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Jackson Laboratory pbrm1 f f strain

Loss of <t>Pbrm1</t> enhances the activation of hepatic progenitor cells in response to cholestatic injury. ( A ) Immunohistochemical staining confirms the loss of PBRM1 expression in hepatocytes and cholangiocytes in the interlobular bile ducts of Pbrm1 KO mice. Scale bar: 100 μm. ( B ) Overview of the DDC diet treatment protocol. ( C – G ) Serum levels of AST ( C ), ALT ( D ), total bilirubin ( E ), direct bilirubin ( F ), and ALP ( G ) in WT and Pbrm1 KO mice following DDC diet treatment (n = 11 for each group for A – E , n = 5 for each group for F and G ). ∗ P < .05 and ∗∗ P < .01.

Pbrm1 F F Strain, supplied by Jackson Laboratory, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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pbrm1 f f strain - by Bioz Stars, 2026-09

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1) Product Images from "Pbrm1 Loss Induces a Permissive Chromatin State for Cholangiocytic Differentiation and Cholangiocarcinoma Formation"

Article Title: Pbrm1 Loss Induces a Permissive Chromatin State for Cholangiocytic Differentiation and Cholangiocarcinoma Formation

Journal: Cellular and Molecular Gastroenterology and Hepatology

doi: 10.1016/j.jcmgh.2025.101720

Loss of Pbrm1 enhances the activation of hepatic progenitor cells in response to cholestatic injury. ( A ) Immunohistochemical staining confirms the loss of PBRM1 expression in hepatocytes and cholangiocytes in the interlobular bile ducts of Pbrm1 KO mice. Scale bar: 100 μm. ( B ) Overview of the DDC diet treatment protocol. ( C – G ) Serum levels of AST ( C ), ALT ( D ), total bilirubin ( E ), direct bilirubin ( F ), and ALP ( G ) in WT and Pbrm1 KO mice following DDC diet treatment (n = 11 for each group for A – E , n = 5 for each group for F and G ). ∗ P < .05 and ∗∗ P < .01.

Figure Legend Snippet: Loss of Pbrm1 enhances the activation of hepatic progenitor cells in response to cholestatic injury. ( A ) Immunohistochemical staining confirms the loss of PBRM1 expression in hepatocytes and cholangiocytes in the interlobular bile ducts of Pbrm1 KO mice. Scale bar: 100 μm. ( B ) Overview of the DDC diet treatment protocol. ( C – G ) Serum levels of AST ( C ), ALT ( D ), total bilirubin ( E ), direct bilirubin ( F ), and ALP ( G ) in WT and Pbrm1 KO mice following DDC diet treatment (n = 11 for each group for A – E , n = 5 for each group for F and G ). ∗ P < .05 and ∗∗ P < .01.

Techniques Used: Activation Assay, Immunohistochemical staining, Staining, Expressing

Histologic and molecular evidence of enhanced hepatic progenitor cell activation in response to cholestatic injury in Pbrm1 KO liver. ( A ) Histological analysis of H&E and KRT19-stained sections reveals increased bile ductular proliferation in the livers of Pbrm1 KO mice after DDC diet treatment. ( B ) Quantification of KRT19-positive areas in the livers of WT and Pbrm1 KO mice post-DDC diet treatment (n = 14 for each group). ( C ) Immunostaining demonstrates loss of PBRM1 expression in exaggerated ductular reaction in Pbrm1 KO liver. ( D ) Quantification of SOX9-positive hepatocytes in the livers of WT and Pbrm1 KO mice post-DDC diet treatment (n = 14 for each group). ( E and F ) RNA-seq data shows downregulation of hepatocyte markers Fabp1 and C2, and upregulation of cholangiocyte marker Krt19 and progenitor marker Lgr5 in Pbrm1 KO mice on the DDC diet ( E ), with no differences observed in untreated mice (n = 3 for each group) ( F ). ( G ) Forty-eight hours post-partial hepatectomy, the liver-to-body weight ratio, an indicator of liver regeneration, shows no significant difference between Pbrm1 KO (n = 5) and WT mice (n = 7). ∗ P < .05; ∗∗ P < .01; and ∗∗∗ P < .001. Scale bars for ( A ): 500 μm; for ( C ) and ( D ): 100 μm.

Figure Legend Snippet: Histologic and molecular evidence of enhanced hepatic progenitor cell activation in response to cholestatic injury in Pbrm1 KO liver. ( A ) Histological analysis of H&E and KRT19-stained sections reveals increased bile ductular proliferation in the livers of Pbrm1 KO mice after DDC diet treatment. ( B ) Quantification of KRT19-positive areas in the livers of WT and Pbrm1 KO mice post-DDC diet treatment (n = 14 for each group). ( C ) Immunostaining demonstrates loss of PBRM1 expression in exaggerated ductular reaction in Pbrm1 KO liver. ( D ) Quantification of SOX9-positive hepatocytes in the livers of WT and Pbrm1 KO mice post-DDC diet treatment (n = 14 for each group). ( E and F ) RNA-seq data shows downregulation of hepatocyte markers Fabp1 and C2, and upregulation of cholangiocyte marker Krt19 and progenitor marker Lgr5 in Pbrm1 KO mice on the DDC diet ( E ), with no differences observed in untreated mice (n = 3 for each group) ( F ). ( G ) Forty-eight hours post-partial hepatectomy, the liver-to-body weight ratio, an indicator of liver regeneration, shows no significant difference between Pbrm1 KO (n = 5) and WT mice (n = 7). ∗ P < .05; ∗∗ P < .01; and ∗∗∗ P < .001. Scale bars for ( A ): 500 μm; for ( C ) and ( D ): 100 μm.

Techniques Used: Activation Assay, Staining, Immunostaining, Expressing, RNA Sequencing, Marker

Loss of Pbrm1 reduces chromatin accessibility of genes associated with hepatocyte differentiation. ( A ) ATAC-seq peaks are concentrated near TSSs in both WT and Pbrm1 KO livers. ( B ) Overall decrease in chromatin accessibility observed in Pbrm1 KO livers. ( C ) ATAC-seq reveals reduced chromatin accessibility in liver-specific genes, particularly those related to hepatocyte differentiation and metabolism, in Pbrm1 KO livers. ( D ) ATAC-seq shows decreased chromatin accessibility in genes downregulated during tumor progression in Pbrm1 KO livers. ( E ) ATAC-seq demonstrates reduced accessibility in genes regulated by hepatocyte-enriched transcription factors such as HNF-4α, HNF-1α, and FOXA2 in Pbrm1 KO livers. ( F ) Motif analysis indicates diminished accessibility at binding sites for liver-enriched transcription factors KLF15, HNF-1α, HNF-4α, and CEBPA in Pbrm1 KO livers. ( G ) Two gene sets linked with H3K27me3 show increased accessibility in Pbrm1 KO livers. (n = 3 for each group).

Figure Legend Snippet: Loss of Pbrm1 reduces chromatin accessibility of genes associated with hepatocyte differentiation. ( A ) ATAC-seq peaks are concentrated near TSSs in both WT and Pbrm1 KO livers. ( B ) Overall decrease in chromatin accessibility observed in Pbrm1 KO livers. ( C ) ATAC-seq reveals reduced chromatin accessibility in liver-specific genes, particularly those related to hepatocyte differentiation and metabolism, in Pbrm1 KO livers. ( D ) ATAC-seq shows decreased chromatin accessibility in genes downregulated during tumor progression in Pbrm1 KO livers. ( E ) ATAC-seq demonstrates reduced accessibility in genes regulated by hepatocyte-enriched transcription factors such as HNF-4α, HNF-1α, and FOXA2 in Pbrm1 KO livers. ( F ) Motif analysis indicates diminished accessibility at binding sites for liver-enriched transcription factors KLF15, HNF-1α, HNF-4α, and CEBPA in Pbrm1 KO livers. ( G ) Two gene sets linked with H3K27me3 show increased accessibility in Pbrm1 KO livers. (n = 3 for each group).

Techniques Used: Binding Assay

Correlation between chromatin accessibility and RNA expression in mice with or without DDC diet treatment. ( A ) Volcano plots display differentially expressed genes between Pbrm1 KO and WT livers, both with and without DDC diet treatment. Pbrm1 KO livers exhibit a greater number of downregulated genes compared with WT in both conditions. ( B ) Correlation analysis of RNA expression and chromatin accessibility in Pbrm1 KO and WT livers with or without DDC diet treatment. ( C and D ) Pathway analysis of genes that are downregulated and exhibit reduced chromatin accessibility in Pbrm1 KO livers without ( C ) and with ( D ) DDC diet treatment. ( E and F ) Inhbe ( E ) and Fads1 ( F ) show reduced chromatin accessibility in Pbrm1 KO livers without DDC diet treatment, whereas RNA expression remains similar between Pbrm1 KO and WT. However, after DDC diet treatment, RNA expression of these genes decreases in Pbrm1 KO mice. (n = 3 for each group).

Figure Legend Snippet: Correlation between chromatin accessibility and RNA expression in mice with or without DDC diet treatment. ( A ) Volcano plots display differentially expressed genes between Pbrm1 KO and WT livers, both with and without DDC diet treatment. Pbrm1 KO livers exhibit a greater number of downregulated genes compared with WT in both conditions. ( B ) Correlation analysis of RNA expression and chromatin accessibility in Pbrm1 KO and WT livers with or without DDC diet treatment. ( C and D ) Pathway analysis of genes that are downregulated and exhibit reduced chromatin accessibility in Pbrm1 KO livers without ( C ) and with ( D ) DDC diet treatment. ( E and F ) Inhbe ( E ) and Fads1 ( F ) show reduced chromatin accessibility in Pbrm1 KO livers without DDC diet treatment, whereas RNA expression remains similar between Pbrm1 KO and WT. However, after DDC diet treatment, RNA expression of these genes decreases in Pbrm1 KO mice. (n = 3 for each group).

Techniques Used: RNA Expression

Loss of Pbrm1 increases vulnerability to high-fat diet-induced fatty liver. ( A ) After high-fat diet treatment, the liver weight/body weight ratio is increased in Pbrm1 KO mice (n = 7 for each group). ( B and C ) Following high-fat diet treatment, Pbrm1 KO livers exhibit more pronounced fatty changes in H&E-stained histological sections (n = 7 for each group). Scale bar: 500 μm. ( D and E ) Fresh frozen liver specimens stained with Oil Red show increased fat droplet accumulation in Pbrm1 KO liver, with quantification of fat-occupied areas (n = 7 for each group). Scale bar: 500 μm. ( F ) Quantification of triglyceride levels in Pbrm1 KO and WT livers using a colorimetric assay (n = 6 for each group). ( G and H ) Serum levels of AST ( G ) and ALT ( H ) are similar in both Pbrm1 KO and WT mice after high-fat diet treatment (n = 7 for each group). ∗ P < .05 and ∗∗ P < .01.

Figure Legend Snippet: Loss of Pbrm1 increases vulnerability to high-fat diet-induced fatty liver. ( A ) After high-fat diet treatment, the liver weight/body weight ratio is increased in Pbrm1 KO mice (n = 7 for each group). ( B and C ) Following high-fat diet treatment, Pbrm1 KO livers exhibit more pronounced fatty changes in H&E-stained histological sections (n = 7 for each group). Scale bar: 500 μm. ( D and E ) Fresh frozen liver specimens stained with Oil Red show increased fat droplet accumulation in Pbrm1 KO liver, with quantification of fat-occupied areas (n = 7 for each group). Scale bar: 500 μm. ( F ) Quantification of triglyceride levels in Pbrm1 KO and WT livers using a colorimetric assay (n = 6 for each group). ( G and H ) Serum levels of AST ( G ) and ALT ( H ) are similar in both Pbrm1 KO and WT mice after high-fat diet treatment (n = 7 for each group). ∗ P < .05 and ∗∗ P < .01.

Techniques Used: Staining, Colorimetric Assay

Interaction between Pbrm1 loss and mutant KRAS in iCCA development. ( A ) Schematic overview of the mouse tumorigenesis model. ( B ) Kaplan-Meier analysis comparing AK (n = 8) and AKP male mice (n = 9) showing the time until illness requiring euthanasia or up to 12 months. ( C ) Representative images of AK and AKP livers, both displaying multiple tumors. ( D ) Histological images showing HCC in an AK mouse and iCCA in an AKP mouse. Scale bar: 100 μm. ( E – G ) Age-matched AKP livers have a higher density of iCCAs per unit area ( E ), whereas the number of hepatocellular neoplasms (HCA and HCC) is similar between AK and AKP livers ( F ). The percentage of iCCAs in the total tumor count is significantly higher in AKP livers ( G ). ( H ) Photographs of 2 AK livers with a dominant HCC in each liver. ( I ) The total tumor areas per unit area is larger in AK livers. ( J ) The total iCCA tumor areas per unit area is larger in AKP livers. ( K ) The total hepatocellular neoplasm tumor areas per unit area is larger in AK livers. (n = 6 for AK mice and n = 5 for AKP mice in E – K ). ∗ P < .05; ∗∗ P < .01; and ∗∗∗ P < .001.

Figure Legend Snippet: Interaction between Pbrm1 loss and mutant KRAS in iCCA development. ( A ) Schematic overview of the mouse tumorigenesis model. ( B ) Kaplan-Meier analysis comparing AK (n = 8) and AKP male mice (n = 9) showing the time until illness requiring euthanasia or up to 12 months. ( C ) Representative images of AK and AKP livers, both displaying multiple tumors. ( D ) Histological images showing HCC in an AK mouse and iCCA in an AKP mouse. Scale bar: 100 μm. ( E – G ) Age-matched AKP livers have a higher density of iCCAs per unit area ( E ), whereas the number of hepatocellular neoplasms (HCA and HCC) is similar between AK and AKP livers ( F ). The percentage of iCCAs in the total tumor count is significantly higher in AKP livers ( G ). ( H ) Photographs of 2 AK livers with a dominant HCC in each liver. ( I ) The total tumor areas per unit area is larger in AK livers. ( J ) The total iCCA tumor areas per unit area is larger in AKP livers. ( K ) The total hepatocellular neoplasm tumor areas per unit area is larger in AK livers. (n = 6 for AK mice and n = 5 for AKP mice in E – K ). ∗ P < .05; ∗∗ P < .01; and ∗∗∗ P < .001.

Techniques Used: Mutagenesis

Representative histology and immunophenotype of tumors from AKP and AK mice. ( A – F ) Histology and immunophenotype of an iCCA derived from an AKP liver. Low magnification ( A , 40×) and high magnification ( B , 200×) views of an H&E-stained section show tumor cells arranged in glandular patterns or as isolated cells within a fibrous stroma. IHC analysis reveals that the tumor cells do not express PBRM1 ( C ) or HNF-4α ( D ), but are positive for KRT19 ( E ) and SOX9 ( F ). Histology and immunophenotype analysis of an HCC derived from an AK liver. ( G and H ) Low magnification ( G , 40×) and high magnification ( H , 200×) views of an H&E-stained section reveal tumor cells with abundant eosinophilic cytoplasm arranged in trabecular patterns. IHC staining shows that the tumor cells express PBRM1 ( I ) and HNF-4α ( J ), but lack expression of KRT19 ( K ) and SOX9 ( L ). Scale bars for ( A ) and ( G ): 500 μm; B - F and H - L : 100 μm.

Figure Legend Snippet: Representative histology and immunophenotype of tumors from AKP and AK mice. ( A – F ) Histology and immunophenotype of an iCCA derived from an AKP liver. Low magnification ( A , 40×) and high magnification ( B , 200×) views of an H&E-stained section show tumor cells arranged in glandular patterns or as isolated cells within a fibrous stroma. IHC analysis reveals that the tumor cells do not express PBRM1 ( C ) or HNF-4α ( D ), but are positive for KRT19 ( E ) and SOX9 ( F ). Histology and immunophenotype analysis of an HCC derived from an AK liver. ( G and H ) Low magnification ( G , 40×) and high magnification ( H , 200×) views of an H&E-stained section reveal tumor cells with abundant eosinophilic cytoplasm arranged in trabecular patterns. IHC staining shows that the tumor cells express PBRM1 ( I ) and HNF-4α ( J ), but lack expression of KRT19 ( K ) and SOX9 ( L ). Scale bars for ( A ) and ( G ): 500 μm; B - F and H - L : 100 μm.

Techniques Used: Derivative Assay, Staining, Isolation, Immunohistochemistry, Expressing

Image Search Results

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Pbrm1 Loss Induces a Permissive Chromatin State for Cholangiocytic Differentiation and Cholangiocarcinoma Formation

doi: 10.1016/j.jcmgh.2025.101720

Figure Lengend Snippet: Loss of Pbrm1 enhances the activation of hepatic progenitor cells in response to cholestatic injury. ( A ) Immunohistochemical staining confirms the loss of PBRM1 expression in hepatocytes and cholangiocytes in the interlobular bile ducts of Pbrm1 KO mice. Scale bar: 100 μm. ( B ) Overview of the DDC diet treatment protocol. ( C – G ) Serum levels of AST ( C ), ALT ( D ), total bilirubin ( E ), direct bilirubin ( F ), and ALP ( G ) in WT and Pbrm1 KO mice following DDC diet treatment (n = 11 for each group for A – E , n = 5 for each group for F and G ). ∗ P < .05 and ∗∗ P < .01.

Article Snippet: The Pbrm1 f/f strain (B6;129- Pbrm1 tm1Zhwa/J ), Kras LSL-G12D strain (B6.129S4- Kras tm4Tyj/J ), and Alb -Cre strain (B6.Cg-Speer6-ps1 Tg( Alb -cre)21Mgn/J ) were obtained from the Jackson Laboratories.

Techniques: Activation Assay, Immunohistochemical staining, Staining, Expressing

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Pbrm1 Loss Induces a Permissive Chromatin State for Cholangiocytic Differentiation and Cholangiocarcinoma Formation

doi: 10.1016/j.jcmgh.2025.101720

Figure Lengend Snippet: Histologic and molecular evidence of enhanced hepatic progenitor cell activation in response to cholestatic injury in Pbrm1 KO liver. ( A ) Histological analysis of H&E and KRT19-stained sections reveals increased bile ductular proliferation in the livers of Pbrm1 KO mice after DDC diet treatment. ( B ) Quantification of KRT19-positive areas in the livers of WT and Pbrm1 KO mice post-DDC diet treatment (n = 14 for each group). ( C ) Immunostaining demonstrates loss of PBRM1 expression in exaggerated ductular reaction in Pbrm1 KO liver. ( D ) Quantification of SOX9-positive hepatocytes in the livers of WT and Pbrm1 KO mice post-DDC diet treatment (n = 14 for each group). ( E and F ) RNA-seq data shows downregulation of hepatocyte markers Fabp1 and C2, and upregulation of cholangiocyte marker Krt19 and progenitor marker Lgr5 in Pbrm1 KO mice on the DDC diet ( E ), with no differences observed in untreated mice (n = 3 for each group) ( F ). ( G ) Forty-eight hours post-partial hepatectomy, the liver-to-body weight ratio, an indicator of liver regeneration, shows no significant difference between Pbrm1 KO (n = 5) and WT mice (n = 7). ∗ P < .05; ∗∗ P < .01; and ∗∗∗ P < .001. Scale bars for ( A ): 500 μm; for ( C ) and ( D ): 100 μm.

Techniques: Activation Assay, Staining, Immunostaining, Expressing, RNA Sequencing, Marker

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Pbrm1 Loss Induces a Permissive Chromatin State for Cholangiocytic Differentiation and Cholangiocarcinoma Formation

doi: 10.1016/j.jcmgh.2025.101720

Figure Lengend Snippet: Loss of Pbrm1 reduces chromatin accessibility of genes associated with hepatocyte differentiation. ( A ) ATAC-seq peaks are concentrated near TSSs in both WT and Pbrm1 KO livers. ( B ) Overall decrease in chromatin accessibility observed in Pbrm1 KO livers. ( C ) ATAC-seq reveals reduced chromatin accessibility in liver-specific genes, particularly those related to hepatocyte differentiation and metabolism, in Pbrm1 KO livers. ( D ) ATAC-seq shows decreased chromatin accessibility in genes downregulated during tumor progression in Pbrm1 KO livers. ( E ) ATAC-seq demonstrates reduced accessibility in genes regulated by hepatocyte-enriched transcription factors such as HNF-4α, HNF-1α, and FOXA2 in Pbrm1 KO livers. ( F ) Motif analysis indicates diminished accessibility at binding sites for liver-enriched transcription factors KLF15, HNF-1α, HNF-4α, and CEBPA in Pbrm1 KO livers. ( G ) Two gene sets linked with H3K27me3 show increased accessibility in Pbrm1 KO livers. (n = 3 for each group).

Techniques: Binding Assay

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Pbrm1 Loss Induces a Permissive Chromatin State for Cholangiocytic Differentiation and Cholangiocarcinoma Formation

doi: 10.1016/j.jcmgh.2025.101720

Figure Lengend Snippet: Correlation between chromatin accessibility and RNA expression in mice with or without DDC diet treatment. ( A ) Volcano plots display differentially expressed genes between Pbrm1 KO and WT livers, both with and without DDC diet treatment. Pbrm1 KO livers exhibit a greater number of downregulated genes compared with WT in both conditions. ( B ) Correlation analysis of RNA expression and chromatin accessibility in Pbrm1 KO and WT livers with or without DDC diet treatment. ( C and D ) Pathway analysis of genes that are downregulated and exhibit reduced chromatin accessibility in Pbrm1 KO livers without ( C ) and with ( D ) DDC diet treatment. ( E and F ) Inhbe ( E ) and Fads1 ( F ) show reduced chromatin accessibility in Pbrm1 KO livers without DDC diet treatment, whereas RNA expression remains similar between Pbrm1 KO and WT. However, after DDC diet treatment, RNA expression of these genes decreases in Pbrm1 KO mice. (n = 3 for each group).

Techniques: RNA Expression

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Pbrm1 Loss Induces a Permissive Chromatin State for Cholangiocytic Differentiation and Cholangiocarcinoma Formation

doi: 10.1016/j.jcmgh.2025.101720

Figure Lengend Snippet: Loss of Pbrm1 increases vulnerability to high-fat diet-induced fatty liver. ( A ) After high-fat diet treatment, the liver weight/body weight ratio is increased in Pbrm1 KO mice (n = 7 for each group). ( B and C ) Following high-fat diet treatment, Pbrm1 KO livers exhibit more pronounced fatty changes in H&E-stained histological sections (n = 7 for each group). Scale bar: 500 μm. ( D and E ) Fresh frozen liver specimens stained with Oil Red show increased fat droplet accumulation in Pbrm1 KO liver, with quantification of fat-occupied areas (n = 7 for each group). Scale bar: 500 μm. ( F ) Quantification of triglyceride levels in Pbrm1 KO and WT livers using a colorimetric assay (n = 6 for each group). ( G and H ) Serum levels of AST ( G ) and ALT ( H ) are similar in both Pbrm1 KO and WT mice after high-fat diet treatment (n = 7 for each group). ∗ P < .05 and ∗∗ P < .01.

Techniques: Staining, Colorimetric Assay

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Pbrm1 Loss Induces a Permissive Chromatin State for Cholangiocytic Differentiation and Cholangiocarcinoma Formation

doi: 10.1016/j.jcmgh.2025.101720

Figure Lengend Snippet: Interaction between Pbrm1 loss and mutant KRAS in iCCA development. ( A ) Schematic overview of the mouse tumorigenesis model. ( B ) Kaplan-Meier analysis comparing AK (n = 8) and AKP male mice (n = 9) showing the time until illness requiring euthanasia or up to 12 months. ( C ) Representative images of AK and AKP livers, both displaying multiple tumors. ( D ) Histological images showing HCC in an AK mouse and iCCA in an AKP mouse. Scale bar: 100 μm. ( E – G ) Age-matched AKP livers have a higher density of iCCAs per unit area ( E ), whereas the number of hepatocellular neoplasms (HCA and HCC) is similar between AK and AKP livers ( F ). The percentage of iCCAs in the total tumor count is significantly higher in AKP livers ( G ). ( H ) Photographs of 2 AK livers with a dominant HCC in each liver. ( I ) The total tumor areas per unit area is larger in AK livers. ( J ) The total iCCA tumor areas per unit area is larger in AKP livers. ( K ) The total hepatocellular neoplasm tumor areas per unit area is larger in AK livers. (n = 6 for AK mice and n = 5 for AKP mice in E – K ). ∗ P < .05; ∗∗ P < .01; and ∗∗∗ P < .001.

Techniques: Mutagenesis

Journal: Cellular and Molecular Gastroenterology and Hepatology

Article Title: Pbrm1 Loss Induces a Permissive Chromatin State for Cholangiocytic Differentiation and Cholangiocarcinoma Formation

doi: 10.1016/j.jcmgh.2025.101720

Figure Lengend Snippet: Representative histology and immunophenotype of tumors from AKP and AK mice. ( A – F ) Histology and immunophenotype of an iCCA derived from an AKP liver. Low magnification ( A , 40×) and high magnification ( B , 200×) views of an H&E-stained section show tumor cells arranged in glandular patterns or as isolated cells within a fibrous stroma. IHC analysis reveals that the tumor cells do not express PBRM1 ( C ) or HNF-4α ( D ), but are positive for KRT19 ( E ) and SOX9 ( F ). Histology and immunophenotype analysis of an HCC derived from an AK liver. ( G and H ) Low magnification ( G , 40×) and high magnification ( H , 200×) views of an H&E-stained section reveal tumor cells with abundant eosinophilic cytoplasm arranged in trabecular patterns. IHC staining shows that the tumor cells express PBRM1 ( I ) and HNF-4α ( J ), but lack expression of KRT19 ( K ) and SOX9 ( L ). Scale bars for ( A ) and ( G ): 500 μm; B - F and H - L : 100 μm.

Techniques: Derivative Assay, Staining, Isolation, Immunohistochemistry, Expressing

Reduced proportion of iNKT cells in the periphery of Pbrm1 deficient mice. Eight‐week‐old Lckcre + Pbrm1 +/+ (WT) and Lckcre + Pbrm1 f/f (KO) mice were analyzed for CD4 + T cells, CD8 + T cells and iNKT cells by flow cytometry ( n = 3). (A) Representative FACS plots of CD4 + and CD8 + T cells in the thymi and spleens from WT and Pbrm1 KO mice. (B, C) Statistical percentages of CD4 + and CD8 + thymocytes. (D, E) Statistical percentages of CD4 + and CD8 + splenocytes. (F) Representative FACS plots of CD3 and CD1d‐tetramer staining for thymocytes and splenocytes. (G, H) Percentages and numbers of thymic iNKT cells from WT and Pbrm1 KO mice. (I, J) Percentages and numbers of iNKT cells in the spleens from WT and Pbrm1 KO mice. The results shown are representative of three independent experiments. ** p < 0.01. Data were shown as Mean ± SD

Journal: Journal of Cellular and Molecular Medicine

Article Title: Pbrm1 intrinsically controls the development and effector differentiation of iNKT cells

doi: 10.1111/jcmm.17445

Figure Lengend Snippet: Reduced proportion of iNKT cells in the periphery of Pbrm1 deficient mice. Eight‐week‐old Lckcre + Pbrm1 +/+ (WT) and Lckcre + Pbrm1 f/f (KO) mice were analyzed for CD4 + T cells, CD8 + T cells and iNKT cells by flow cytometry ( n = 3). (A) Representative FACS plots of CD4 + and CD8 + T cells in the thymi and spleens from WT and Pbrm1 KO mice. (B, C) Statistical percentages of CD4 + and CD8 + thymocytes. (D, E) Statistical percentages of CD4 + and CD8 + splenocytes. (F) Representative FACS plots of CD3 and CD1d‐tetramer staining for thymocytes and splenocytes. (G, H) Percentages and numbers of thymic iNKT cells from WT and Pbrm1 KO mice. (I, J) Percentages and numbers of iNKT cells in the spleens from WT and Pbrm1 KO mice. The results shown are representative of three independent experiments. ** p < 0.01. Data were shown as Mean ± SD

Article Snippet: The Pbrm1 f/f strain was purchased from The Jackson Laboratory.

Techniques: Flow Cytometry, Staining

Pbrm1 is intrinsically required for the presence of iNKT cells in the periphery. CD45.1 + WT mice were irradiated with 7.5 Gy X‐ray and injected with lineage negative bone marrow cells from CD45.2 + Lckcre + Pbrm1 +/+ (WT) or Lckcre + Pbrm1 f/f (KO), respectively. Recipient mice were sacrificed and analyzed 7 weeks after transplantation ( n = 3). (A) Representative FACS plots showing CD3 + and CD1d‐tetramer + iNKT cells from the thymi and spleens. (B) Statistical frequency and numbers of thymic iNKT cells from WT and Pbrm1 KO mice. (C) Statistical frequency and numbers of iNKT cells in the spleens from WT and Pbrm1 KO mice. The results shown are representative of three independent experiments. * p < 0.05. Data were shown as Mean ± SD

Journal: Journal of Cellular and Molecular Medicine

Article Title: Pbrm1 intrinsically controls the development and effector differentiation of iNKT cells

doi: 10.1111/jcmm.17445

Figure Lengend Snippet: Pbrm1 is intrinsically required for the presence of iNKT cells in the periphery. CD45.1 + WT mice were irradiated with 7.5 Gy X‐ray and injected with lineage negative bone marrow cells from CD45.2 + Lckcre + Pbrm1 +/+ (WT) or Lckcre + Pbrm1 f/f (KO), respectively. Recipient mice were sacrificed and analyzed 7 weeks after transplantation ( n = 3). (A) Representative FACS plots showing CD3 + and CD1d‐tetramer + iNKT cells from the thymi and spleens. (B) Statistical frequency and numbers of thymic iNKT cells from WT and Pbrm1 KO mice. (C) Statistical frequency and numbers of iNKT cells in the spleens from WT and Pbrm1 KO mice. The results shown are representative of three independent experiments. * p < 0.05. Data were shown as Mean ± SD

Article Snippet: The Pbrm1 f/f strain was purchased from The Jackson Laboratory.

Techniques: Irradiation, Injection, Transplantation Assay

Pbrm1 deficiency has no effect on iNKT cell proliferation and survival. 1 mg of BrdU per mouse was i.p. injected to WT and Pbrm1 KO mice. 4 hours post injection, the thymi and spleens were harvested for FACS analysis ( n = 3). (A) Representative FACS plots of CD1d‐tetramer and BrdU staining for thymic iNKT cells from WT and Pbrm1 KO mice. (B) Statistical frequency of BrdU + cells in thymic iNKT cells. (C) Representative histograms of Annexin V staining of iNKT cells in the thymi. (D) Statistical frequency of Annexin V + cells in thymic iNKT cells. (E) Representative FACS plots of CD1d‐tetramer and BrdU staining in the spleens. (F) Statistical percentage of BrdU + cells in iNKT cells from the spleens. (G) Representative histograms of Annexin V staining of iNKT cells in the spleens. (H) Statistical percentage of Annexin V + cells in iNKT cells from the spleens. The results shown are representative of three independent experiments

Journal: Journal of Cellular and Molecular Medicine

Article Title: Pbrm1 intrinsically controls the development and effector differentiation of iNKT cells

doi: 10.1111/jcmm.17445

Figure Lengend Snippet: Pbrm1 deficiency has no effect on iNKT cell proliferation and survival. 1 mg of BrdU per mouse was i.p. injected to WT and Pbrm1 KO mice. 4 hours post injection, the thymi and spleens were harvested for FACS analysis ( n = 3). (A) Representative FACS plots of CD1d‐tetramer and BrdU staining for thymic iNKT cells from WT and Pbrm1 KO mice. (B) Statistical frequency of BrdU + cells in thymic iNKT cells. (C) Representative histograms of Annexin V staining of iNKT cells in the thymi. (D) Statistical frequency of Annexin V + cells in thymic iNKT cells. (E) Representative FACS plots of CD1d‐tetramer and BrdU staining in the spleens. (F) Statistical percentage of BrdU + cells in iNKT cells from the spleens. (G) Representative histograms of Annexin V staining of iNKT cells in the spleens. (H) Statistical percentage of Annexin V + cells in iNKT cells from the spleens. The results shown are representative of three independent experiments

Article Snippet: The Pbrm1 f/f strain was purchased from The Jackson Laboratory.

Techniques: Injection, BrdU Staining, Staining

Effect of Pbrm1 deletion on developmental stages of iNKT cells. (A) Representative FACS plots showing developmental stages of iNKT cells from the the thymi. The developmental stages of thymic iNKT cells were analyzed based on the expression of CD24, CD44 and NK1.1. The upper plots are gated on CD1d‐tetramer + cells and the lower plots are gated on CD24 − CD1d‐tetramer + cells. (B) Statistical frequency of iNKT cells at different developmental stages for (A). (C) Representative FACS plot showing developmental stages of iNKT cells from the thymi of mixed bone marrow chimeric mice as described in Figure . (D) Statistical frequency of iNKT cells at the indicated developmental stages for (C). n = 3 for each group. The results shown are representative of three independent experiments. * p < 0.05; ** p < 0.01. Data were shown as Mean ± SD

Journal: Journal of Cellular and Molecular Medicine

Article Title: Pbrm1 intrinsically controls the development and effector differentiation of iNKT cells

doi: 10.1111/jcmm.17445

Figure Lengend Snippet: Effect of Pbrm1 deletion on developmental stages of iNKT cells. (A) Representative FACS plots showing developmental stages of iNKT cells from the the thymi. The developmental stages of thymic iNKT cells were analyzed based on the expression of CD24, CD44 and NK1.1. The upper plots are gated on CD1d‐tetramer + cells and the lower plots are gated on CD24 − CD1d‐tetramer + cells. (B) Statistical frequency of iNKT cells at different developmental stages for (A). (C) Representative FACS plot showing developmental stages of iNKT cells from the thymi of mixed bone marrow chimeric mice as described in Figure . (D) Statistical frequency of iNKT cells at the indicated developmental stages for (C). n = 3 for each group. The results shown are representative of three independent experiments. * p < 0.05; ** p < 0.01. Data were shown as Mean ± SD

Article Snippet: The Pbrm1 f/f strain was purchased from The Jackson Laboratory.

Techniques: Expressing

Pbrm1 deletion impairs iNKT17 cell differentiation, but not iNKT1 and iNKT2 generation. Eight‐week‐old Lckcre + Pbrm1 +/+ (WT) and Lckcre + Pbrm1 f/f (KO) mice were analyzed for iNKT cells differentiation in both thymus and spleen by flow cytometry ( n = 3). (A) PLZF and RORγt staining of thymic and splenic iNKT cells. iNKT cell effector lineages were in the indicated FACS plot. (B) Percentages and cell numbers of iNKT effector lineages in the thymi. (C) Percentages and cell numbers of iNKT effector lineages in the spleens. (D) The overlay histogram of RORγt expression in thymic iNKT17 cells from WT and Pbrm1 KO mice. (E) Mean fluorescence intensity (MFI) of RORγt expression in thymic iNKT17 cells from WT and Pbrm1 KO mice. The results shown are representative of three independent experiments. * p < 0.05; ** p < 0.01; *** p < 0.001. Data were shown as Mean ± SD

Journal: Journal of Cellular and Molecular Medicine

Article Title: Pbrm1 intrinsically controls the development and effector differentiation of iNKT cells

doi: 10.1111/jcmm.17445

Figure Lengend Snippet: Pbrm1 deletion impairs iNKT17 cell differentiation, but not iNKT1 and iNKT2 generation. Eight‐week‐old Lckcre + Pbrm1 +/+ (WT) and Lckcre + Pbrm1 f/f (KO) mice were analyzed for iNKT cells differentiation in both thymus and spleen by flow cytometry ( n = 3). (A) PLZF and RORγt staining of thymic and splenic iNKT cells. iNKT cell effector lineages were in the indicated FACS plot. (B) Percentages and cell numbers of iNKT effector lineages in the thymi. (C) Percentages and cell numbers of iNKT effector lineages in the spleens. (D) The overlay histogram of RORγt expression in thymic iNKT17 cells from WT and Pbrm1 KO mice. (E) Mean fluorescence intensity (MFI) of RORγt expression in thymic iNKT17 cells from WT and Pbrm1 KO mice. The results shown are representative of three independent experiments. * p < 0.05; ** p < 0.01; *** p < 0.001. Data were shown as Mean ± SD

Article Snippet: The Pbrm1 f/f strain was purchased from The Jackson Laboratory.

Techniques: Cell Differentiation, Flow Cytometry, Staining, Expressing, Fluorescence

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1) Product Images from "Pbrm1 Loss Induces a Permissive Chromatin State for Cholangiocytic Differentiation and Cholangiocarcinoma Formation"

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