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

Michael Bitzer, Sorin Armeanu, Florian Prinz, Guy Ungerechts, Wolfgang Wybranietz, Martin Spiegel, Christian Bernlöhr, Francesco Cecconi, Michael Gregor, Wolfgang J. Neubert, Klaus Schulze-Osthoff, Ulrich M. Lauer

Research output: Contribution to journalArticlepeer-review

Abstract

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.

Original languageEnglish
Pages (from-to)29817-29824
Number of pages8
JournalJournal of Biological Chemistry
Volume277
Issue number33
Publication statusPublished - Aug 16 2002

ASJC Scopus subject areas

  • Biochemistry

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