Abstract
The mammalian interleukin-1 beta-converting enzyme (ICE) has sequence similarity to the C. elegans cell death gene ced-3. We show here that overexpression of the murine ICE (mICE) gene or of the C. elegans ced-3 gene causes Rat-1 cells to undergo programmed cell death. Point mutations in a region homologous between mICE and CED-3 eliminate the ability of mICE and ced-3 to cause cell death. The cell death caused by mICE can be suppressed by overexpression of the crmA gene, a specific inhibitor of ICE, as well as by bcl-2, a mammalian oncogene that can act to prevent programmed cell death. Our results suggest that ICE may function during mammalian development to cause programmed cell death.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Apoptosis*
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Base Sequence
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Caspase 1
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Cell Line
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DNA Primers / chemistry
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In Vitro Techniques
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Metalloendopeptidases / antagonists & inhibitors
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Metalloendopeptidases / physiology*
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Mice
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Molecular Sequence Data
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Mutagenesis, Site-Directed
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Proto-Oncogene Proteins / pharmacology
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Proto-Oncogene Proteins c-bcl-2
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Rats
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Recombinant Fusion Proteins / metabolism
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Serpins / metabolism
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Viral Proteins*
Substances
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DNA Primers
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Proto-Oncogene Proteins
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Proto-Oncogene Proteins c-bcl-2
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Recombinant Fusion Proteins
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Serpins
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Viral Proteins
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interleukin-1beta-converting enzyme inhibitor
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Caspase 1
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Metalloendopeptidases