| First Author | Kuida K | Year | 1998 |
| Journal | Cell | Volume | 94 |
| Issue | 3 | Pages | 325-37 |
| PubMed ID | 9708735 | Mgi Jnum | J:49088 |
| Mgi Id | MGI:1276658 | Doi | 10.1016/s0092-8674(00)81476-2 |
| Citation | Kuida K, et al. (1998) Reduced apoptosis and cytochrome c-mediated caspase activation in mice lacking caspase 9. Cell 94(3):325-37 |
| abstractText | Caspases are essential components of the mammalian cell death machinery. Here we test the hypothesis that Caspase 9 (Casp9) is a critical upstream activator of caspases through gene targeting in mice. The majority of Casp9 knockout mice die perinatally with a markedly enlarged and malformed cerebrum caused by reduced apoptosis during brain development. Casp9 deletion prevents activation of Casp3 in embryonic brains in vivo, and Casp9-deficient thymocytes show resistance to a subset of apoptotic stimuli, including absence of Casp3-like cleavage and delayed DNA fragmentation. Moreover, the cytochrome c-mediated cleavage of Casp3 is absent in the cytosolic extracts of Casp9-deficient cells but is restored after addition of in vitro-translated Casp9. Together, these results indicate that Casp9 is a critical upstream activator of the caspase cascade in vivo. |
