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Cell. 2000 May 12;101(4):389-99.

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

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1
Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75390, USA.

Abstract

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.

PMID:
10830166
[Indexed for MEDLINE]
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