Sci. Aging Knowl. Environ., 8 March 2006
Caspases 3 and 7: Key Mediators of Mitochondrial Events of Apoptosis
Saquib A. Lakhani, Ali Masud, Keisuke Kuida, George A. Porter, Jr., Carmen J. Booth, Wajahat Z. Mehal, Irteza Inayat, and Richard A. Flavellhttp://sageke.sciencemag.org/cgi/content/abstract/2006/6/or5
Abstract: Science 311, 847-851 (2006).
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.
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