Apaf1 and the apoptotic machinery

Research output: Contribution to journalArticle

104 Citations (Scopus)

Abstract

The molecular characterization of the Caenorhabditis elegans cell death genes has been crucial in revealing some of the biochemical mechanisms underlying apoptosis in all animals. Four C. elegans genes, egl-1, ced-9, ced-4 and ced-3 are required for all somatic programmed cell death to occur. This genetic network is highly conserved during evolution. The pro-death gene egl-1 and the anti-death gene ced-9 have structural and functional similarities to the vertebrate Bcl2 gene family. The killer gene ced-3 encodes a cystein-aspartate protease (caspase), which is the archetype of a family of conserved proteins known as effecters of apoptosis in mammals. Zou and collaborators reported the biochemical identification of an apoptotic protease activating factor (Apaf1), a human homolog of C. elegans CED-4, providing important clues to how CED-4 and its potential relatives could work. A number of proteins have been shown to interact with Apaf1 or to be determinant for its activity as an apoptotic adapter. The aim of this review is to provide an overview of the recent progress made in the field of developmental apoptosis by means of the murine Apaf1 targeted mutations. The central role of Apaf1 in the cell death machinery (apoptosome) and its involvement in different apoptotic pathways will also be discussed.

Original languageEnglish
Pages (from-to)1087-1098
Number of pages12
JournalCell Death and Differentiation
Volume6
Issue number11
Publication statusPublished - 1999

Fingerprint

Caenorhabditis elegans
Genes
Cell Death
Apoptosis
Peptide Hydrolases
Apoptosomes
Aspartic Acid
Vertebrates
Mammals
Proteins
Mutation

Keywords

  • Bax
  • BcIX(L)
  • Boo
  • CARD
  • Caspases
  • Cytochrome c

ASJC Scopus subject areas

  • Cell Biology

Cite this

Apaf1 and the apoptotic machinery. / Cecconi, F.

In: Cell Death and Differentiation, Vol. 6, No. 11, 1999, p. 1087-1098.

Research output: Contribution to journalArticle

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