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co treatment with bortezomib  (Tocris)


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    Tocris co treatment with bortezomib
    Cells expressing Rpn13(1–128)-HTP-FLAG (A, C, E and G; blue bar graphs) were treated with the indicated chemicals. The cells were lysed and the levels of BRD2 were assessed by SDS-PAGE and Western blotting. The bars represent the average of two - three biological replicates and the individual data points are shown as dots. A) Effect of the Nedd activating enzyme inhibitor TAK-924. C) Effect of the ubiquitin activating enzyme inhibitor TAK-243. E) Effect of the proteasome inhibitor <t>Bortezomib.</t> G) Effect of Added JQ1. The data show that the inhibitors of protein ubiquitylation had no effect on the activity of the three Halo-UIDs tested but blocked the activity of the ubiquitin-dependent degrader MZ1. Targeted degradation of BRD2 was blocked in all cases by the proteasome inhibitor Bortezomib or excess JQ1. The red panels (B, D, F and H) show the results of the same set of experiments in cells that express HTP-FLAG, which is not tethered to the proteasome.
    Co Treatment With Bortezomib, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 34 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/co treatment with bortezomib/product/Tocris
    Average 94 stars, based on 34 article reviews
    co treatment with bortezomib - by Bioz Stars, 2026-02
    94/100 stars

    Images

    1) Product Images from "Chemically Induced Degradation of Native Proteins by Direct Recruitment to the 26S Proteasome"

    Article Title: Chemically Induced Degradation of Native Proteins by Direct Recruitment to the 26S Proteasome

    Journal: bioRxiv

    doi: 10.1101/2023.07.19.549534

    Cells expressing Rpn13(1–128)-HTP-FLAG (A, C, E and G; blue bar graphs) were treated with the indicated chemicals. The cells were lysed and the levels of BRD2 were assessed by SDS-PAGE and Western blotting. The bars represent the average of two - three biological replicates and the individual data points are shown as dots. A) Effect of the Nedd activating enzyme inhibitor TAK-924. C) Effect of the ubiquitin activating enzyme inhibitor TAK-243. E) Effect of the proteasome inhibitor Bortezomib. G) Effect of Added JQ1. The data show that the inhibitors of protein ubiquitylation had no effect on the activity of the three Halo-UIDs tested but blocked the activity of the ubiquitin-dependent degrader MZ1. Targeted degradation of BRD2 was blocked in all cases by the proteasome inhibitor Bortezomib or excess JQ1. The red panels (B, D, F and H) show the results of the same set of experiments in cells that express HTP-FLAG, which is not tethered to the proteasome.
    Figure Legend Snippet: Cells expressing Rpn13(1–128)-HTP-FLAG (A, C, E and G; blue bar graphs) were treated with the indicated chemicals. The cells were lysed and the levels of BRD2 were assessed by SDS-PAGE and Western blotting. The bars represent the average of two - three biological replicates and the individual data points are shown as dots. A) Effect of the Nedd activating enzyme inhibitor TAK-924. C) Effect of the ubiquitin activating enzyme inhibitor TAK-243. E) Effect of the proteasome inhibitor Bortezomib. G) Effect of Added JQ1. The data show that the inhibitors of protein ubiquitylation had no effect on the activity of the three Halo-UIDs tested but blocked the activity of the ubiquitin-dependent degrader MZ1. Targeted degradation of BRD2 was blocked in all cases by the proteasome inhibitor Bortezomib or excess JQ1. The red panels (B, D, F and H) show the results of the same set of experiments in cells that express HTP-FLAG, which is not tethered to the proteasome.

    Techniques Used: Expressing, SDS Page, Western Blot, Ubiquitin Proteomics, Activity Assay



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    co treatment with bortezomib  (Tocris)
    94
    Tocris co treatment with bortezomib
    Cells expressing Rpn13(1–128)-HTP-FLAG (A, C, E and G; blue bar graphs) were treated with the indicated chemicals. The cells were lysed and the levels of BRD2 were assessed by SDS-PAGE and Western blotting. The bars represent the average of two - three biological replicates and the individual data points are shown as dots. A) Effect of the Nedd activating enzyme inhibitor TAK-924. C) Effect of the ubiquitin activating enzyme inhibitor TAK-243. E) Effect of the proteasome inhibitor <t>Bortezomib.</t> G) Effect of Added JQ1. The data show that the inhibitors of protein ubiquitylation had no effect on the activity of the three Halo-UIDs tested but blocked the activity of the ubiquitin-dependent degrader MZ1. Targeted degradation of BRD2 was blocked in all cases by the proteasome inhibitor Bortezomib or excess JQ1. The red panels (B, D, F and H) show the results of the same set of experiments in cells that express HTP-FLAG, which is not tethered to the proteasome.
    Co Treatment With Bortezomib, supplied by Tocris, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/co treatment with bortezomib/product/Tocris
    Average 94 stars, based on 1 article reviews
    co treatment with bortezomib - by Bioz Stars, 2026-02
    94/100 stars
    		  Buy from Supplier

    Image Search Results


    Cells expressing Rpn13(1–128)-HTP-FLAG (A, C, E and G; blue bar graphs) were treated with the indicated chemicals. The cells were lysed and the levels of BRD2 were assessed by SDS-PAGE and Western blotting. The bars represent the average of two - three biological replicates and the individual data points are shown as dots. A) Effect of the Nedd activating enzyme inhibitor TAK-924. C) Effect of the ubiquitin activating enzyme inhibitor TAK-243. E) Effect of the proteasome inhibitor Bortezomib. G) Effect of Added JQ1. The data show that the inhibitors of protein ubiquitylation had no effect on the activity of the three Halo-UIDs tested but blocked the activity of the ubiquitin-dependent degrader MZ1. Targeted degradation of BRD2 was blocked in all cases by the proteasome inhibitor Bortezomib or excess JQ1. The red panels (B, D, F and H) show the results of the same set of experiments in cells that express HTP-FLAG, which is not tethered to the proteasome.

    Journal: bioRxiv

    Article Title: Chemically Induced Degradation of Native Proteins by Direct Recruitment to the 26S Proteasome

    doi: 10.1101/2023.07.19.549534

    Figure Lengend Snippet: Cells expressing Rpn13(1–128)-HTP-FLAG (A, C, E and G; blue bar graphs) were treated with the indicated chemicals. The cells were lysed and the levels of BRD2 were assessed by SDS-PAGE and Western blotting. The bars represent the average of two - three biological replicates and the individual data points are shown as dots. A) Effect of the Nedd activating enzyme inhibitor TAK-924. C) Effect of the ubiquitin activating enzyme inhibitor TAK-243. E) Effect of the proteasome inhibitor Bortezomib. G) Effect of Added JQ1. The data show that the inhibitors of protein ubiquitylation had no effect on the activity of the three Halo-UIDs tested but blocked the activity of the ubiquitin-dependent degrader MZ1. Targeted degradation of BRD2 was blocked in all cases by the proteasome inhibitor Bortezomib or excess JQ1. The red panels (B, D, F and H) show the results of the same set of experiments in cells that express HTP-FLAG, which is not tethered to the proteasome.

    Article Snippet: The proteasome-dependence of WJ704-706 degradation of BRD2 was assayed by co-treatment with bortezomib (Tocris 7282), a proteasome inhibitor.

    Techniques: Expressing, SDS Page, Western Blot, Ubiquitin Proteomics, Activity Assay