In vitro transcription of capped mRNA with modified nucleotides and Poly(A) tail
Tyramide Signal Amplification (TSA)
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Phos Binding Reagent Acrylamide
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
Cell Counting Kit-8 (CCK-8)
A convenient and sensitive way for cell proliferation assay and cytotoxicity assay
SYBR Safe DNA Gel Stain
Safe and sensitive stain for visualization of DNA or RNA in agarose or acrylamide gels.
Protect the integrity of proteins from multiple proteases and phosphatases for different applications.
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 .
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].
. Jastroch M, Divakaruni AS, Mookerjee S, et al. Mitochondrial proton and electron leaks. Essays Biochemistry, 2010, 47:53-67.
. 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.
. 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.
. 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.
|Physical Appearance||A solid|
|Storage||Store at -20°C|
|Solubility||≥9.9mg/mL in DMSO, ≥17.43 mg/mL in EtOH,insoluble in H2O|
|Shipping Condition||Evaluation sample solution: ship with blue ice. All other available sizes: ship with RT, or blue ice upon request.|
|General tips||For obtaining a higher solubility, please warm the tube at 37°C and shake it in the ultrasonic bath for a while. Stock solution can be stored below -20°C for several months.|
Human laryngeal cancer docetaxel-resistant DRHEp2 cells
The solubility of this compound in DMSO is > 9.9mg/mL. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months.
72 h, 2 µg/ml
Oligomycin A is an Fo-ATPase inhibitor. Oligomycin A increased the sensitivity of DRHEp2 cells to docetaxel in a dose-dependent manner and combining oligomycin A and docetaxel increased the generation of mitochondrial ROS.
. Mizumachi T, Suzuki S, Naito A, et al. Increased mitochondrial DNA induces acquired docetaxel resistance in head and neck cancer cells[J]. Oncogene, 2008, 27(6): 831-838.