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Oligomycin A
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
Oligomycin A图片
CAS NO:579-13-5
规格:98%
分子量:791.06
包装与价格:
包装价格(元)
5mg电议
25mg电议

产品介绍
Mitochondrial ATP synthase Inhibitor
CAS:579-13-5
分子式:C45H74O11
分子量:791.06
纯度:98%
存储:Store at -20°C

Background:

Oligomycin A is an inhibitor of ATP synthase, which inhibits the process taking place on mitochondria coupling membrane that depended on ATP and oxidative phosphorylation [1].


Oligomycin A blocks proton channel of ATP synthase, which is necessary for transforming ADP to ATP by oxidative phosphorylation, accomplishing the inhibition of ATP synthase. The process which oligomycin A inhibits ATP synthesis can significantly reduce electron flow through the electron transport chain.


Experiments which performed in testing against 60 human cancer cell lines that from the National Cancer Institute showed that oligomycin is among the top 0.1% of the most cell line selective cytotoxic agents of 37,000 molecules. In the HeLa carcinoma cell line, the inhibitors of H+ -ATP-synthase oligomycin (5 mg/ml) was shown to strongly suppress, and the cell respiration, showing that it is tightly coupled to ATP synthesis. It was reported that Oligomycin at 100 ng/ml completely inhibits the activity of oxidative phosphorylation in 1h and induces different levels of glycolysis gains by 6 h in a group of cancer cell. As an inhibitor of the F0 part of H+-ATP-synthase, Oligomycin also suppresses the apoptosis which was induced by TNF. Treatment with different concentrations of oligomycin and rotenone severely reduced the oxygen consumption by up to 94%, indicating a major role for mitochondria in this process. And treatment with oligomycin could abolish the H2O2 increase completely [2-4].


参考文献:
[1].  Jastroch M, Divakaruni AS, Mookerjee S, et al. Mitochondrial proton and electron leaks. Essays Biochemistry, 2010, 47:53-67.
[2].  Shchepina LA, Pletjushkina OY, Avetisyan AV, et al. Oligomycin, inhibitor of the F-0 part of H+-ATP-synthase, suppresses the TNF-induced apoptosis. Oncogene, 2002, 53: 8149-8157.
[3].  Salomon AR, Voehringer DW, Herzenberg LA, et al. Understanding and exploiting the mechanistic basis for selectivity of polyketide inhibitors of F0F1-ATPase. Proceedings of The National Academy of Sciences of The United States of America, 2000, 97(26): 14766-14771.
[4].  Alexander R, Adina V, Ivan B, et al. Overcoming intrinsic multi-drug resistance in melanoma by blocking the mitochondrial respiratory chain of slow-cycling JARID1Bhigh cells. Cancer Cell, 2013, 23(6): 811-825.