 at this early timepoint. Dots corresponding to SOCS2, CISH, and CXCL11 are labelled with black borders. (E) Heatmaps of changes in BCL6 target gene expression at 4, 8 and 24 h show that EB-TCIP induces faster and/or higher expression of these select genes. (F) GSEA comparing EB-TCIP treated EWS502 FKBP-E::F cells to BCL6 KO EWS502 parental cells (LFC ≥ 1.65) at 4 (top), 8 (middle) and 24 h (bottom) show significant positive correlation between the two gene sets. RNA-seq data is shown as the average of three independent replicates.

Techniques: Gene Expression, Expressing, Targeted Gene Expression, RNA Sequencing

(A) ChIP-seq tornado plots of HA (FKBP-E::F) binding signal of EB-TCIP (red) versus DMSO (black) peaks that are decreasing (DEC; 92), non-significantly changing (NS; 8656), and increasing (INC; 2296) at 24 h. Differential peaks between EB-TCIP and DMSO are shown for all compounds. Compared to BI3812 (brown) and BI3802 ( DEG , purple), EB-TCIP increases FKBP-E::F binding at a subset of genes. Line plots for all compound treatments in each cluster are shown to the right. (B) Scatter plot portraying top enriched motifs of HA binding sites in DMSO treated cells. (C) Scatter plot portraying top motifs of HA increased peaks enriched in EB-TCIP treated cells. The BCL6 motif scores 29 th . (D) Scatter plot portraying top motifs of HA decreased peaks enriched in EB-TCIP treated cells. IGV visualization of input, HA (FKBP-E::F), BCL6, ATAC-seq signal, and RNA-seq signal at the SOCS2 (E) and CISH (F) with treatments DMSO (black), 1 µM BI3812 (brown), 1 µM BI3802 (DEG , purple), and 1 µM EB-TCIP (red). All ChIP-seq and ATAC-seq is portrayed as the average of two independent replicates. RNA-seq is portrayed as the average of three independent replicates.

Journal: Journal of the American Chemical Society

Article Title: Rewiring the fusion oncoprotein EWSR1::FLI1 in Ewing sarcoma with bivalent small molecules

doi: 10.1021/jacs.5c05634

Figure Lengend Snippet: (A) ChIP-seq tornado plots of HA (FKBP-E::F) binding signal of EB-TCIP (red) versus DMSO (black) peaks that are decreasing (DEC; 92), non-significantly changing (NS; 8656), and increasing (INC; 2296) at 24 h. Differential peaks between EB-TCIP and DMSO are shown for all compounds. Compared to BI3812 (brown) and BI3802 ( DEG , purple), EB-TCIP increases FKBP-E::F binding at a subset of genes. Line plots for all compound treatments in each cluster are shown to the right. (B) Scatter plot portraying top enriched motifs of HA binding sites in DMSO treated cells. (C) Scatter plot portraying top motifs of HA increased peaks enriched in EB-TCIP treated cells. The BCL6 motif scores 29 th . (D) Scatter plot portraying top motifs of HA decreased peaks enriched in EB-TCIP treated cells. IGV visualization of input, HA (FKBP-E::F), BCL6, ATAC-seq signal, and RNA-seq signal at the SOCS2 (E) and CISH (F) with treatments DMSO (black), 1 µM BI3812 (brown), 1 µM BI3802 (DEG , purple), and 1 µM EB-TCIP (red). All ChIP-seq and ATAC-seq is portrayed as the average of two independent replicates. RNA-seq is portrayed as the average of three independent replicates.

Techniques: ChIP-sequencing, Binding Assay, RNA Sequencing

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