XIAP discriminates between type I and type II FAS-induced apoptosis

Philipp J. Jost, Stephanie Grabow, Daniel Gray, Mark D. McKenzie, Ueli Nachbur, David C. S. Huang, Philippe Bouillet, Helen E. Thomas, Christoph Borner, John Silke, Andreas Strasser () and Thomas Kaufmann ()
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Philipp J. Jost: The Walter and Eliza Hall Institute of Medical Research,
Stephanie Grabow: The Walter and Eliza Hall Institute of Medical Research,
Daniel Gray: The Walter and Eliza Hall Institute of Medical Research,
Mark D. McKenzie: Melbourne University, Parkville, Victoria 3050, Australia
Ueli Nachbur: Institute of Biochemistry, LaTrobe University, Bundoora, Victoria 3086, Australia
David C. S. Huang: The Walter and Eliza Hall Institute of Medical Research,
Philippe Bouillet: The Walter and Eliza Hall Institute of Medical Research,
Helen E. Thomas: St Vincent’s Institute of Medical Research, Fitzroy, Victoria 3065, Australia
Christoph Borner: Institute of Molecular Medicine and Cell Research, Centre for Biochemistry and Molecular Cell Research, Freiburg, D79104, Germany
John Silke: Institute of Biochemistry, LaTrobe University, Bundoora, Victoria 3086, Australia
Andreas Strasser: The Walter and Eliza Hall Institute of Medical Research,
Thomas Kaufmann: The Walter and Eliza Hall Institute of Medical Research,

Nature, 2009, vol. 460, issue 7258, 1035-1039

Abstract: Divergent routes to cell death One of the current problems in cell death research is to understand why distinct cell types (type I versus type II cells) differ so markedly in the mechanisms by which the 'death receptor' FAS triggers their apoptosis. Type I cells die by FAS-induced activation of caspase-8 and downstream effector caspases, leading a quick demise; type II cells, however, have to amplify the caspase cascade through caspase-8-mediated activation of the 'death agonist' BID, and subsequent activation of caspase-9. Jost et al. now show that the inhibitor of apoptosis, XIAP, makes all the difference for these cells: without XIAP a type II cell dies just like any cell type I. The authors suggest that IAP inhibitors should be used with caution in cancer patients with underlying liver conditions since they might unintentionally sensitize non-target cells to die.

Date: 2009
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DOI: 10.1038/nature08229

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