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

Cell | May 12, 2000

http://www.ncbi.nlm.nih.gov/pubmed/10830166

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 RIS Download

Mesh terms: Animals | Apoptosis | Cytochrome c Group | Embryo Loss | Embryo, Mammalian | Embryonic and Fetal Development | Gene Expression Regulation, Developmental | Mice

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Mouse Genome Informatics (Data, Gene Annotation)

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