| First Author | Yoshida H | Year | 1998 |
| Journal | Cell | Volume | 94 |
| Issue | 6 | Pages | 739-50 |
| PubMed ID | 9753321 | Mgi Jnum | J:49841 |
| Mgi Id | MGI:1289118 | Doi | 10.1016/s0092-8674(00)81733-x |
| Citation | Yoshida H, et al. (1998) Apaf1 is required for mitochondrial pathways of apoptosis and brain development. Cell 94(6):739-50 |
| abstractText | Apoptosis is essential for the precise regulation of cellular homeostasis and development. The role in vivo of Apaf1, a mammalian homolog of C. elegans CED-4, was investigated in gene-targeted Apaf1-/- mice. Apaf1-deficient mice exhibited reduced apoptosis in the brain and striking craniofacial abnormalities with hyperproliferation of neuronal cells. Apaf1-deficient cells were resistant to a variety of apoptotic stimuli, and the processing of Caspases 2, 3, and 8 was impaired. However, both Apaf1-/- thymocytes and activated T lymphocytes were sensitive to Fas-induced killing, showing that Fas-mediated apoptosis in these cells is independent of Apaf1. These data indicate that Apaf1 plays a central role in the common events of mitochondria-dependent apoptosis in most death pathways and that this role is critical for normal development. |
