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bcl10 mutations  (TargetMol)


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    TargetMol bcl10 mutations
    Fig. 1 Gene expression impact of <t>BCL10</t> mutations. A Heatmap of differentially expressed genes in RIVA cells containing vector or BCL10 mutants, (FC ≥1.5x up or down). B Venn diagram of the number of differentially expressed genes in BCL10 mutants compared to vector. C Top 10 upregulated (adjusted p value ≤0.001) Jensen compartment complexes using genes upregulated with a FC ≥2. D The top overlapping Hallmark gene set pathways upregulated (FDR q-value ≤0.25) in BCL10 mutants. E Western blot of RIVA and HBL1 cells induced with doxycycline for 24 h and probed as indicated. F TNFα ELISA assay on cell supernatant from RIVA, HBL1, and U2932 cells containing vector or BCL10 mutants. G Boxplot of gene expression levels of TNFRSF13B and USP2 of untreated DLBCL cases comparing mutant versus wildtype BCL10 cases.
    Bcl10 Mutations, supplied by TargetMol, used in various techniques. Bioz Stars score: 93/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/bcl10 mutations/product/TargetMol
    Average 93 stars, based on 2 article reviews
    bcl10 mutations - by Bioz Stars, 2026-04
    93/100 stars

    Images

    1) Product Images from "Bruton's tyrosine kinase inhibition re-sensitizes multidrug-resistant DLBCL tumors driven by BCL10 gain-of-function mutants to venetoclax."

    Article Title: Bruton's tyrosine kinase inhibition re-sensitizes multidrug-resistant DLBCL tumors driven by BCL10 gain-of-function mutants to venetoclax.

    Journal: Blood cancer journal

    doi: 10.1038/s41408-025-01214-y

    Fig. 1 Gene expression impact of BCL10 mutations. A Heatmap of differentially expressed genes in RIVA cells containing vector or BCL10 mutants, (FC ≥1.5x up or down). B Venn diagram of the number of differentially expressed genes in BCL10 mutants compared to vector. C Top 10 upregulated (adjusted p value ≤0.001) Jensen compartment complexes using genes upregulated with a FC ≥2. D The top overlapping Hallmark gene set pathways upregulated (FDR q-value ≤0.25) in BCL10 mutants. E Western blot of RIVA and HBL1 cells induced with doxycycline for 24 h and probed as indicated. F TNFα ELISA assay on cell supernatant from RIVA, HBL1, and U2932 cells containing vector or BCL10 mutants. G Boxplot of gene expression levels of TNFRSF13B and USP2 of untreated DLBCL cases comparing mutant versus wildtype BCL10 cases.
    Figure Legend Snippet: Fig. 1 Gene expression impact of BCL10 mutations. A Heatmap of differentially expressed genes in RIVA cells containing vector or BCL10 mutants, (FC ≥1.5x up or down). B Venn diagram of the number of differentially expressed genes in BCL10 mutants compared to vector. C Top 10 upregulated (adjusted p value ≤0.001) Jensen compartment complexes using genes upregulated with a FC ≥2. D The top overlapping Hallmark gene set pathways upregulated (FDR q-value ≤0.25) in BCL10 mutants. E Western blot of RIVA and HBL1 cells induced with doxycycline for 24 h and probed as indicated. F TNFα ELISA assay on cell supernatant from RIVA, HBL1, and U2932 cells containing vector or BCL10 mutants. G Boxplot of gene expression levels of TNFRSF13B and USP2 of untreated DLBCL cases comparing mutant versus wildtype BCL10 cases.

    Techniques Used: Gene Expression, Plasmid Preparation, Western Blot, Enzyme-linked Immunosorbent Assay, Mutagenesis

    Fig. 3 BCL10 mutants mediate lymphomagenesis through activation of key transcription factors. A Genes that were upregulated (FC ≥2) in both mutants were analyzed for enrichment in regulation by transcription factors from the ENCODE project through the online transcription factor analysis tool ChIP-X Enrichment Analysis Version 3 (ChEA3). Sixteen transcription factors were significantly upregulated in BCL10 mutants (FDR ≤0.05). B Schematic of transcription factors identified to be upregulated in (A). C Boxplot of gene expression levels of BATF and IRF4 of untreated DLBCL cases comparing mutant versus wildtype BCL10 cases. D Western blot of RIVA and HBL1 cells induced with doxycycline for 24 h and probed as indicated. E Western blot of RIVA and U2932 cells induced with doxycycline for 24 h and probed as indicated. F ELISA assays in RIVA AND U2932 cell supernatant probing for CXCL10 (RIVA - S136X: p = 0.0046, R58Q: p = 0.0003, U2932- S136X: p = 0.0003, R58Q: p = 0.0028).
    Figure Legend Snippet: Fig. 3 BCL10 mutants mediate lymphomagenesis through activation of key transcription factors. A Genes that were upregulated (FC ≥2) in both mutants were analyzed for enrichment in regulation by transcription factors from the ENCODE project through the online transcription factor analysis tool ChIP-X Enrichment Analysis Version 3 (ChEA3). Sixteen transcription factors were significantly upregulated in BCL10 mutants (FDR ≤0.05). B Schematic of transcription factors identified to be upregulated in (A). C Boxplot of gene expression levels of BATF and IRF4 of untreated DLBCL cases comparing mutant versus wildtype BCL10 cases. D Western blot of RIVA and HBL1 cells induced with doxycycline for 24 h and probed as indicated. E Western blot of RIVA and U2932 cells induced with doxycycline for 24 h and probed as indicated. F ELISA assays in RIVA AND U2932 cell supernatant probing for CXCL10 (RIVA - S136X: p = 0.0046, R58Q: p = 0.0003, U2932- S136X: p = 0.0003, R58Q: p = 0.0028).

    Techniques Used: Activation Assay, Gene Expression, Mutagenesis, Western Blot, Enzyme-linked Immunosorbent Assay

    Fig. 4 BCL10 mutants drive resistance to multiple drug classes. A Dose response viability assays of RIVA cells treated with pirtobrutinib (S136X: p = 0.033, R58Q: p = 0.019), acalabrutinib (S136X: p = 0.07, R58Q: p = 0.07), and ibrutinib (S136X: p = 0.023, R58Q: p = < 0.0001). B Epigenetic Library (TargetMol) on doxycycline induced RIVA cells. Hits are compounds that significantly inhibited cell viability and compounds that had an increase or decrease in viability two standard deviations from the mean of the difference between BCL10 S136X and vector after 72 h of 10 μM drug treatment. Targets in red highlight mutant-driven resistance, mutant-sensitive targets are in blue, and compounds that sensitized both vector and BCL10 S136X are in purple. C Schematic of hits from 4B. D Dose response viability assays of RIVA cells treated with selcidemstat (p=ns), tovorafenib (p = ns), ulixertinib (S136X: p = 0.0125, R58Q: p = 0.0103), JNKi (p = ns), duvelisib (S136X: p = 0.126, R58Q: p = 0.0264), idelalisib (S136X: p = ns, R58Q: p = 0.004), capivasertib (S136X: p = 0.0002, R58Q: p = 0.005), venetoclax (S136X: p = 0.008, R58Q: p = 0. 0.046), and AZD1208 (PIMi) (S136X: p = 0.019, R58Q: p = 0.040).
    Figure Legend Snippet: Fig. 4 BCL10 mutants drive resistance to multiple drug classes. A Dose response viability assays of RIVA cells treated with pirtobrutinib (S136X: p = 0.033, R58Q: p = 0.019), acalabrutinib (S136X: p = 0.07, R58Q: p = 0.07), and ibrutinib (S136X: p = 0.023, R58Q: p = < 0.0001). B Epigenetic Library (TargetMol) on doxycycline induced RIVA cells. Hits are compounds that significantly inhibited cell viability and compounds that had an increase or decrease in viability two standard deviations from the mean of the difference between BCL10 S136X and vector after 72 h of 10 μM drug treatment. Targets in red highlight mutant-driven resistance, mutant-sensitive targets are in blue, and compounds that sensitized both vector and BCL10 S136X are in purple. C Schematic of hits from 4B. D Dose response viability assays of RIVA cells treated with selcidemstat (p=ns), tovorafenib (p = ns), ulixertinib (S136X: p = 0.0125, R58Q: p = 0.0103), JNKi (p = ns), duvelisib (S136X: p = 0.126, R58Q: p = 0.0264), idelalisib (S136X: p = ns, R58Q: p = 0.004), capivasertib (S136X: p = 0.0002, R58Q: p = 0.005), venetoclax (S136X: p = 0.008, R58Q: p = 0. 0.046), and AZD1208 (PIMi) (S136X: p = 0.019, R58Q: p = 0.040).

    Techniques Used: Plasmid Preparation, Mutagenesis



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    bcl10 mutations  (TargetMol)
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    TargetMol bcl10 mutations
    Fig. 1 Gene expression impact of <t>BCL10</t> mutations. A Heatmap of differentially expressed genes in RIVA cells containing vector or BCL10 mutants, (FC ≥1.5x up or down). B Venn diagram of the number of differentially expressed genes in BCL10 mutants compared to vector. C Top 10 upregulated (adjusted p value ≤0.001) Jensen compartment complexes using genes upregulated with a FC ≥2. D The top overlapping Hallmark gene set pathways upregulated (FDR q-value ≤0.25) in BCL10 mutants. E Western blot of RIVA and HBL1 cells induced with doxycycline for 24 h and probed as indicated. F TNFα ELISA assay on cell supernatant from RIVA, HBL1, and U2932 cells containing vector or BCL10 mutants. G Boxplot of gene expression levels of TNFRSF13B and USP2 of untreated DLBCL cases comparing mutant versus wildtype BCL10 cases.
    Bcl10 Mutations, supplied by TargetMol, 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/result/bcl10 mutations/product/TargetMol
    Average 93 stars, based on 1 article reviews
    bcl10 mutations - by Bioz Stars, 2026-04
    93/100 stars
    		  Buy from Supplier

    Image Search Results


    Fig. 1 Gene expression impact of BCL10 mutations. A Heatmap of differentially expressed genes in RIVA cells containing vector or BCL10 mutants, (FC ≥1.5x up or down). B Venn diagram of the number of differentially expressed genes in BCL10 mutants compared to vector. C Top 10 upregulated (adjusted p value ≤0.001) Jensen compartment complexes using genes upregulated with a FC ≥2. D The top overlapping Hallmark gene set pathways upregulated (FDR q-value ≤0.25) in BCL10 mutants. E Western blot of RIVA and HBL1 cells induced with doxycycline for 24 h and probed as indicated. F TNFα ELISA assay on cell supernatant from RIVA, HBL1, and U2932 cells containing vector or BCL10 mutants. G Boxplot of gene expression levels of TNFRSF13B and USP2 of untreated DLBCL cases comparing mutant versus wildtype BCL10 cases.

    Journal: Blood cancer journal

    Article Title: Bruton's tyrosine kinase inhibition re-sensitizes multidrug-resistant DLBCL tumors driven by BCL10 gain-of-function mutants to venetoclax.

    doi: 10.1038/s41408-025-01214-y

    Figure Lengend Snippet: Fig. 1 Gene expression impact of BCL10 mutations. A Heatmap of differentially expressed genes in RIVA cells containing vector or BCL10 mutants, (FC ≥1.5x up or down). B Venn diagram of the number of differentially expressed genes in BCL10 mutants compared to vector. C Top 10 upregulated (adjusted p value ≤0.001) Jensen compartment complexes using genes upregulated with a FC ≥2. D The top overlapping Hallmark gene set pathways upregulated (FDR q-value ≤0.25) in BCL10 mutants. E Western blot of RIVA and HBL1 cells induced with doxycycline for 24 h and probed as indicated. F TNFα ELISA assay on cell supernatant from RIVA, HBL1, and U2932 cells containing vector or BCL10 mutants. G Boxplot of gene expression levels of TNFRSF13B and USP2 of untreated DLBCL cases comparing mutant versus wildtype BCL10 cases.

    Article Snippet: To more fully assess impact of BCL10 mutations on treatment resistance, we interrogated the 960-compound TargetMol Epigenetic Library.

    Techniques: Gene Expression, Plasmid Preparation, Western Blot, Enzyme-linked Immunosorbent Assay, Mutagenesis

    Fig. 3 BCL10 mutants mediate lymphomagenesis through activation of key transcription factors. A Genes that were upregulated (FC ≥2) in both mutants were analyzed for enrichment in regulation by transcription factors from the ENCODE project through the online transcription factor analysis tool ChIP-X Enrichment Analysis Version 3 (ChEA3). Sixteen transcription factors were significantly upregulated in BCL10 mutants (FDR ≤0.05). B Schematic of transcription factors identified to be upregulated in (A). C Boxplot of gene expression levels of BATF and IRF4 of untreated DLBCL cases comparing mutant versus wildtype BCL10 cases. D Western blot of RIVA and HBL1 cells induced with doxycycline for 24 h and probed as indicated. E Western blot of RIVA and U2932 cells induced with doxycycline for 24 h and probed as indicated. F ELISA assays in RIVA AND U2932 cell supernatant probing for CXCL10 (RIVA - S136X: p = 0.0046, R58Q: p = 0.0003, U2932- S136X: p = 0.0003, R58Q: p = 0.0028).

    Journal: Blood cancer journal

    Article Title: Bruton's tyrosine kinase inhibition re-sensitizes multidrug-resistant DLBCL tumors driven by BCL10 gain-of-function mutants to venetoclax.

    doi: 10.1038/s41408-025-01214-y

    Figure Lengend Snippet: Fig. 3 BCL10 mutants mediate lymphomagenesis through activation of key transcription factors. A Genes that were upregulated (FC ≥2) in both mutants were analyzed for enrichment in regulation by transcription factors from the ENCODE project through the online transcription factor analysis tool ChIP-X Enrichment Analysis Version 3 (ChEA3). Sixteen transcription factors were significantly upregulated in BCL10 mutants (FDR ≤0.05). B Schematic of transcription factors identified to be upregulated in (A). C Boxplot of gene expression levels of BATF and IRF4 of untreated DLBCL cases comparing mutant versus wildtype BCL10 cases. D Western blot of RIVA and HBL1 cells induced with doxycycline for 24 h and probed as indicated. E Western blot of RIVA and U2932 cells induced with doxycycline for 24 h and probed as indicated. F ELISA assays in RIVA AND U2932 cell supernatant probing for CXCL10 (RIVA - S136X: p = 0.0046, R58Q: p = 0.0003, U2932- S136X: p = 0.0003, R58Q: p = 0.0028).

    Article Snippet: To more fully assess impact of BCL10 mutations on treatment resistance, we interrogated the 960-compound TargetMol Epigenetic Library.

    Techniques: Activation Assay, Gene Expression, Mutagenesis, Western Blot, Enzyme-linked Immunosorbent Assay

    Fig. 4 BCL10 mutants drive resistance to multiple drug classes. A Dose response viability assays of RIVA cells treated with pirtobrutinib (S136X: p = 0.033, R58Q: p = 0.019), acalabrutinib (S136X: p = 0.07, R58Q: p = 0.07), and ibrutinib (S136X: p = 0.023, R58Q: p = < 0.0001). B Epigenetic Library (TargetMol) on doxycycline induced RIVA cells. Hits are compounds that significantly inhibited cell viability and compounds that had an increase or decrease in viability two standard deviations from the mean of the difference between BCL10 S136X and vector after 72 h of 10 μM drug treatment. Targets in red highlight mutant-driven resistance, mutant-sensitive targets are in blue, and compounds that sensitized both vector and BCL10 S136X are in purple. C Schematic of hits from 4B. D Dose response viability assays of RIVA cells treated with selcidemstat (p=ns), tovorafenib (p = ns), ulixertinib (S136X: p = 0.0125, R58Q: p = 0.0103), JNKi (p = ns), duvelisib (S136X: p = 0.126, R58Q: p = 0.0264), idelalisib (S136X: p = ns, R58Q: p = 0.004), capivasertib (S136X: p = 0.0002, R58Q: p = 0.005), venetoclax (S136X: p = 0.008, R58Q: p = 0. 0.046), and AZD1208 (PIMi) (S136X: p = 0.019, R58Q: p = 0.040).

    Journal: Blood cancer journal

    Article Title: Bruton's tyrosine kinase inhibition re-sensitizes multidrug-resistant DLBCL tumors driven by BCL10 gain-of-function mutants to venetoclax.

    doi: 10.1038/s41408-025-01214-y

    Figure Lengend Snippet: Fig. 4 BCL10 mutants drive resistance to multiple drug classes. A Dose response viability assays of RIVA cells treated with pirtobrutinib (S136X: p = 0.033, R58Q: p = 0.019), acalabrutinib (S136X: p = 0.07, R58Q: p = 0.07), and ibrutinib (S136X: p = 0.023, R58Q: p = < 0.0001). B Epigenetic Library (TargetMol) on doxycycline induced RIVA cells. Hits are compounds that significantly inhibited cell viability and compounds that had an increase or decrease in viability two standard deviations from the mean of the difference between BCL10 S136X and vector after 72 h of 10 μM drug treatment. Targets in red highlight mutant-driven resistance, mutant-sensitive targets are in blue, and compounds that sensitized both vector and BCL10 S136X are in purple. C Schematic of hits from 4B. D Dose response viability assays of RIVA cells treated with selcidemstat (p=ns), tovorafenib (p = ns), ulixertinib (S136X: p = 0.0125, R58Q: p = 0.0103), JNKi (p = ns), duvelisib (S136X: p = 0.126, R58Q: p = 0.0264), idelalisib (S136X: p = ns, R58Q: p = 0.004), capivasertib (S136X: p = 0.0002, R58Q: p = 0.005), venetoclax (S136X: p = 0.008, R58Q: p = 0. 0.046), and AZD1208 (PIMi) (S136X: p = 0.019, R58Q: p = 0.040).

    Article Snippet: To more fully assess impact of BCL10 mutations on treatment resistance, we interrogated the 960-compound TargetMol Epigenetic Library.

    Techniques: Plasmid Preparation, Mutagenesis