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Requirement of an Ice/Ced-3 Protease for Fas/Apo-1-Mediated Apoptosis
Institute of Biochemistry, Albert-Ludwigs-University, Hermann-Heder-Strasse 7, D79104 Freiburg im Breisgau, Germany.
Laboratory of Molecular Biology, University of Ghent, Ghent, Belgium.
Laboratory of Molecular Biology, University of Ghent, Ghent, Belgium.
Divisions of Immunochemistry § Divisions of Immunogenetics, Tumorimmunology Program, German Cancer Research Center, Heidelberg, Germany.
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1995 (English)In: Nature, ISSN 0028-0836, Vol. 375, no 6526, 81-83 p.Article in journal (Refereed) Published
Abstract [en]

THE Fas/APO-1 receptor is one of the major regulators of apoptosis(1-7). We report here that Fas/APO-1-mediated apoptosis requires the activation of a new class of cysteine proteases, including interleukin-1 beta-converting enzyme (ICE)(8-10) which are homologous to the product of the Caenorhabditis elegans cell-death gene ced-3 (refs 11, 12). Triggering of Fas/APO-1 rapidly stimulated the proteolytic activity of ICE. Overexpression of ICE, achieved by electroporation and microinjection, strongly potentiated Fas/APO-1-mediated cell death. In addition, inhibition of ICE activity by protease inhibitors, as well as by transient expression of the pox virus-derived serpin inhibitor CrmA or an antisense ICE construct, substantially suppressed Fas/APO-1-triggered cell death. We conclude that activation of ICE or an ICE-related protease is a critical event in Fas/APO-1-mediated cell death.

Place, publisher, year, edition, pages
1995. Vol. 375, no 6526, 81-83 p.
Keyword [en]
cell-surface antigen, death gene ced-3, fas, induction, interleukin-1-beta converting enzyme, molecular-cloning, monoclonal-antibody, receptor, tumor-necrosis-factor, virus encodes
National Category
Biochemistry and Molecular Biology Cell Biology
URN: urn:nbn:se:liu:diva-87080DOI: 10.1038/375081a0ISI: A1995QW60400060OAI: diva2:584839
Available from: 2013-01-09 Created: 2013-01-09 Last updated: 2013-01-28

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