| First Author | Li K | Year | 2000 |
| Journal | Cell | Volume | 101 |
| Issue | 4 | Pages | 389-99 |
| PubMed ID | 10830166 | Mgi Jnum | J:62276 |
| Mgi Id | MGI:1858667 | Doi | 10.1016/s0092-8674(00)80849-1 |
| Citation | Li K, et al. (2000) Cytochrome c deficiency causes embryonic lethality and attenuates stress-induced apoptosis. Cell 101(4):389-99 |
| abstractText | 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. |
