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Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis.

Cytochrome c released from mitochondria has been proposed to be an essential component of an apoptotic pathway responsive to DNA damage and other forms of cell stress. Murine embryos devoid of cytochrome c die in utero by midgestation, but cell lines established from early cytochrome c null embryos are viable under conditions that compensate for defective oxidative phosphorylation. As compared to cell lines established from wild-type embryos, cells lacking cytochrome c show reduced caspase-3 activation and are resistant to the proapoptotic effects of UV irradiation, serum withdrawal, or staurosporine. In contrast, cells lacking cytochrome c demonstrate increased sensitivity to cell death signals triggered by TNFalpha. These results define the role of cytochrome c in different apoptotic signaling cascades.

Pubmed ID: 10830166


  • Li K
  • Li Y
  • Shelton JM
  • Richardson JA
  • Spencer E
  • Chen ZJ
  • Wang X
  • Williams RS



Publication Data

May 12, 2000

Associated Grants


Mesh Terms

  • Animals
  • Apoptosis
  • Cytochrome c Group
  • Embryo Loss
  • Embryo, Mammalian
  • Embryonic and Fetal Development
  • Gene Expression Regulation, Developmental
  • Mice