Induction of apoptosis in fibroblasts by IL-1β-converting enzyme, a mammalian homolog of the C. elegans cell death gene ced-3
The mammalian interleukin-lfl-converting enzyme (ICE) has sequence similarity to the C.
elegans cell death gene ted-3. We show here that overexpression of the murine ICE (mlCE)
gene or of the C. elegans ted-3 gene causes Rat-l cells to undergo programmed cell death.
Point mutations in a region homologous between mlCE and CED-3 eliminate the ability of
mlCE and ted-3 to cause cell death. The cell death caused by mlCE can be suppressed by
overexpression of the crmA gene, a specific inhibitor of ICE, as well as by bcl-2, a …
elegans cell death gene ted-3. We show here that overexpression of the murine ICE (mlCE)
gene or of the C. elegans ted-3 gene causes Rat-l cells to undergo programmed cell death.
Point mutations in a region homologous between mlCE and CED-3 eliminate the ability of
mlCE and ted-3 to cause cell death. The cell death caused by mlCE can be suppressed by
overexpression of the crmA gene, a specific inhibitor of ICE, as well as by bcl-2, a …
Summary
The mammalian interleukin-lfl-converting enzyme (ICE) has sequence similarity to the C. elegans cell death gene ted-3. We show here that overexpression of the murine ICE (mlCE) gene or of the C. elegans ted-3 gene causes Rat-l cells to undergo programmed cell death. Point mutations in a region homologous between mlCE and CED-3 eliminate the ability of mlCE and ted-3 to cause cell death. The cell death caused by mlCE 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.
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