Caspases 3 and 7: key mediators of mitochondrial events of apoptosis |
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Authors: | Lakhani Saquib A Masud Ali Kuida Keisuke Porter George A Booth Carmen J Mehal Wajahat Z Inayat Irteza Flavell Richard A |
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Institution: | Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA. |
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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. |
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