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bortezomib  (StressMarq)


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    Structured Review

    StressMarq bortezomib
    The tumor-suppressing potency of proteasome inhibitor is enhanced through combination with PPM1D inhibitor. A , B Cells were treated for 8 h with <t>bortezomib:</t> U87MG (64 nM), A549 (32 nM), HCT116 (16 nM), and U2OS (32 nM) using DMSO as vehicle control (n = 3). Representative immunoblots ( A ) and quantification ( B ) of PPM1D mutant (PPM1D-mut) or PPM1D full-length (PPM1D-FL) protein levels are shown. Protein levels were normalized to vinculin. C – N Cells were treated for 48 h with various concentrations of bortezomib, GSK2830371, or their combination at a fixed molar ratio based on the IC 50 values of each drug. Cell viability was assessed using the Cell Counting Kit-8 assay (n = 3). Dose–response curves for bortezomib alone and in combination with GSK2830371 are shown in panels C , F , I , and L , while those for GSK2830371 alone and in combination with bortezomib are shown in panels D , G , J , and M . Data represent mean ± SD. Combination Index (CI) plots ( E , H , K , and N ), extracted from CompuSyn reports, depict the relationship between the fraction affected (Fa, x-axis) and CI (y-axis). CI values < 1 indicate synergistic interaction between the two drugs
    Bortezomib, supplied by StressMarq, used in various techniques. Bioz Stars score: 93/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/SIH-328/Bortezomib/pmc12424213-61-28-30
    Average 93 stars, based on 7 article reviews
    bortezomib - by Bioz Stars, 2026-09
    93/100 stars

    Images

    1) Product Images from "PPM1D is directly degraded by proteasomes in a ubiquitination-independent manner through its carboxyl-terminal region"

    Article Title: PPM1D is directly degraded by proteasomes in a ubiquitination-independent manner through its carboxyl-terminal region

    Journal: Journal of Biomedical Science

    doi: 10.1186/s12929-025-01185-z

    The tumor-suppressing potency of proteasome inhibitor is enhanced through combination with PPM1D inhibitor. A , B Cells were treated for 8 h with bortezomib: U87MG (64 nM), A549 (32 nM), HCT116 (16 nM), and U2OS (32 nM) using DMSO as vehicle control (n = 3). Representative immunoblots ( A ) and quantification ( B ) of PPM1D mutant (PPM1D-mut) or PPM1D full-length (PPM1D-FL) protein levels are shown. Protein levels were normalized to vinculin. C – N Cells were treated for 48 h with various concentrations of bortezomib, GSK2830371, or their combination at a fixed molar ratio based on the IC 50 values of each drug. Cell viability was assessed using the Cell Counting Kit-8 assay (n = 3). Dose–response curves for bortezomib alone and in combination with GSK2830371 are shown in panels C , F , I , and L , while those for GSK2830371 alone and in combination with bortezomib are shown in panels D , G , J , and M . Data represent mean ± SD. Combination Index (CI) plots ( E , H , K , and N ), extracted from CompuSyn reports, depict the relationship between the fraction affected (Fa, x-axis) and CI (y-axis). CI values < 1 indicate synergistic interaction between the two drugs
    Figure Legend Snippet: The tumor-suppressing potency of proteasome inhibitor is enhanced through combination with PPM1D inhibitor. A , B Cells were treated for 8 h with bortezomib: U87MG (64 nM), A549 (32 nM), HCT116 (16 nM), and U2OS (32 nM) using DMSO as vehicle control (n = 3). Representative immunoblots ( A ) and quantification ( B ) of PPM1D mutant (PPM1D-mut) or PPM1D full-length (PPM1D-FL) protein levels are shown. Protein levels were normalized to vinculin. C – N Cells were treated for 48 h with various concentrations of bortezomib, GSK2830371, or their combination at a fixed molar ratio based on the IC 50 values of each drug. Cell viability was assessed using the Cell Counting Kit-8 assay (n = 3). Dose–response curves for bortezomib alone and in combination with GSK2830371 are shown in panels C , F , I , and L , while those for GSK2830371 alone and in combination with bortezomib are shown in panels D , G , J , and M . Data represent mean ± SD. Combination Index (CI) plots ( E , H , K , and N ), extracted from CompuSyn reports, depict the relationship between the fraction affected (Fa, x-axis) and CI (y-axis). CI values < 1 indicate synergistic interaction between the two drugs

    Techniques Used: Control, Western Blot, Mutagenesis, Cell Counting

    Bortezomib and GSK2830371 exhibit synergistic cytotoxicity in bortezomib-resistant cells. Bortezomib-resistant (BR) cells were treated for 48 h with various concentrations of bortezomib, GSK2830371, or their combination at a fixed molar ratio based on the IC 50 values of each drug. Cell viability was assessed using the Cell Counting Kit-8 assay (n = 3). Dose–response curves are shown in panels A , B , D , E , G , H , J , and K , comparing single-drug treatments with the combination. Data represent mean ± SD. Combination index (CI) plots extracted from CompuSyn reports are shown in panels C , F , I , and L . The x-axis represents the fraction affected (Fa), and the y-axis indicates the CI value. CI < 1 denotes synergism between the two drugs
    Figure Legend Snippet: Bortezomib and GSK2830371 exhibit synergistic cytotoxicity in bortezomib-resistant cells. Bortezomib-resistant (BR) cells were treated for 48 h with various concentrations of bortezomib, GSK2830371, or their combination at a fixed molar ratio based on the IC 50 values of each drug. Cell viability was assessed using the Cell Counting Kit-8 assay (n = 3). Dose–response curves are shown in panels A , B , D , E , G , H , J , and K , comparing single-drug treatments with the combination. Data represent mean ± SD. Combination index (CI) plots extracted from CompuSyn reports are shown in panels C , F , I , and L . The x-axis represents the fraction affected (Fa), and the y-axis indicates the CI value. CI < 1 denotes synergism between the two drugs

    Techniques Used: Cell Counting

    Related Articles

    Lysis:

    Article Title: Ethylene promotes SMAX1 accumulation to inhibit arbuscular mycorrhiza symbiosis
    Article Snippet: .. The tissue powder was homogenized in 300 μl lysis buffer (62.6 mM Tris, 2% SDS, 10% Glycerol, 1 mM DTT, 10 μM Bortezomib (StressMarq Biosciences, Canada, Cat. No. SIH-328)) by vortexing. ..

    Article Title: Ethylene promotes SMAX1 accumulation to inhibit arbuscular mycorrhiza symbiosis.
    Article Snippet: .. The tissue powder was homogenized in 300 μl lysis buffer (62.6mM Tris, 2% SDS, 10% Glycerol, 1mM DTT, 10 μM Bortezomib (StressMarq Biosciences, Canada, Cat. No. SIH-328)) by vortexing. ..

    DNA Synthesis:

    Article Title: A novel homozygous Y140X mutation of ISG15 causes diverse type I interferonopathies in sibling patients with cutaneous lesions or recurrent parenchymal pneumonia.
    Article Snippet: Purpose: Interferon-stimulated gene 15 (ISG15) deficiency, a rare human inborn error of immunity characterized by susceptibility to Bacillus Calmette-Guerin (BCG) diseases, neuropathic and dermatological manifestations.. Methods: The clinical and immunological features of two siblings with ISG15 deficiency combined with asymptomatic myeloperoxidase (MPO) mutations were analyzed, and their pathogenesis, as well as target therapeutic candidates, were explored.. Results: The manifestation in patient 2 was skin lesions, while those in patient 1 were intracranial calcification and recurrent pneumonia.

    Article Title: Dual novel homozygous mutations in ISG15 and MPO lead to classic type I interferonopathy and a new phenotype of recurrent parenchymal pneumonia
    Article Snippet: .. Inhibitors Baricitinib (S2851, Selleck), a speci c inhibitor of JAK1 and JAK2; udarabine (S1491, Selleck), a STAT1 and DNA synthesis inhibitor; and bortezomib (SIH328, Stressmarq), a proteasome inhibitor, were used in the study. ..



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    Image Search Results


    The tumor-suppressing potency of proteasome inhibitor is enhanced through combination with PPM1D inhibitor. A , B Cells were treated for 8 h with bortezomib: U87MG (64 nM), A549 (32 nM), HCT116 (16 nM), and U2OS (32 nM) using DMSO as vehicle control (n = 3). Representative immunoblots ( A ) and quantification ( B ) of PPM1D mutant (PPM1D-mut) or PPM1D full-length (PPM1D-FL) protein levels are shown. Protein levels were normalized to vinculin. C – N Cells were treated for 48 h with various concentrations of bortezomib, GSK2830371, or their combination at a fixed molar ratio based on the IC 50 values of each drug. Cell viability was assessed using the Cell Counting Kit-8 assay (n = 3). Dose–response curves for bortezomib alone and in combination with GSK2830371 are shown in panels C , F , I , and L , while those for GSK2830371 alone and in combination with bortezomib are shown in panels D , G , J , and M . Data represent mean ± SD. Combination Index (CI) plots ( E , H , K , and N ), extracted from CompuSyn reports, depict the relationship between the fraction affected (Fa, x-axis) and CI (y-axis). CI values < 1 indicate synergistic interaction between the two drugs

    Journal: Journal of Biomedical Science

    Article Title: PPM1D is directly degraded by proteasomes in a ubiquitination-independent manner through its carboxyl-terminal region

    doi: 10.1186/s12929-025-01185-z

    Figure Lengend Snippet: The tumor-suppressing potency of proteasome inhibitor is enhanced through combination with PPM1D inhibitor. A , B Cells were treated for 8 h with bortezomib: U87MG (64 nM), A549 (32 nM), HCT116 (16 nM), and U2OS (32 nM) using DMSO as vehicle control (n = 3). Representative immunoblots ( A ) and quantification ( B ) of PPM1D mutant (PPM1D-mut) or PPM1D full-length (PPM1D-FL) protein levels are shown. Protein levels were normalized to vinculin. C – N Cells were treated for 48 h with various concentrations of bortezomib, GSK2830371, or their combination at a fixed molar ratio based on the IC 50 values of each drug. Cell viability was assessed using the Cell Counting Kit-8 assay (n = 3). Dose–response curves for bortezomib alone and in combination with GSK2830371 are shown in panels C , F , I , and L , while those for GSK2830371 alone and in combination with bortezomib are shown in panels D , G , J , and M . Data represent mean ± SD. Combination Index (CI) plots ( E , H , K , and N ), extracted from CompuSyn reports, depict the relationship between the fraction affected (Fa, x-axis) and CI (y-axis). CI values < 1 indicate synergistic interaction between the two drugs

    Article Snippet: The reagents used in this study included MG132 (474790, Merck, Darmstadt, Germany), carfilzomib (17554, Cayman Chemical, Ann Arbor, MI, USA), bafilomycin A1 (11038, Cayman Chemical), chloroquine (C6628, Sigma-Aldrich), bortezomib (SIH-328, StressMarq Biosciences, British Columbia, Canada), and GSK2830371 (S7573, Selleck Biotechnology, Kanagawa, Japan).

    Techniques: Control, Western Blot, Mutagenesis, Cell Counting

    Bortezomib and GSK2830371 exhibit synergistic cytotoxicity in bortezomib-resistant cells. Bortezomib-resistant (BR) cells were treated for 48 h with various concentrations of bortezomib, GSK2830371, or their combination at a fixed molar ratio based on the IC 50 values of each drug. Cell viability was assessed using the Cell Counting Kit-8 assay (n = 3). Dose–response curves are shown in panels A , B , D , E , G , H , J , and K , comparing single-drug treatments with the combination. Data represent mean ± SD. Combination index (CI) plots extracted from CompuSyn reports are shown in panels C , F , I , and L . The x-axis represents the fraction affected (Fa), and the y-axis indicates the CI value. CI < 1 denotes synergism between the two drugs

    Journal: Journal of Biomedical Science

    Article Title: PPM1D is directly degraded by proteasomes in a ubiquitination-independent manner through its carboxyl-terminal region

    doi: 10.1186/s12929-025-01185-z

    Figure Lengend Snippet: Bortezomib and GSK2830371 exhibit synergistic cytotoxicity in bortezomib-resistant cells. Bortezomib-resistant (BR) cells were treated for 48 h with various concentrations of bortezomib, GSK2830371, or their combination at a fixed molar ratio based on the IC 50 values of each drug. Cell viability was assessed using the Cell Counting Kit-8 assay (n = 3). Dose–response curves are shown in panels A , B , D , E , G , H , J , and K , comparing single-drug treatments with the combination. Data represent mean ± SD. Combination index (CI) plots extracted from CompuSyn reports are shown in panels C , F , I , and L . The x-axis represents the fraction affected (Fa), and the y-axis indicates the CI value. CI < 1 denotes synergism between the two drugs

    Article Snippet: The reagents used in this study included MG132 (474790, Merck, Darmstadt, Germany), carfilzomib (17554, Cayman Chemical, Ann Arbor, MI, USA), bafilomycin A1 (11038, Cayman Chemical), chloroquine (C6628, Sigma-Aldrich), bortezomib (SIH-328, StressMarq Biosciences, British Columbia, Canada), and GSK2830371 (S7573, Selleck Biotechnology, Kanagawa, Japan).

    Techniques: Cell Counting