| Autor: |
Shchepina, Liarisa A, Pletjushkina, Olga Y, Avetisyan, Armine V, Bakeeva, Liora E, Fetisova, Elena K, Izyumov, Denis S, Saprunova, Valeria B, Vyssokikh, Mikhail Y, Chernyak, Boris V, Skulachev, Vladimir P |
| Předmět: |
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| Zdroj: |
Oncogene; 11/21/2002, Vol. 21 Issue 53, p8149, 9p |
| Abstrakt: |
The release of cytochrome c from the intermembrane space of mitochondria into the cytosol is one of the critical events in apoptotic cell death. In the present study, it is shown that release of cytochrome c and apoptosis induced by tumor necrosis factor α (TNF) in HeLa cells can be inhibited by (i) overexpression of an oncoprotein Bcl-2, (ii) Cyclosporin A, an inhibitor of the mitochondrial permeability transition pore (PTP) or (iii) oligomycin, an inhibitor of H+- ATP-synthase. Staurosporine-induced apoptosis is sensitive to Bcl-2 but insensitive to Cyclosporin A and oligomycin. The effect of oligomycin is not due to changes in mitochondrial membrane potential or to inhibition of ATP synthesis/hydrolysis since (a) uncouplers (CCCP, DNP) which discharge the membrane potential fail to abolish the protective action of oligomycin and (b) aurovertin B (another inhibitor of H+-ATP-synthase, affecting its F1 component) do not affect apoptosis. A role of oligomycin-sensitive F0 component of H+-ATP-synthase in the TNF-induced PTP opening and apoptosis is suggested.Oncogene (2002) 21, 8149–8157. doi:10.1038/sj.onc.1206053 [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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