Posttranslational regulation of Bim by caspase-3
- PMID: 17584989
- DOI: 10.1196/annals.1402.001
Posttranslational regulation of Bim by caspase-3
Abstract
Bim is a proapoptotic BH3-domain-only member of the Bcl-2 family, and its expression is regulated both transcriptionally and posttranslationally. We developed an in vitro system examining the posttranslational regulation of Bim. Since Bim is a strong mediator of apoptosis, it has been quite difficult to establish cell lines stably overexpressing Bim. Coexpression of Bcl-2 enabled us to obtain mouse embryonic fibroblasts (MEFs) in which Bim is overexpressed and Bcl-2 expression is regulated by Tet-off system. Reduction of Bcl-2 levels by doxycycline treatment induced caspase-3 and caspase-7 activation, which was followed by Bim degradation. Bim degradation was suppressed by gene knockdown of caspase-3, but not by caspase-7 knockdown. The same posttranslational regulation of Bim was observed in osteoclasts. These results suggest that caspase-3 negatively regulates Bim expression by stimulating its degradation, thus creating a negative feedback loop in the Bim-caspase axis.
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