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MG132

Cat. No. M1902

All AbMole products are for research use only, cannot be used for human consumption.

MG132 Structure
Synonym:

Z-Leu-Leu-Leu-al; MG-132

Size Price Availability Quantity
Free Sample (0.5-1 mg)  USD 0 In stock
10mM*1mL in DMSO USD 50  USD50 In stock
5mg USD 35  USD35 In stock
10mg USD 45  USD45 In stock
50mg USD 155  USD155 In stock
100mg USD 245  USD245 In stock
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Quality Control & Documentation
Biological Activity

MG132 is a potent cell-permeable inhibitor of proteasome and calpain with IC50 of 100 nM and 1.2 μM respectively. MG132 inhibited the growth of HeLa cells via inducing the cell cycle arrest as well as triggering apoptosis. MG132 also inhibits NF-κB activation with an IC50 of 3 µM and prevents β-secretase cleavage. MG132 induces cell apoptosis through formation of reactive oxygen species or the upregulation and downregulation of these factors, which is ultimately dependent upon the activation of the caspase family of cysteine proteases.

In vitro, it induces neurite outgrowth in PC12 cells and has anticancer properties. Besides its apoptotic effect alone, MG132 also enhanced the antiglioma effect of the chemotherapeutics cisplatin, taxol and doxorubicin in C6 and U138MG cells, indicating an adjuvant/chemosensitizer potential.

Product Citations
Customer Product Validations & Biological Datas
Source New Phytol (2020 Jan). Figure 7. MG132 (Abmole Bioscience, Houston, TX, USA)
Method Quantitative cell-free degradation assay
Cell Lines tobacco leaf epidermis cells
Concentrations 100 μM
Incubation Time 0, 60, 120 and 240 min
Results Proteasomal inhibitor MG132 antagonized this degradation and confirmed proteasomal involvement in FIT protein turnover.
Source Current Biology (2018). Figure 3. MG132 (Abmole Bioscience)
Method In vivo CoIP
Cell Lines Total protein
Concentrations 20 mM
Incubation Time 12 h
Results PAC-treated WT seedlings incubated with MG132 (a proteasome inhibitor) had increased TOC159 levels, implicating degradation by the UPS.
Source Oncotarget (2018 Feb). Figure5. MG132 (Abmole Bioscience, Houston, USA)
Method Co-immunoprecipitation
Cell Lines MCF-7 cells
Concentrations 20 μM
Incubation Time 4 h
Results When MCF-7 & SKBR3 cells were treated with both cycloheximide and MG132, a proteasome inhibitor, NDRG1-OT1_v4 no longer promoted NDRG1 degradation
Source Journal of Hematology & Oncology (2017). Figure 5. MG132 (Abmole Bioscience)
Method Immunofluorescence analysis
Cell Lines U251, U87 and U118 cell lines
Concentrations 20 μM
Incubation Time 2 h
Results Astrocytoma patients with a low expression of SIX3 and mutant p53 are more sensitive to treatment with aurora kinase inhibitors.
Source Journal of Hematology & Oncology (2017). Figure 3. MG132 (Abmole Bioscience)
Method Western blotting
Cell Lines U251, U87 and U118 cell lines
Concentrations 20 μM
Incubation Time 2 h
Results When we knocked down AURKA, MG132 resulted in increased AURKB expression and had less effect on AURKA (Fig. 3e).
Source Institut für Biochemie der Universität Stuttgart (2014). Figure 21. MG132 (Abmole Bioscience)
Method MG-132 was dissolved in DMSO. To verify that the activity was sufficiently inhibited, peptide cleavage assays were performed.
Cell Lines
Concentrations 200 μM
Incubation Time 2 h
Results As shown above, GST-Nup53 was immobilized on glutathione sepharose beads (Figure 21A, load, bottom lane; Coomassie blue stained gel) and incubated with equal amounts of CP or Blm10-CP. To confirm that equal amounts of proteasome were used, the loads were separated by SDS-PAGE, and the gel was subsequently stained with Coomassie blue and immunoblotted against the HA-tag of 4 (Figure 21A, load).
Source Faculté de Médecine (2015). Figure 5. MG132 (Abmole Bioscience)
Method
Cell Lines CFBE-wt cells
Concentrations 5 μM
Incubation Time 18h
Results In fact, our data obtained in the presence of MG132 and/or cycloheximide (Fig. 4 and 5) indicated that CFTR synthesis may also be affected by PsaDM. Our study, as well as data from the literature, thus indicated that P. aeruginosa exoproducts may impact CFTR protein synthesis, degradation and trafficking/recycling to the cell membrane.
Source Faculté de Médecine (2015). Figure 4. MG132 (Abmole Bioscience)
Method
Cell Lines CFBE-wt cells
Concentrations 5 μM
Incubation Time 18h
Results In fact, our data obtained in the presence of MG132 and/or cycloheximide (Fig. 4 and 5) indicated that CFTR synthesis may also be affected by PsaDM. Our study, as well as data from the literature, thus indicated that P. aeruginosa exoproducts may impact CFTR protein synthesis, degradation and trafficking/recycling to the cell membrane.
Source ERJ Express.(2015). Figure 5. MG132 (Abmole Bioscience, Kowloon, Honk Hong)
Method Immunoblotting
Cell Lines CFBE-ΔF508 and CFBE-wt cell lines
Concentrations
Incubation Time 18 h
Results To confirm that the huge accumulation of CFTR protein observed after proteasomal inhibition with MG132 (MG132+LB at 18 h) (fig. 5a and b) was secondary to newly synthesised CFTR proteins, we verified that a co treatment with CHX (MG132+CHX+LB) totally prevented CFTR accumulation.
Source ERJ Express.(2015). Figure 4. MG132 (Abmole Bioscience, Kowloon, Honk Hong)
Method Immunoblotting
Cell Lines CFBE-ΔF508 and CFBE-wt cell lines
Concentrations
Incubation Time 2 h, 8 h, 18 h
Results In fact, our data obtained in the presence of MG132 and/or CHX (figs 4 and 5) indicated that CFTR synthesis may also be affected by PsaDM.
Source Autophage (2016) . Figure 2. MG132 (Abmole BioScience, M1902)
Method Western blot
Cell Lines HEK293T, MCF7 or MDA-MB-231 cells
Concentrations 10 μM
Incubation Time 6 h
Results Results showed that NH4Cl, but not MG132, 3-MA or wortmannin, induced the accumulation of HSD17B4 protein (Fig. 2A ), indicating that the degradation of HSD17B4 is independent of the proteasome and macroautophagy pathways.
Protocol (for reference only)
Cell Experiment
Cell lines Lung cancer cell lines A549 and H1299
Preparation method Cell viability assay. Cell viability was determined using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. Cells were seeded in 96-well plates at a density of 2.5x103/well 1 day prior to treatment. Then, cells were treated with MG132 or/and irradiation. After treatment, 20 µl of 5 mg/ml MTT solution was added into each well and incubated for 4 h. After the supernatant was removed, 100 µl of DMSO was added, and then placed in a microplate reader to measure OD value. Cell viability rate (vR) was calculated according to the following formula: vR = (OD in observed group/OD in 0 Gy group) x 100%. All assays were repeated 3 times in quintuplicate.
Concentrations 200 nM
Incubation time 6h
Animal Experiment
Animal models Male mdx (C57BL/10ScSn DMD mdx) mice
Formulation Dissolved in DMSO, and diluted in PBS
Dosages ~10 μg/kg/day
Administration Injection
Chemical Information
Molecular Weight 475.62
Formula C26H41N3O5
CAS Number 133407-82-6
Solubility (25°C) DMSO 80 mg/mL
Ethanol 20 mg/mL
Storage Powder          -20°C   3 years ;  4°C   2 years
In solvent       -80°C   6 months ;  -20°C   1 month
References

[1] Andrew Sandstrom, et al. Science. Functional degradation: A mechanism of NLRP1 inflammasome activation by diverse pathogen enzymes

[2] Ashley J Chui, et al. Science. N-terminal degradation activates the NLRP1B inflammasome

[3] Guo N, et al. Asia Pac J Clin Oncol. MG132, a proteasome inhibitor, induces apoptosis in tumor cells.

[4] Zanotto-Filho A, et al. Invest New Drugs. Proteasome inhibitor MG132 induces selective apoptosis in glioblastoma cells through inhibition of PI3K/Akt and NFkappaB pathways, mitochondrial dysfunction, and activation of p38-JNK1/2 signaling.

[5] Han YH, et al. Oncol Rep. The effect of MG132, a proteasome inhibitor on HeLa cells in relation to cell growth, reactive oxygen species and GSH.

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Keywords: MG132, Z-Leu-Leu-Leu-al; MG-132 supplier, Proteasome, inhibitors, activators

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