| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
| 500mg | 电议 |
MG-132 (Z-Leu-Leu-Leu-al) 是一种有效的蛋白酶体和钙蛋白酶抑制剂，IC50 分别为 100 nM 和 1.2 μM。 MG-132 有效阻断 26S 蛋白酶体复合物的蛋白水解活性。 MG-132 是一种肽醛，也是一种自噬激活剂。 MG-132 还诱导细胞凋亡。
Cell lines | KIM-2 |
Preparation Method | MG-132 were diluted in Me2SO. Cells were treated with protease inhibitors or dilutant alone. Supernatant and monolayer cells were harvested by centrifugation and fixed in 70% ethanol in PBS for staining with acridine orange. Equal volumes of cells and acridine orange (5 mg/ml in PBS) were mixed on a microscope slide and examined by fluorescence microscopy. |
Reaction Conditions | 0, 1.5, 5 μM, 24 h |
Applications | MG-132 treatment induces apoptosis in a cell cycle dependent manner. |
Animal models | C57BL/10ScSn DMD mdx mice |
Preparation Method | Localized administration was performed by injection of MG-132 into the gastrocnemius muscles of mdx mice. To visualize the injected muscle, MG-132 (final concentration of 20 μmol/L) was pre-mixed with 1% India ink in phosphate-buffered saline (PBS) for a total volume of 100 μl. Mice were sacrificed 24 hours after injection, and skeletal muscles were quickly isolated for further analysis. To systemically administer MG-132, Alzet Minipumps was subcutaneously implanted in the anterior back region of mdx mice. Experiments were conducted on 6-month-old mdx mice. For 8 days, administration of either different concentrations of MG-132 (delivered at rate of either 1 μg, or 5 μg or 10 μg/kg/24 hours) or the inhibitor-diluent (PBS only) was enforced, as a negative control. Skeletal muscle tissues were collected from untreated (PBS only) and MG-132-treated mdx mice for further analysis. |
Dosage form | 1 μg, 5 μg, 10 μg/kg, injection into the gastrocnemius muscles or subcutaneously implanted Alzet Minipumps |
Applications | MG-132, as a proteasomal inhibitor, effectively rescues the expression levels and plasma membrane localization of dystrophin, β-dystroglycan, α-dystroglycan, and α-sarcoglycan in skeletal muscle fibers from mdx mice. Furthermore, MG-132 reduces muscle membrane damage, as revealed by vital staining of the diaphragm and gastrocnemius muscle isolated from treated mdx mice, and ameliorates the histopathological signs of muscular dystrophy, as judged by hematoxylin and eosin staining of muscle biopsies taken from treated mdx mice. |
| 文献引用 | |
| 产品描述 | MG-132 is a potent, reversible, and cell-permeable proteasome inhibitor. It belongs to the class of synthetic peptide aldehydes. It reduces the degradation of ubiquitin-conjugated proteins in mammalian cells and permeable strains of yeast by the 26S complex without affecting its ATPase or isopeptidase activities.MG-132 activates c-Jun N-terminal kinase (JNK1), which initiates apoptosis.MG-132 also inhibits NF-κB activation and prevents β-secretase cleavage. MG-132 inhibits 20S proteasome with IC50 of 100 nM in vitro. Furthermore,MG-132 treatment induces apoptosis in a cell cycle dependent manner.[1][2] MG-132 can treat mdx Mice by rescuing the Expression and Membrane Localization of Dystrophin and Dystrophin-Associated Proteins. For in vivo experiment,MG-132 was administrated into mdx mice by injection into the gastrocnemius muscles or subcutaneously implanted Alzet Minipumps. As a result,MG-132, as a proteasomal inhibitor, effectively rescues the expression levels and plasma membrane localization of dystrophin, β-dystroglycan, α-dystroglycan, and α-sarcoglycan in skeletal muscle fibers from mdx mice. Furthermore,MG-132 reduces muscle membrane damage, as revealed by vital staining of the diaphragm and gastrocnemius muscle isolated from treated mdx mice, and ameliorates the histopathological signs of muscular dystrophy, as judged by hematoxylin and eosin staining of muscle biopsies taken from treated mdx mice.[3] References: |
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