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Product Details
Oligomycin A,579-13-5,IC-0201659
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 produced a concentration-dependent block of Icrac with similar characteristics, but with lower potency than oligomycin B. Fits of averaged concentration-response data to a logistic function yielded IC50 values and slope factor coefficients (respectively) of 13.5 μM and 0.85 for oligomycin A, and 2.3 μM and 0.82 for oligomycin B. A two-way analysis of variance confirmed a significantly greater inhibition by oligomycin B over the concentration range tested [2]. Oligomycin A treated Wt(widetype) mice have decreased ATP levels in the liver. Concomitantly, these mice showed an enhanced apoptosis in hepatocytes as Tg mice after LPS/GalN administration [3]. Further activation of AMPK was detected in Wt mice after treatment with oligomycin A. Collectively, these data demonstrated that UCP2 expression in hepatocytes could alter mitochondrial parameters leading to activation of AMPK [3].
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 produced a concentration-dependent block of Icrac with similar characteristics, but with lower potency than oligomycin B. Fits of averaged concentration-response data to a logistic function yielded IC50 values and slope factor coefficients (respectively) of 13.5 μM and 0.85 for oligomycin A, and 2.3 μM and 0.82 for oligomycin B. A two-way analysis of variance confirmed a significantly greater inhibition by oligomycin B over the concentration range tested [2]. Oligomycin A treated Wt(widetype) mice have decreased ATP levels in the liver. Concomitantly, these mice showed an enhanced apoptosis in hepatocytes as Tg mice after LPS/GalN administration [3]. Further activation of AMPK was detected in Wt mice after treatment with oligomycin A. Collectively, these data demonstrated that UCP2 expression in hepatocytes could alter mitochondrial parameters leading to activation of AMPK [3].
