| First Author | Lakhani SA | Year | 2006 |
| Journal | Science | Volume | 311 |
| Issue | 5762 | Pages | 847-51 |
| PubMed ID | 16469926 | Mgi Jnum | J:105496 |
| Mgi Id | MGI:3615714 | Doi | 10.1126/science.1115035 |
| Citation | Lakhani SA, et al. (2006) Caspases 3 and 7: key mediators of mitochondrial events of apoptosis. Science 311(5762):847-51 |
| abstractText | The current model of apoptosis holds that upstream signals lead to activation of downstream effector caspases. We generated mice deficient in the two effectors, caspase 3 and caspase 7, which died immediately after birth with defects in cardiac development. Fibroblasts lacking both enzymes were highly resistant to both mitochondrial and death receptor-mediated apoptosis, displayed preservation of mitochondrial membrane potential, and had defective nuclear translocation of apoptosis-inducing factor (AIF). Furthermore, the early apoptotic events of Bax translocation and cytochrome c release were also delayed. We conclude that caspases 3 and 7 are critical mediators of mitochondrial events of apoptosis. |
