Review



proteasome inhibitor mg132  (MedChemExpress)


Bioz Verified Symbol MedChemExpress is a verified supplier
Bioz Manufacturer Symbol MedChemExpress manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
    • 99
      Buy from Supplier

    Structured Review

    MedChemExpress proteasome inhibitor mg132
    TRIM28 ubiquitinates RFC4 with K29‐linked polyubiquitin chains. (A) MDA‐MB‐231 cells were transduced with lentiviruses carrying empty vector or oeTRIM28 and treated with cycloheximide (CHX) for 0, 4, 8, and 12 h. (B) TRIM28 knockdown promoted RFC4 protein degradation through the proteasome pathway. (C) Analysis of the ubiquitin chain types on RFC4 affected by TRIM28. Ubiquitinated proteins were pulled down using anti‐Flag agarose under denaturing conditions from HEK293T cells transfected with the indicated constructs and analyzed by western blotting with the indicated antibodies. At 24 h after transfection, cells were treated with <t>MG132</t> (10 µM) for an additional 4 h. (D) Analysis of endogenous RFC4 ubiquitination in MDA‐MB‐231 cells following siRNA‐mediated TRIM28 knockdown. (E) TRIM28‐mediated K29‐linked polyubiquitination of RFC4. (F) Effect of mutation of the TRIM28 enzymatic active site on the half‐life of RFC4. (G) Quantitative analysis of RFC4 protein levels after mutation of the TRIM28 enzymatic active site. (H) TRIM28 ubiquitinated RFC4 at K205 and K217. (I–K) Analysis of the half‐lives of Flag‐RFC4 wild‐type, K205R, K217R, and K205/217R mutant proteins in HEK293T cells.
    Proteasome Inhibitor Mg132, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 2226 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/proteasome+inhibitor+mg132/MG-132/pmc13635811-213-1-18
    Average 99 stars, based on 2226 article reviews
    proteasome inhibitor mg132 - by Bioz Stars, 2026-10
    99/100 stars

    Images

    1) Product Images from "TRIM28 Increases RFC4 Protein Expression to Promote Triple‐Negative Breast Cancer Progression"

    Article Title: TRIM28 Increases RFC4 Protein Expression to Promote Triple‐Negative Breast Cancer Progression

    Journal: MedComm

    doi: 10.1002/mco2.71043

    TRIM28 ubiquitinates RFC4 with K29‐linked polyubiquitin chains. (A) MDA‐MB‐231 cells were transduced with lentiviruses carrying empty vector or oeTRIM28 and treated with cycloheximide (CHX) for 0, 4, 8, and 12 h. (B) TRIM28 knockdown promoted RFC4 protein degradation through the proteasome pathway. (C) Analysis of the ubiquitin chain types on RFC4 affected by TRIM28. Ubiquitinated proteins were pulled down using anti‐Flag agarose under denaturing conditions from HEK293T cells transfected with the indicated constructs and analyzed by western blotting with the indicated antibodies. At 24 h after transfection, cells were treated with MG132 (10 µM) for an additional 4 h. (D) Analysis of endogenous RFC4 ubiquitination in MDA‐MB‐231 cells following siRNA‐mediated TRIM28 knockdown. (E) TRIM28‐mediated K29‐linked polyubiquitination of RFC4. (F) Effect of mutation of the TRIM28 enzymatic active site on the half‐life of RFC4. (G) Quantitative analysis of RFC4 protein levels after mutation of the TRIM28 enzymatic active site. (H) TRIM28 ubiquitinated RFC4 at K205 and K217. (I–K) Analysis of the half‐lives of Flag‐RFC4 wild‐type, K205R, K217R, and K205/217R mutant proteins in HEK293T cells.
    Figure Legend Snippet: TRIM28 ubiquitinates RFC4 with K29‐linked polyubiquitin chains. (A) MDA‐MB‐231 cells were transduced with lentiviruses carrying empty vector or oeTRIM28 and treated with cycloheximide (CHX) for 0, 4, 8, and 12 h. (B) TRIM28 knockdown promoted RFC4 protein degradation through the proteasome pathway. (C) Analysis of the ubiquitin chain types on RFC4 affected by TRIM28. Ubiquitinated proteins were pulled down using anti‐Flag agarose under denaturing conditions from HEK293T cells transfected with the indicated constructs and analyzed by western blotting with the indicated antibodies. At 24 h after transfection, cells were treated with MG132 (10 µM) for an additional 4 h. (D) Analysis of endogenous RFC4 ubiquitination in MDA‐MB‐231 cells following siRNA‐mediated TRIM28 knockdown. (E) TRIM28‐mediated K29‐linked polyubiquitination of RFC4. (F) Effect of mutation of the TRIM28 enzymatic active site on the half‐life of RFC4. (G) Quantitative analysis of RFC4 protein levels after mutation of the TRIM28 enzymatic active site. (H) TRIM28 ubiquitinated RFC4 at K205 and K217. (I–K) Analysis of the half‐lives of Flag‐RFC4 wild‐type, K205R, K217R, and K205/217R mutant proteins in HEK293T cells.

    Techniques Used: Transduction, Plasmid Preparation, Knockdown, Analysis, Ubiquitin Proteomics, Transfection, Construct, Western Blot, Mutagenesis

    Related Articles

    Control:

    Article Title: UHMK1 regulates VM formation in OSCC by interacting with STMN1.
    Article Snippet: Oral squamous cell carcinoma (OSCC) is a common malignant tumor in the head and neck region and clinically characterized by relatively high invasiveness and a propensity for metastasis.. Patients generally exhibit nonsatisfactory prognosis.. Beyond the classical endothelium-dependent angiogenesis pathway, vasculogenic mimicry (VM), a nonclassical blood supply mechanism whereby tumor cells themselves form microcirculatory conduits, plays a significant role in tumor progression.

    Article Title: STING Aggravates Ferroptosis in Septic Acute Kidney Injury by Promoting Ubiquitin–Proteasome–Dependent Degradation of FSP1
    Article Snippet: .. iFSP1 was used at a final concentration of 0.5 μM for 24 h. The corresponding control groups were treated with an equal volume of vehicle.To explore the mechanism by which STING regulates FSP1 protein stability, HK-2 1 3 Article in Press Inflammation https://doi.org/10.1007/s10753-026-02608-1 cells were stimulated with the STING agonist 2′3′-cGAMP (MCE, Monmouth Junction, NJ, USA; HY-100564) at a final concentration of 40 μg/mL for 6 h. To distinguish the degradation pathway of FSP1, cells were pretreated with the proteasome inhibitor MG132 (MCE, Monmouth Junction, NJ, USA; HY-13259; 20μM) or the lysosome inhibitor chloroquine (CQ; MCE, Monmouth Junction, NJ, USA; HY-17589 A; 10μM) for 0.5 h, followed by combined treatment with cGAMP. ..

    Recombinant:

    Article Title: CAF-derived TGF-β1 activates an LBH-mediated β-catenin stabilization program to drive gastric cancer progression
    Article Snippet: .. Recombinant human TGF-β1 (HY-P70543), the TGF-β receptor I kinase inhibitor TGF-β1-IN-1 (HY-151427), the Wnt/β-catenin pathway activator LiCl (HY-Y0649), the Wnt inhibitor XAV-939 ( HY-15147), the proteasome inhibitor MG132 (HY-13259), and the lysosome inhibitor Chloroquine (CQ; HY-17589A) were all obtained from MedChemExpress (MCE, USA). ..

    Concentration Assay:

    Article Title: STING Aggravates Ferroptosis in Septic Acute Kidney Injury by Promoting Ubiquitin–Proteasome–Dependent Degradation of FSP1
    Article Snippet: .. iFSP1 was used at a final concentration of 0.5 μM for 24 h. The corresponding control groups were treated with an equal volume of vehicle.To explore the mechanism by which STING regulates FSP1 protein stability, HK-2 1 3 Article in Press Inflammation https://doi.org/10.1007/s10753-026-02608-1 cells were stimulated with the STING agonist 2′3′-cGAMP (MCE, Monmouth Junction, NJ, USA; HY-100564) at a final concentration of 40 μg/mL for 6 h. To distinguish the degradation pathway of FSP1, cells were pretreated with the proteasome inhibitor MG132 (MCE, Monmouth Junction, NJ, USA; HY-13259; 20μM) or the lysosome inhibitor chloroquine (CQ; MCE, Monmouth Junction, NJ, USA; HY-17589 A; 10μM) for 0.5 h, followed by combined treatment with cGAMP. ..

    Stability:

    Article Title: STING Aggravates Ferroptosis in Septic Acute Kidney Injury by Promoting Ubiquitin–Proteasome–Dependent Degradation of FSP1
    Article Snippet: .. iFSP1 was used at a final concentration of 0.5 μM for 24 h. The corresponding control groups were treated with an equal volume of vehicle.To explore the mechanism by which STING regulates FSP1 protein stability, HK-2 1 3 Article in Press Inflammation https://doi.org/10.1007/s10753-026-02608-1 cells were stimulated with the STING agonist 2′3′-cGAMP (MCE, Monmouth Junction, NJ, USA; HY-100564) at a final concentration of 40 μg/mL for 6 h. To distinguish the degradation pathway of FSP1, cells were pretreated with the proteasome inhibitor MG132 (MCE, Monmouth Junction, NJ, USA; HY-13259; 20μM) or the lysosome inhibitor chloroquine (CQ; MCE, Monmouth Junction, NJ, USA; HY-17589 A; 10μM) for 0.5 h, followed by combined treatment with cGAMP. ..

    Western Blot:

    Article Title: A Small‐Molecule DEPTAC Rescues Cognitive Deficits by Targeted Dephosphorylation of Pathological Tau
    Article Snippet: .. To identify the degradation pathway, cells were co‐treated with 10 μ m TP2 and either the proteasome inhibitor MG132 (10 μ m , MCE, #HY‐13259) or the autophagy–lysosome inhibitor bafilomycin A1 (BafA1, 100 nM, MCE, #HY‐100558) for 8 h, and cell lysates were subjected to Western blotting for AT8, Tau5, and β‐actin. ..

    Article Title: UPF1-dependent glycolysis driven by LINC00887 facilitates macrophage M2 polarization in clear cell renal cell carcinoma
    Article Snippet: .. To investigate the mechanism by which LINC00887 negatively regulates UPF1, Caki-1 cells transfected with sh-NC or sh-LINC00887 were treated with the proteasome inhibitor MG132 (10 μM, HY-13259, MCE, USA) for 6 h, followed by Western blot analysis of UPF1 protein expression. ..

    Transfection:

    Article Title: UPF1-dependent glycolysis driven by LINC00887 facilitates macrophage M2 polarization in clear cell renal cell carcinoma
    Article Snippet: .. To investigate the mechanism by which LINC00887 negatively regulates UPF1, Caki-1 cells transfected with sh-NC or sh-LINC00887 were treated with the proteasome inhibitor MG132 (10 μM, HY-13259, MCE, USA) for 6 h, followed by Western blot analysis of UPF1 protein expression. ..

    Analysis:

    Article Title: UPF1-dependent glycolysis driven by LINC00887 facilitates macrophage M2 polarization in clear cell renal cell carcinoma
    Article Snippet: .. To investigate the mechanism by which LINC00887 negatively regulates UPF1, Caki-1 cells transfected with sh-NC or sh-LINC00887 were treated with the proteasome inhibitor MG132 (10 μM, HY-13259, MCE, USA) for 6 h, followed by Western blot analysis of UPF1 protein expression. ..

    Expressing:

    Article Title: UPF1-dependent glycolysis driven by LINC00887 facilitates macrophage M2 polarization in clear cell renal cell carcinoma
    Article Snippet: .. To investigate the mechanism by which LINC00887 negatively regulates UPF1, Caki-1 cells transfected with sh-NC or sh-LINC00887 were treated with the proteasome inhibitor MG132 (10 μM, HY-13259, MCE, USA) for 6 h, followed by Western blot analysis of UPF1 protein expression. ..



    Similar Products

    proteasome inhibitor mg132  (Aladdin Scientific Corporation)
    94
    Aladdin Scientific Corporation proteasome inhibitor mg132
    Proteasome Inhibitor Mg132, supplied by Aladdin Scientific Corporation, 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/product/proteasome+inhibitor+mg132/AS-605240/pm42843084-105-11-14
    Average 94 stars, based on 1 article reviews
    proteasome inhibitor mg132 - by Bioz Stars, 2026-10
    94/100 stars
    		  Buy from Supplier
    proteasome inhibitor mg132  (MedChemExpress)
    99
    MedChemExpress proteasome inhibitor mg132
    TRIM28 ubiquitinates RFC4 with K29‐linked polyubiquitin chains. (A) MDA‐MB‐231 cells were transduced with lentiviruses carrying empty vector or oeTRIM28 and treated with cycloheximide (CHX) for 0, 4, 8, and 12 h. (B) TRIM28 knockdown promoted RFC4 protein degradation through the proteasome pathway. (C) Analysis of the ubiquitin chain types on RFC4 affected by TRIM28. Ubiquitinated proteins were pulled down using anti‐Flag agarose under denaturing conditions from HEK293T cells transfected with the indicated constructs and analyzed by western blotting with the indicated antibodies. At 24 h after transfection, cells were treated with <t>MG132</t> (10 µM) for an additional 4 h. (D) Analysis of endogenous RFC4 ubiquitination in MDA‐MB‐231 cells following siRNA‐mediated TRIM28 knockdown. (E) TRIM28‐mediated K29‐linked polyubiquitination of RFC4. (F) Effect of mutation of the TRIM28 enzymatic active site on the half‐life of RFC4. (G) Quantitative analysis of RFC4 protein levels after mutation of the TRIM28 enzymatic active site. (H) TRIM28 ubiquitinated RFC4 at K205 and K217. (I–K) Analysis of the half‐lives of Flag‐RFC4 wild‐type, K205R, K217R, and K205/217R mutant proteins in HEK293T cells.
    Proteasome Inhibitor Mg132, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/proteasome+inhibitor+mg132/MG-132/pmc13635811-213-1-18
    Average 99 stars, based on 1 article reviews
    proteasome inhibitor mg132 - by Bioz Stars, 2026-10
    99/100 stars
    		  Buy from Supplier
    proteasome inhibitors mg132  (MedChemExpress)
    99
    MedChemExpress proteasome inhibitors mg132
    TRIM28 ubiquitinates RFC4 with K29‐linked polyubiquitin chains. (A) MDA‐MB‐231 cells were transduced with lentiviruses carrying empty vector or oeTRIM28 and treated with cycloheximide (CHX) for 0, 4, 8, and 12 h. (B) TRIM28 knockdown promoted RFC4 protein degradation through the proteasome pathway. (C) Analysis of the ubiquitin chain types on RFC4 affected by TRIM28. Ubiquitinated proteins were pulled down using anti‐Flag agarose under denaturing conditions from HEK293T cells transfected with the indicated constructs and analyzed by western blotting with the indicated antibodies. At 24 h after transfection, cells were treated with <t>MG132</t> (10 µM) for an additional 4 h. (D) Analysis of endogenous RFC4 ubiquitination in MDA‐MB‐231 cells following siRNA‐mediated TRIM28 knockdown. (E) TRIM28‐mediated K29‐linked polyubiquitination of RFC4. (F) Effect of mutation of the TRIM28 enzymatic active site on the half‐life of RFC4. (G) Quantitative analysis of RFC4 protein levels after mutation of the TRIM28 enzymatic active site. (H) TRIM28 ubiquitinated RFC4 at K205 and K217. (I–K) Analysis of the half‐lives of Flag‐RFC4 wild‐type, K205R, K217R, and K205/217R mutant proteins in HEK293T cells.
    Proteasome Inhibitors Mg132, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/proteasome+inhibitor+mg132/MG-132/pm42785594-102-13-18
    Average 99 stars, based on 1 article reviews
    proteasome inhibitors mg132 - by Bioz Stars, 2026-10
    99/100 stars
    		  Buy from Supplier

    Image Search Results


    TRIM28 ubiquitinates RFC4 with K29‐linked polyubiquitin chains. (A) MDA‐MB‐231 cells were transduced with lentiviruses carrying empty vector or oeTRIM28 and treated with cycloheximide (CHX) for 0, 4, 8, and 12 h. (B) TRIM28 knockdown promoted RFC4 protein degradation through the proteasome pathway. (C) Analysis of the ubiquitin chain types on RFC4 affected by TRIM28. Ubiquitinated proteins were pulled down using anti‐Flag agarose under denaturing conditions from HEK293T cells transfected with the indicated constructs and analyzed by western blotting with the indicated antibodies. At 24 h after transfection, cells were treated with MG132 (10 µM) for an additional 4 h. (D) Analysis of endogenous RFC4 ubiquitination in MDA‐MB‐231 cells following siRNA‐mediated TRIM28 knockdown. (E) TRIM28‐mediated K29‐linked polyubiquitination of RFC4. (F) Effect of mutation of the TRIM28 enzymatic active site on the half‐life of RFC4. (G) Quantitative analysis of RFC4 protein levels after mutation of the TRIM28 enzymatic active site. (H) TRIM28 ubiquitinated RFC4 at K205 and K217. (I–K) Analysis of the half‐lives of Flag‐RFC4 wild‐type, K205R, K217R, and K205/217R mutant proteins in HEK293T cells.

    Journal: MedComm

    Article Title: TRIM28 Increases RFC4 Protein Expression to Promote Triple‐Negative Breast Cancer Progression

    doi: 10.1002/mco2.71043

    Figure Lengend Snippet: TRIM28 ubiquitinates RFC4 with K29‐linked polyubiquitin chains. (A) MDA‐MB‐231 cells were transduced with lentiviruses carrying empty vector or oeTRIM28 and treated with cycloheximide (CHX) for 0, 4, 8, and 12 h. (B) TRIM28 knockdown promoted RFC4 protein degradation through the proteasome pathway. (C) Analysis of the ubiquitin chain types on RFC4 affected by TRIM28. Ubiquitinated proteins were pulled down using anti‐Flag agarose under denaturing conditions from HEK293T cells transfected with the indicated constructs and analyzed by western blotting with the indicated antibodies. At 24 h after transfection, cells were treated with MG132 (10 µM) for an additional 4 h. (D) Analysis of endogenous RFC4 ubiquitination in MDA‐MB‐231 cells following siRNA‐mediated TRIM28 knockdown. (E) TRIM28‐mediated K29‐linked polyubiquitination of RFC4. (F) Effect of mutation of the TRIM28 enzymatic active site on the half‐life of RFC4. (G) Quantitative analysis of RFC4 protein levels after mutation of the TRIM28 enzymatic active site. (H) TRIM28 ubiquitinated RFC4 at K205 and K217. (I–K) Analysis of the half‐lives of Flag‐RFC4 wild‐type, K205R, K217R, and K205/217R mutant proteins in HEK293T cells.

    Article Snippet: The proteasome inhibitor MG132, protein synthesis inhibitor CHX, autophagy inhibitor CQ and PI3K inhibitor LY294004 were purchased from MedChem Express (Shanghai, China).

    Techniques: Transduction, Plasmid Preparation, Knockdown, Analysis, Ubiquitin Proteomics, Transfection, Construct, Western Blot, Mutagenesis