Requirement of an Ice/Ced-3 Protease for Fas/Apo-1-Mediated Apoptosis
1995 (English)In: Nature, ISSN 0028-0836, Vol. 375, no 6526, 81-83 p.Article in journal (Refereed) Published
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.
cell-surface antigen, death gene ced-3, fas, induction, interleukin-1-beta converting enzyme, molecular-cloning, monoclonal-antibody, receptor, tumor-necrosis-factor, virus encodes
Biochemistry and Molecular Biology Cell Biology
IdentifiersURN: urn:nbn:se:liu:diva-87080DOI: 10.1038/375081a0ISI: A1995QW60400060OAI: oai:DiVA.org:liu-87080DiVA: diva2:584839