Oligomycin

貨號 Cat. No.: O-500
規格 Size: 10 x 1 mg 5mg 5x5mg

Description

Oligomycin

Mitochondrial ATP Synthase Inhibitor

Product#:

O-500

Sizes:

10 x 1 mg

5 mg

5 x 5 mg

M.W.:

789.3

CAS No.:

[14110-64-6]

Structure:

Bioassay:

Oligomycin inhibits ATP dependent adipogenesis in 3T3-L1 cells. 3T3-L1 preadipocytes were induced to undergo adipocyte differentiation (A-D). 5 days post differentiation, different concentrations of Oligomycin (#O-500) were added (A=0, B=1, C=2, and D=10mg/ml). After 10 days the cells were stained with Oil Red 0 and visualized by light microscopy.

References:

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5.	Arato-Oshima, T. et al. (1996) J. Biol. Chem. 271, 25604.
6.	Fortes, P.A. and Lee, J.A. (1984) J. Biol. Chem. 259, 11176.
7.	Garrahan, P.J. and Glynn, I.M. (1967) J. Physiol. 192, 217.
8.	Cornelius, F. and Skou, J.C. (1985) Biochim. Biophys. Acta 818, 211.
9.	Martin, W.H. et al. (1994) Proc. Natl. Acad. Sci USA 91, 9881.
10.	Hegyvary, C. (1976) Biochim. Biophys. Acta 422, 365.
11.	Fahn, S. et al. (1966) J. Biol. Chem. 241, 1882.
12.	Fahn, S. et al. (1968) J. Biol. Chem. 243, 1993.
13.	Inturrisi, C.E. and Titus, E. (1968) Mol. Pharmacol. 4, 591.

Oligomycin is a natural antibiotic isolated from Streptomyces diastatochromogenes

which inhibits mitochondrial H⁺-ATP synthase. It is primarily found to act as an inhibitor of mitochondrial respiration and swelling. This antibiotic is widely used as an inhibitor of oxidative phosphorylation.^1-2 ^6-16

These inhibitory properties have been attributed to its ability to occlude the transition of E₁~P (high energy intermediate) to E₂-P (low energy intermediate) by oligomycin binding to E₁~P.¹⁷

Oligomycin inhibits the H⁺- ATP-synthase by binding to the Oligomycin sensitivity-conferring protein(OSCP) at the F(o) subunits 6 and 9 which are found in the stalk of the F₁F₀-ATPase complex. This binding blocks the proton conductance and inhibits the synthesis of mitochondrial ATP.^3-4 Because of its activity, it can also be used to reduce the number of parameters(such as ER Ca²⁺ release, exocytotoxicity and apopotosis) which are affected by mitochondrial depolarization.⁵

Oligomycin at high concentrationsmay also inhibit the plasma membrane Na⁺-K⁺-ATPase. Interaction of Oligomycin with the Na⁺ occlusion site on the extracellular side of Na/K-ATPase, delays Na⁺ release to the extracellular side without inducing a conformational change. Although Oligomycin stimulated Na⁺ binding to Na⁺/K⁺-ATPase, it inhibited Na⁺/Na⁺ exchange, and did not affect either Na⁺-dependent AD/-ATP exchange or K⁺-dependent phosphatase activity.

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