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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Solary, E., Giordanetto, F. & Kroemer, G. Re-examining the role of cytochrome c in cell death. Nat Genet 40, 379–380 (2008). https://doi.org/10.1038/ng0408-379
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DOI: https://doi.org/10.1038/ng0408-379
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