Examples of caspase

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A minority of apoptotic cells showed only fragmented nuclear morphology or fragmented nuclear morphology with the presence of active caspase-3 in the cytoplasm.
From animal studies, pro-apoptotic caspases (-2 and -3) have been implicated in the pathways of germ cell apoptosis.
This suggests the possibility that caspase inhibitors might protect hepatocytes from apoptosis during viral or other instances of liver inflammation.
An antiapoptotic protein human survivin is a direct inhibitor of caspase-3 and -7.
Thus, fertilization does not seem to affect the endogenous levels of caspase-3, caspase-8 or caspase-9 in the oocyteto-zygote transition.
Caspase-3 gene knockout defines cell lineage specificity for programmed cell death signaling in the ovary.
These data suggest that caspase-6 might play a critical role in apoptosis induction following chemotherapy.
The incidence of cytoplasmic fragmentation in mouse embryos in vitro is not affected by inhibition of caspase activity.
Their expression has been detected in the human fetal ovary (cleaved caspase-3) between 14-19 weeks, a time leading to primordial follicle formation.
The first caspases to become activated in the path to apoptosis are the 'initiator caspases', namely caspase-8 and caspase-9.
Apoptosis is associated with the activation of caspases.
These proteins can physically interact with, and block, caspase activity.
Caspase-independent photoreceptor apoptosis in vivo and differential expression of apoptotic protease activating factor-1 and caspase-3 during retinal development.
Profiles of such induced apoptosis were usually characterized by increased occurrence of active caspase-3 in the cytoplasm of apoptotic blastomeres.
These amounts of caspase substrates were determined from titration curves that were run on oocytes assayed with each of the substrates (data not shown).
Caspase-3 activation therefore appears to be a convergent event in the induction o f apoptosis by a variety of death stimuli.

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