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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Reduced apoptosis and cytochrome c- mediated caspase activation in mice lacking caspase 9.

Caspases are essential components of the mammalian cell death machinery. Here we test the hypothesis that Caspase 9 ( Casp9) is a critical upstream activator of caspases through gene targeting in mice. The majority of Casp9 knockout mice die perinatally with a markedly enlarged and malformed cerebrum caused by reduced apoptosis during brain development. Casp9 deletion prevents activation of Casp3 in embryonic brains in vivo, and Casp9-deficient thymocytes show resistance to a subset of apoptotic stimuli, including absence of Casp3-like cleavage and delayed DNA fragmentation. Moreover, the cytochrome c- mediated cleavage of Casp3 is absent in the cytosolic extracts of Casp9-deficient cells but is restored after addition of in vitro-translated Casp9. Together, these results indicate that Casp9 is a critical upstream activator of the caspase cascade in vivo.[1]

References

  1. Reduced apoptosis and cytochrome c-mediated caspase activation in mice lacking caspase 9. Kuida, K., Haydar, T.F., Kuan, C.Y., Gu, Y., Taya, C., Karasuyama, H., Su, M.S., Rakic, P., Flavell, R.A. Cell (1998) [Pubmed]
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