| 包装 | 价格(元) |
| 1mg | 电议 |
| 5mg | 电议 |
Preparation Method | The reaction mixture for 20S proteasome inhibitory assay contained 0.1 M Tris-acetate, pH 7.0, 20S proteasome, MG-132 and 25 μM substrate dissolved in DMSO in a final volume of 1 ml. |
Reaction Conditions | After incubation at 37 ℃ for 15 min, the reaction was stopped by the addition of 0.1 ml of 10% SDS and 0.9 ml of 0.1 M Tris-acetate, pH 9.0. |
Applications | After measurement of fluorescence of reaction products, the IC50of MG-132 against m-calpain and 20S proteasome can be determined. MG-132 inhibits 20S proteasome with IC50of 100 nM. |
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. |
| 产品描述 | Uridine diphosphate glucose (uracil-diphosphate glucose, UDPG) is a nucleotide sugar. It is used in nucleotide sugar metabolism as an activated form of glucose, a substrate for enzymes called glucosyltransferases.[1]Uridine diphosphate glucose has been shown to have tissue-specific effects that have proved to be of clinical value in the treatment of some liver ailments. It is also known to have multiple effects on intrahepatic bilirubin metabolism which, in turn, are related to the glycogen synthesis occurring in the liver.[2] In vitro study demonstrated that the effects of UDPG on cell metabolism do not appear to be limited to enzyme induction. Others have reported that UDPG can have effects under conditions that bar enzyme induction. Results showed that a significant amount of the UDPG, even though it is a highly polar compound, does pass through the membrane unchanged. A large fraction of the UDPG added to incubation media, however, was found in the cell as glucose phosphate, indicating cleavage after penetration of the cell. Eventually. all the UDPG that entered the cells was degraded to glucose phosphate and glucose. The in vitro studies show that G-6-P is not the active form, and several tests show that uridine does not lead to changes like those seen with UDPG.[2] In vivo study indicated that indicate that the intracellular level of PRPP in animal tissues is greatly affected by extracellular UDPG. The alteration of PRPP level by UDPG is not linearly dose-related. The changes in PRPP that were induced by UDPG were also tissue-specific: mouse liver was more sensitive than was the spleen. This latter specificity may well be related to the therapeutically beneficial effects of UDPG.[2] References: |
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