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mutant myc  (Addgene inc)


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    Addgene inc mutant myc
    (A) RNF43 -mutant/ RSPO -fusion cancer xenografts were analysed by western blotting for 6 reported substrates of FBXW7. β-actin was used as loading control. Each lane represents an independent tumor. In the panel of SNU1411 ± FBXW7 mutant, ETC-159-treated samples were from the 5 mg/kg group shown in . (B, C) Ectopic expression of human phosphorylation site <t>mutant</t> <t>Cyclin</t> E1 (CCNE1) or <t>MYC</t> that are resistant to GSK3/FBXW7-mediated degradation caused resistance to PORCN inhibition in HPAF-II cells. (B) HPAF-II cells or cells stably expressing the mutants were treated with DMSO or 100 nM ETC-159 for 4 days, followed by western blotting analysis. The exogenous MYC mutant was fused with 3xHA tag that led to the mobility shift on the gel. endo, endogenous. n = 2 biological replicates/condition. (C) HPAF-II cells or cells stably expressing the mutants were seeded in soft agar and treated with the indicated concentrations of ETC-159 for ∼2 weeks. Colony numbers were quantified and normalized to the DMSO control. Data are represented as mean ± SD (n = 3 biological replicates/condition). IC50 values are shown. (D) RNF43 -mutant tumors with or without pre-existing FBXW7 mutations and treated with vehicle or ETC-159 were analysed by western blotting. Each lane represents an independent tumor. (E) GSEA of the hallmark “MYC targets” gene set for RSPO3 -fusion PDXs treated with the RSPO3-neutralizing mAb versus control. The transcriptomic data were extracted from GSE73906.
    Mutant Myc, supplied by Addgene inc, used in various techniques. Bioz Stars score: 91/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/mutant myc/product/Addgene inc
    Average 91 stars, based on 2 article reviews
    mutant myc - by Bioz Stars, 2026-02
    91/100 stars

    Images

    1) Product Images from "Recurrent FBXW7 mutations bypass Wnt/β-catenin addiction in cancer"

    Article Title: Recurrent FBXW7 mutations bypass Wnt/β-catenin addiction in cancer

    Journal: bioRxiv

    doi: 10.1101/2023.07.28.550933

    (A) RNF43 -mutant/ RSPO -fusion cancer xenografts were analysed by western blotting for 6 reported substrates of FBXW7. β-actin was used as loading control. Each lane represents an independent tumor. In the panel of SNU1411 ± FBXW7 mutant, ETC-159-treated samples were from the 5 mg/kg group shown in . (B, C) Ectopic expression of human phosphorylation site mutant Cyclin E1 (CCNE1) or MYC that are resistant to GSK3/FBXW7-mediated degradation caused resistance to PORCN inhibition in HPAF-II cells. (B) HPAF-II cells or cells stably expressing the mutants were treated with DMSO or 100 nM ETC-159 for 4 days, followed by western blotting analysis. The exogenous MYC mutant was fused with 3xHA tag that led to the mobility shift on the gel. endo, endogenous. n = 2 biological replicates/condition. (C) HPAF-II cells or cells stably expressing the mutants were seeded in soft agar and treated with the indicated concentrations of ETC-159 for ∼2 weeks. Colony numbers were quantified and normalized to the DMSO control. Data are represented as mean ± SD (n = 3 biological replicates/condition). IC50 values are shown. (D) RNF43 -mutant tumors with or without pre-existing FBXW7 mutations and treated with vehicle or ETC-159 were analysed by western blotting. Each lane represents an independent tumor. (E) GSEA of the hallmark “MYC targets” gene set for RSPO3 -fusion PDXs treated with the RSPO3-neutralizing mAb versus control. The transcriptomic data were extracted from GSE73906.
    Figure Legend Snippet: (A) RNF43 -mutant/ RSPO -fusion cancer xenografts were analysed by western blotting for 6 reported substrates of FBXW7. β-actin was used as loading control. Each lane represents an independent tumor. In the panel of SNU1411 ± FBXW7 mutant, ETC-159-treated samples were from the 5 mg/kg group shown in . (B, C) Ectopic expression of human phosphorylation site mutant Cyclin E1 (CCNE1) or MYC that are resistant to GSK3/FBXW7-mediated degradation caused resistance to PORCN inhibition in HPAF-II cells. (B) HPAF-II cells or cells stably expressing the mutants were treated with DMSO or 100 nM ETC-159 for 4 days, followed by western blotting analysis. The exogenous MYC mutant was fused with 3xHA tag that led to the mobility shift on the gel. endo, endogenous. n = 2 biological replicates/condition. (C) HPAF-II cells or cells stably expressing the mutants were seeded in soft agar and treated with the indicated concentrations of ETC-159 for ∼2 weeks. Colony numbers were quantified and normalized to the DMSO control. Data are represented as mean ± SD (n = 3 biological replicates/condition). IC50 values are shown. (D) RNF43 -mutant tumors with or without pre-existing FBXW7 mutations and treated with vehicle or ETC-159 were analysed by western blotting. Each lane represents an independent tumor. (E) GSEA of the hallmark “MYC targets” gene set for RSPO3 -fusion PDXs treated with the RSPO3-neutralizing mAb versus control. The transcriptomic data were extracted from GSE73906.

    Techniques Used: Mutagenesis, Western Blot, Control, Expressing, Phospho-proteomics, Inhibition, Stable Transfection, Mobility Shift



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    (A) RNF43 -mutant/ RSPO -fusion cancer xenografts were analysed by western blotting for 6 reported substrates of FBXW7. β-actin was used as loading control. Each lane represents an independent tumor. In the panel of SNU1411 ± FBXW7 mutant, ETC-159-treated samples were from the 5 mg/kg group shown in . (B, C) Ectopic expression of human phosphorylation site <t>mutant</t> <t>Cyclin</t> E1 (CCNE1) or <t>MYC</t> that are resistant to GSK3/FBXW7-mediated degradation caused resistance to PORCN inhibition in HPAF-II cells. (B) HPAF-II cells or cells stably expressing the mutants were treated with DMSO or 100 nM ETC-159 for 4 days, followed by western blotting analysis. The exogenous MYC mutant was fused with 3xHA tag that led to the mobility shift on the gel. endo, endogenous. n = 2 biological replicates/condition. (C) HPAF-II cells or cells stably expressing the mutants were seeded in soft agar and treated with the indicated concentrations of ETC-159 for ∼2 weeks. Colony numbers were quantified and normalized to the DMSO control. Data are represented as mean ± SD (n = 3 biological replicates/condition). IC50 values are shown. (D) RNF43 -mutant tumors with or without pre-existing FBXW7 mutations and treated with vehicle or ETC-159 were analysed by western blotting. Each lane represents an independent tumor. (E) GSEA of the hallmark “MYC targets” gene set for RSPO3 -fusion PDXs treated with the RSPO3-neutralizing mAb versus control. The transcriptomic data were extracted from GSE73906.
    Mutant Myc, supplied by Addgene inc, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    (A) RNF43 -mutant/ RSPO -fusion cancer xenografts were analysed by western blotting for 6 reported substrates of FBXW7. β-actin was used as loading control. Each lane represents an independent tumor. In the panel of SNU1411 ± FBXW7 mutant, ETC-159-treated samples were from the 5 mg/kg group shown in . (B, C) Ectopic expression of human phosphorylation site <t>mutant</t> <t>Cyclin</t> E1 (CCNE1) or <t>MYC</t> that are resistant to GSK3/FBXW7-mediated degradation caused resistance to PORCN inhibition in HPAF-II cells. (B) HPAF-II cells or cells stably expressing the mutants were treated with DMSO or 100 nM ETC-159 for 4 days, followed by western blotting analysis. The exogenous MYC mutant was fused with 3xHA tag that led to the mobility shift on the gel. endo, endogenous. n = 2 biological replicates/condition. (C) HPAF-II cells or cells stably expressing the mutants were seeded in soft agar and treated with the indicated concentrations of ETC-159 for ∼2 weeks. Colony numbers were quantified and normalized to the DMSO control. Data are represented as mean ± SD (n = 3 biological replicates/condition). IC50 values are shown. (D) RNF43 -mutant tumors with or without pre-existing FBXW7 mutations and treated with vehicle or ETC-159 were analysed by western blotting. Each lane represents an independent tumor. (E) GSEA of the hallmark “MYC targets” gene set for RSPO3 -fusion PDXs treated with the RSPO3-neutralizing mAb versus control. The transcriptomic data were extracted from GSE73906.
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    Average 91 stars, based on 1 article reviews
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    Image Search Results


    (A) RNF43 -mutant/ RSPO -fusion cancer xenografts were analysed by western blotting for 6 reported substrates of FBXW7. β-actin was used as loading control. Each lane represents an independent tumor. In the panel of SNU1411 ± FBXW7 mutant, ETC-159-treated samples were from the 5 mg/kg group shown in . (B, C) Ectopic expression of human phosphorylation site mutant Cyclin E1 (CCNE1) or MYC that are resistant to GSK3/FBXW7-mediated degradation caused resistance to PORCN inhibition in HPAF-II cells. (B) HPAF-II cells or cells stably expressing the mutants were treated with DMSO or 100 nM ETC-159 for 4 days, followed by western blotting analysis. The exogenous MYC mutant was fused with 3xHA tag that led to the mobility shift on the gel. endo, endogenous. n = 2 biological replicates/condition. (C) HPAF-II cells or cells stably expressing the mutants were seeded in soft agar and treated with the indicated concentrations of ETC-159 for ∼2 weeks. Colony numbers were quantified and normalized to the DMSO control. Data are represented as mean ± SD (n = 3 biological replicates/condition). IC50 values are shown. (D) RNF43 -mutant tumors with or without pre-existing FBXW7 mutations and treated with vehicle or ETC-159 were analysed by western blotting. Each lane represents an independent tumor. (E) GSEA of the hallmark “MYC targets” gene set for RSPO3 -fusion PDXs treated with the RSPO3-neutralizing mAb versus control. The transcriptomic data were extracted from GSE73906.

    Journal: bioRxiv

    Article Title: Recurrent FBXW7 mutations bypass Wnt/β-catenin addiction in cancer

    doi: 10.1101/2023.07.28.550933

    Figure Lengend Snippet: (A) RNF43 -mutant/ RSPO -fusion cancer xenografts were analysed by western blotting for 6 reported substrates of FBXW7. β-actin was used as loading control. Each lane represents an independent tumor. In the panel of SNU1411 ± FBXW7 mutant, ETC-159-treated samples were from the 5 mg/kg group shown in . (B, C) Ectopic expression of human phosphorylation site mutant Cyclin E1 (CCNE1) or MYC that are resistant to GSK3/FBXW7-mediated degradation caused resistance to PORCN inhibition in HPAF-II cells. (B) HPAF-II cells or cells stably expressing the mutants were treated with DMSO or 100 nM ETC-159 for 4 days, followed by western blotting analysis. The exogenous MYC mutant was fused with 3xHA tag that led to the mobility shift on the gel. endo, endogenous. n = 2 biological replicates/condition. (C) HPAF-II cells or cells stably expressing the mutants were seeded in soft agar and treated with the indicated concentrations of ETC-159 for ∼2 weeks. Colony numbers were quantified and normalized to the DMSO control. Data are represented as mean ± SD (n = 3 biological replicates/condition). IC50 values are shown. (D) RNF43 -mutant tumors with or without pre-existing FBXW7 mutations and treated with vehicle or ETC-159 were analysed by western blotting. Each lane represents an independent tumor. (E) GSEA of the hallmark “MYC targets” gene set for RSPO3 -fusion PDXs treated with the RSPO3-neutralizing mAb versus control. The transcriptomic data were extracted from GSE73906.

    Article Snippet: The transfer plasmids used in this study included FuCas9Cherry (Addgene #70182, a gift from Marco Herold) for constitutively expressing Cas9 protein, Lenti-dCas9-KRAB-blast (Addgene #89567, a gift from Gary Hon) for constitutively expressing dCas9-KRAB fusion protein, FgH1tUTG (Addgene #70183, a gift from Marco Herold) for expressing doxycycline (dox) inducible sgRNA, pHR’CMV-FBXW7 R465C (a gift from Patrick Tan) for expressing the mutant FBXW7, MSCV MYC T58A puro (Addgene #18773, a gift from Scott Lowe) for expressing the mutant MYC, and MIGR1-Cyclin E-AA (Addgene #47498, a gift from Alex Minella) for expressing the mutant Cyclin E. After transduction, cells were selected with the corresponding antibiotics or fluorescence-activated cell sorting (FACS).

    Techniques: Mutagenesis, Western Blot, Control, Expressing, Phospho-proteomics, Inhibition, Stable Transfection, Mobility Shift