Ricci et al. (page 65) show that, in both isolated mitochondria and living cells, caspase-3 induces a loss of membrane potential in mitochondria that have been permeabilized by proapoptotic proteins. Inhibition of caspase activity prevented this loss in potential, which places membrane potential loss downstream of cytochrome c release and subsequent activation of caspases.
Mitochondria lost membrane potential because complexes I and II were injured. Caspase-treated permeabilized mitochondria did not consume oxygen in response to substrates used by complexes I and...
The Rockefeller University Press
2003
The Rockefeller University Press
2003
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