Reduced Apoptosis and Cytochrome c–Mediated Caspase Activation in Mice Lacking Caspase 9

@article{Kuida1998ReducedAA,
  title={Reduced Apoptosis and Cytochrome c–Mediated Caspase Activation in Mice Lacking Caspase 9},
  author={Keisuke Kuida and Tarik F. Haydar and Chia-Yi Kuan and Yong Gu and Choji Taya and Hajime Karasuyama and Michael S.-S. Su and Pasko Rakic and Richard A. Flavell},
  journal={Cell},
  year={1998},
  volume={94},
  pages={325-337}
}
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… 
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Caspase-3 is essential for certain processes associated with the dismantling of the cell and the formation of apoptotic bodies, but it may also function before or at the stage when commitment to loss of cell viability is made.
Caspase Enzyme Activity Is Not Essential for Apoptosis During Thymocyte Development1
TLDR
Results indicate that caspase-independent signal transduction pathways can mediate thymocyte death during normal T cell development.
Caspase-12 compensates for lack of caspase-2 and caspase-3 in female germ cells
TLDR
Interestingly, DKO oocytes were more resistant to apoptosis induced by methotrexate (MTX) than WT oocytes, and these results revealed that in female germ cells, insults that directly interfere with their metabolic status require caspase-2 and caspasing-3 as obligatory executioners of the ensuing cell death cascade.
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