The α-toxin activates intracellular caspases independently of transmembrane death receptor proteins, and can induce release of cytochrome c from isolated mitochondria. In both cases, however, the mechanism is likely to be indirect. Pores formed by α-toxin are unlikely to be big enough to allow either entry of α-toxin into the cell or exit of cytochrome c from mitochondria. Thus, apoptosis may be...
The Rockefeller University Press
2001
The Rockefeller University Press
2001
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