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Nature Genetics 40, 379 - 380 (2008)
doi:10.1038/ng0408-379
Re-examining the role of cytochrome c in cell death
Eric Solary1, Fabrizio Giordanetto2 & Guido Kroemer3
- Eric Solary is at INSERM U866, 21000 Dijon, France and Institut Gustave Roussy, 94805 Villejuif, France.
- Fabrizio Giordanetto is at SwedenAstraZeneca R&D Mölndal, SE-431 83 Mölndal, Sweden.
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Guido Kroemer is at Institut Gustave Roussy, INSERM U848 and Université Paris-Sud 11, 94805 Villejuif, France.
e-mail: kroemer@igr.fr
Abstract
When cytochrome c is released from mitochondria, it interacts with Apaf-1 to activate death-promoting caspases. Now, a gain-of-function mutation affecting cytochrome c with enhanced caspase-stimulatory activity is shown to have no other consequences for human health than a subclinical thrombocytopenia, showing that, in most settings, enhanced cytochrome c activity per se is not sufficient to disturb normal tissue homeostasis.
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