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

Kang Li, Yucheng Li, John M. Shelton, James A. Richardson, Erika Spencer, Zhijian J. Chen, Xiaodong Wang, R. Sanders Williams

Research output: Contribution to journalArticlepeer-review

439 Scopus citations


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 TNFα. These results define the role of cytochrome c in different apoptotic signaling cascades.

Original languageEnglish (US)
Pages (from-to)389-399
Number of pages11
Issue number4
StatePublished - May 12 2000

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology


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