Caspase 3 inactivation to suppress Fas-mediated apoptosis: identification of binding domain with p21 and ILP and inactivation machinery by p21

Oncogene. 1999 Feb 4;18(5):1239-44. doi: 10.1038/sj.onc.1202409.

Abstract

The death mediator caspase acts as the dominant regulator during cell death induction. The CPP32 subfamily, including caspase 3 (CPP32/Yama/Apopain), is essential for the cell death signaling. We recently reported that activation of caspase 3 is regulated by complex formation with p21 or ILP. In the present study, we investigated the binding domain with p21 and ILP to further characterize the caspase 3 inactivation machinery. Our results show that caspase 3 contains p21 binding domain in the N-terminus and ILP binding domain in the active site. Further, the caspase 3 binding domain in p21 was independent of the Cdk- or PCNA-binding domain. We also found caspase 3 protection by p21 from the p3-site cleavage serineproteinase contributes to the suppression machinery. Here, we propose the caspase 3 inactivation system by p21 and ILP as new essential system in the regulation of cell death.

MeSH terms

  • Apoptosis*
  • Binding Sites
  • Caspase 3
  • Caspases / metabolism*
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins / metabolism*
  • Enzyme Precursors / metabolism
  • Humans
  • Peptide Fragments / metabolism
  • Protein Binding
  • Tumor Cells, Cultured
  • fas Receptor / metabolism*

Substances

  • CDKN1A protein, human
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins
  • Enzyme Precursors
  • Peptide Fragments
  • fas Receptor
  • CASP3 protein, human
  • Caspase 3
  • Caspases