Identification of an endogenous dominant-negative short isoform of caspase-9 that can regulate apoptosis

Cancer Res. 1999 Mar 1;59(5):999-1002.

Abstract

Alternatively spliced isoforms of certain apoptosis regulators, such as Bcl-x, Ced-4, and Ich-1, have been shown to play opposing roles in regulating apoptosis. Here, we describe the identification of an endogenous alternatively spliced isoform of caspase-9, named caspase-9b, which lacks the central large subunit caspase domain. Caspase-9b is detectable in many cell lines by PCR and at the mRNA and protein levels. Caspase-9b can interact with the caspase recruitment domain of Apaf-1, and like the active site mutant of caspase-9, it can inhibit multiple forms of apoptosis, including those triggered by oligomerization of death receptors. It can also block activation of caspase-9 and -3 by Apaf-1 in an in vitro cytochrome c-dependent caspase activation assay. These results suggest that caspase-9b functions as an endogenous apoptosis inhibitory molecule by interfering with the formation of a functional Apaf-1-caspase-9 complex.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Alternative Splicing*
  • Amino Acid Sequence
  • Apoptosis*
  • Base Sequence
  • Binding Sites
  • Caspase 9
  • Caspases / chemistry
  • Caspases / genetics*
  • Caspases / metabolism*
  • Cell Line
  • Cloning, Molecular
  • HeLa Cells
  • Humans
  • Isoenzymes / chemistry
  • Isoenzymes / genetics*
  • Isoenzymes / metabolism
  • Jurkat Cells
  • Molecular Sequence Data
  • Polymerase Chain Reaction
  • Protein Biosynthesis
  • RNA, Messenger / genetics
  • Recombinant Proteins / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Sequence Alignment
  • Sequence Homology, Amino Acid
  • Transcription, Genetic
  • Tumor Cells, Cultured

Substances

  • Isoenzymes
  • RNA, Messenger
  • Recombinant Proteins
  • CASP9 protein, human
  • Caspase 9
  • Caspases

Associated data

  • GENBANK/AF093130