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Caspase-8 and Apaf-1-independent caspase-9 activation in Sendai virus-infected cells

MPG-Autoren
http://pubman.mpdl.mpg.de/cone/persons/resource/persons78448

Neubert,  W. J.
Former Research Groups, Max Planck Institute of Biochemistry, Max Planck Society;

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Zitation

Bitzer, M., Armeanu, S., Prinz, F., Ungerechts, G., Wybranietz, W., Spiegel, M., et al. (2002). Caspase-8 and Apaf-1-independent caspase-9 activation in Sendai virus-infected cells. Journal of Biological Chemistry, 277(33), 29817-29824.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0010-6E7E-5
Zusammenfassung
Apoptotic cell death is of central importance in the pathogenesis of viral infections. Activation of a cascade of cysteine proteases, i.e. caspases, plays a key role in the effector phase of virus-induced apoptosis. However, little is known about pathways leading to the activation of initiator caspases in virus-infected host cells. Recently, we have shown that Sendai virus (SeV) infection triggers apoptotic cell death by activation of the effector caspase-3 and initiator caspase- 8. We now investigated mechanisms leading to the activation of another initiator caspase, caspase-9. Unexpectedly we found that caspase-9 cleavage is not dependent on the presence of active caspases-3 or -8. Furthermore, the presence of caspase-9 in mouse embryonic fibroblast (MEF) cells was a prerequisite for Sendai virus-induced apoptotic cell death. Caspase-9 activation occurred without the release of cytochrome c from mitochondria and was not dependent on the presence of Apaf-1 or reactive oxygen intermediates. Our results therefore suggest an alternative mechanism for caspase-9 activation in virally infected cells beside the well characterized pathways via death receptors or mitochondrial cytochrome c release.