| Evidence for an interleukin-1beta converting enzyme (ICE)-like activity distinct from ICE and responsible for ICE and CPP32 cleavage during apoptosis. | |
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MedLine Citation:
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PMID: 14646547 Owner: NLM Status: PubMed-not-MEDLINE |
Abstract/OtherAbstract:
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IL-1beta converting enzyme (ICE) and ICE-related proteases (IRPs) have been suggested to play a central role in apoptosis. We report the use of peptidic ICE inhibitors to reassess the role of this enzyme in the apoptosis induced by Fas or TNFalpha receptor ligation in Jurkat cells, U937 cells or monocytes. Our results show that inhibition of IL-1beta processing can be dissociated from inhibition of apoptosis. Indeed, two out of three com-pounds active on ICE are not inhibitory for apoptosis. This shows that ICE is not required for progression in the apoptotic pathway, but that one or several IRPs are necessary. In addition, Western blot analysis of cell lysates shows that both ICE and CPP32 precursors disappear rapidly after apoptosis induction, while ICH-1L precursor remains intact. Concomitant appearance of cleavage products can be visualized for CPP32, but not for ICE, suggesting that the former is proteolytically activated. In addition, this precursor cleavage can be blocked by an ICE inhibitor active on apoptosis. Altogether, our data support the hypothesis that one or several IRPs are necessary for apoptosis and are responsible for ICE and CPP32 cleavage during this process. |
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Authors:
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C Miossec; V Dutilleul; L Durand; C Faucheu; L Pilatre; J Golec; F Fassy; A Diu-Hercend |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Apoptosis : an international journal on programmed cell death Volume: 2 ISSN: 1360-8185 ISO Abbreviation: Apoptosis Publication Date: 1997 |
Date Detail:
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Created Date: 2003-12-03 Completed Date: 2003-12-23 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 9712129 Medline TA: Apoptosis Country: United States |
Other Details:
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Languages: eng Pagination: 125-35 Citation Subset: - |
Affiliation:
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Roussel Uclaf, Romainville, France. miossec@mac.rousseluclaf.fr |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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