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Apaf1 is required for mitochondrial pathways of apoptosis and brain development.


Apoptosis is essential for the precise regulation of cellular homeostasis and development. The role in vivo of Apaf1, a mammalian homolog of C. elegans CED-4, was investigated in gene-targeted Apaf1-/- mice. Apaf1-deficient mice exhibited reduced apoptosis in the brain and striking craniofacial abnormalities with hyperproliferation of neuronal cells. Apaf1-deficient cells were resistant to a variety of apoptotic stimuli, and the processing of Caspases 2, 3, and 8 was impaired. However, both Apaf1-/- thymocytes and activated T lymphocytes were sensitive to Fas-induced killing, showing that Fas-mediated apoptosis in these cells is independent of Apaf1. These data indicate that Apaf1 plays a central role in the common events of mitochondria-dependent apoptosis in most death pathways and that this role is critical for normal development.

Pubmed ID: 9753321


  • Yoshida H
  • Kong YY
  • Yoshida R
  • Elia AJ
  • Hakem A
  • Hakem R
  • Penninger JM
  • Mak TW



Publication Data

September 18, 1998

Associated Grants


Mesh Terms

  • Animals
  • Antigens, CD95
  • Apoptosis
  • Apoptotic Protease-Activating Factor 1
  • Brain
  • Brain Chemistry
  • Caspase 2
  • Caspase 3
  • Caspase 8
  • Caspase 9
  • Caspases
  • Cells, Cultured
  • Cysteine Endopeptidases
  • Cytochrome c Group
  • Embryo, Mammalian
  • Enzyme Precursors
  • Fibroblasts
  • Gene Expression
  • Head
  • Membrane Potentials
  • Mice
  • Mice, Knockout
  • Mitochondria
  • Phenotype
  • Proteins
  • Skin Abnormalities
  • Stem Cells
  • T-Lymphocytes
  • Thymus Gland
  • Ultraviolet Rays