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Sci. Aging Knowl. Environ., 8 March 2006
Vol. 2006, Issue 6, p. or5

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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. Flavell

http://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.

[Abstract/Full Text]

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Science of Aging Knowledge Environment. ISSN 1539-6150