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- W4212801976 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. PMID: 16469926 Funding information This work was supported by: NICHD NIH HHS, United States Grant ID: K08 HD044580 NIDDK NIH HHS, United States Grant ID: K08 DK002965-04 NICHD NIH HHS, United States Grant ID: K12 HD001401 NICHD NIH HHS, United States Grant ID: K12 HD000850 NIDDK NIH HHS, United States Grant ID: K08 DK002965 NIDDK NIH HHS, United States Grant ID: NIDDK P30-34989 NICHD NIH HHS, United States Grant ID: 5 K12 HD01401 NICHD NIH HHS, United States Grant ID: K12 HD00850 NICHD NIH HHS, United States Grant ID: 1 K08 HD044580 More Less keyboard_arrow_down" @default.
- W4212801976 created "2022-02-24" @default.
- W4212801976 creator A5072175765 @default.
- W4212801976 date "2006-06-29" @default.
- W4212801976 modified "2023-09-27" @default.
- W4212801976 title "Faculty Opinions recommendation of Caspases 3 and 7: key mediators of mitochondrial events of apoptosis." @default.
- W4212801976 doi "https://doi.org/10.3410/f.1032358.374606" @default.
- W4212801976 hasPublicationYear "2006" @default.
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