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PMID:16469926
| Citation |
Lakhani, SA, Masud, A, Kuida, K, Porter, GA Jr, Booth, CJ, Mehal, WZ, Inayat, I and Flavell, RA (2006) Caspases 3 and 7: key mediators of mitochondrial events of apoptosis. Science 311:847-51 |
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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. |
| Links |
PubMed Online version:10.1126/science.1115035 |
| Keywords |
Animals; Apoptosis; Apoptosis Inducing Factor/metabolism; Caspase 3; Caspase 7; Caspases/deficiency; Caspases/metabolism; Cell Nucleus/metabolism; Cell Shape; Cell Survival; Cells, Cultured; Cytochromes c/metabolism; DNA Fragmentation; Female; Fibroblasts/cytology; Heart/embryology; Heart Defects, Congenital/etiology; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Mitochondria/metabolism; Mitochondria/physiology; Mitochondrial Membranes/physiology; Permeability; T-Lymphocytes/cytology; bcl-2-Associated X Protein/metabolism |
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Significance
Annotations
| Gene product | Qualifier | GO ID | GO term name | Evidence Code | with/from | Aspect | Notes | Status |
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References
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