Caspases 3 and 7: key mediators of mitochondrial events of apoptosis.

ABSTRACT: 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.

SUBMITTER: Lakhani SA 

PROVIDER: S-EPMC3738210 | biostudies-other | 2006 Feb

REPOSITORIES: biostudies-other