Journal
SCIENCE
Volume 311, Issue 5762, Pages 847-851Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1115035
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Funding
- NICHD NIH HHS [K12 HD00850, 1 K08 HD044580, 5 K12 HD01401, K12 HD001401, K12 HD000850, K08 HD044580] Funding Source: Medline
- NIDDK NIH HHS [NIDDK P30-34989, K08 DK002965, K08 DK002965-04] Funding Source: Medline
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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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