Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice

@article{Kuida1996DecreasedAI,
  title={Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice},
  author={Keisuke Kuida and Timothy S. Zheng and Songqing Na and Chia-Yi Kuan and Di Yang and Hajime Karasuyama and Pasko Rakic and Richard A. Flavell},
  journal={Nature},
  year={1996},
  volume={384},
  pages={368-372}
}
PROGRAMMED cell death (apoptosis) is a prominent feature of the development of the immune and nervous systems1,2. The identification of the Caenorhabditis elegans cell death gene, ced-3, as a prototype of the interleukin-lβ converting enzyme (ICE) protease family has led to extensive evidence implicating these enzymes in apoptosis3,4. Among the ten or more members of the ICE protease family, CPP32/yama/apopain5–7 exhibits the highest similarity to CED-3 in both sequence homology and substrate… 
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References

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CPP32, a novel human apoptotic protein with homology to Caenorhabditis elegans cell death protein Ced-3 and mammalian interleukin-1 beta-converting enzyme.
TLDR
The cloned gene encodes a 32-kDa putative cysteine protease (CPP32) with significant homology to Caenorhabditis elegans cell death protein Ced-3, mammalian interleukin-1 beta-converting enzyme (ICE), and the product of the mouse nedd2 gene, which is highly expressed and most abundant in cell lines of lymphocytic origin.
Apoptosis: A Basic Biological Phenomenon with Wide-ranging Implications in Tissue Kinetics
TLDR
Apoptosis seems to be involved in cell turnover in many healthy adult tissues and is responsible for focal elimination of cells during normal embryonic development, and participates in at least some types of therapeutically induced tumour regression.
Mch3, a novel human apoptotic cysteine protease highly related to CPP32.
TLDR
The cloning of a new Ced-3/interleukin 1 beta-converting enzyme-related gene is reported that encodes a protein with the highest degree of homology to CPP32 compared to other family members, suggesting that Mch3 alpha activation in vivo may depend in part on C PP32 activity.
Mch2, a new member of the apoptotic Ced-3/Ice cysteine protease gene family.
TLDR
The data suggest that Mch2 is a Ced-3/interleukin-1 beta converting enzyme-like cysteine protease and could be another important mediator of apoptosis in mammalian cells.
Identification and inhibition of the ICE/CED-3 protease necessary for mammalian apoptosis
TLDR
A potent peptide aldehyde inhibitor has been developed and shown to prevent apoptotic events in vitro, suggesting that apopain/CPP32 is important for the initiation of apoptotic cell death.
Yama/CPP32β, a mammalian homolog of CED-3, is a CrmA-inhibitable protease that cleaves the death substrate poly(ADP-ribose) polymerase
TLDR
It is proposed that Yama may represent an effector component of the mammalian cell death pathway and suggest that CrmA blocks apoptosis by inhibiting Yama.
The Caenorhabditis elegans cell-death protein CED-3 is a cysteine protease with substrate specificities similar to those of the human CPP32 protease.
TLDR
It is suggested that different mammalian CED-3/ICE-like proteases may have distinct roles in mammalian apoptosis and that CPP32 is a candidate for being a mammalian functional equivalent of CED, which was more similar to the mammalian C PP32 protease than to mammalian ICE or NEDD2/ICH-1 protease.
Genetic control of programmed cell death in the nematode C. elegans
TLDR
Ced-3 and ced-4 mutants appear grossly normal in morphology and behavior, indicating that programmed cell death is not an essential aspect of nematode development.
Mutations that affect neural cell lineages and cell fates during the development of the nematode Caenorhabditis elegans.
TLDR
The genes lin-22, lin-12, unc-86, and ced-3 may play decision-making roles during C. elegans neurogenesis, as mutations in each of these genes cause specific transformations in the fates of particular cells.
Early redistribution of plasma membrane phosphatidylserine is a general feature of apoptosis regardless of the initiating stimulus: inhibition by overexpression of Bcl-2 and Abl
TLDR
It is shown that PS externalization is an early and widespread event during apoptosis of a variety of murine and human cell types, regardless of the initiating stimulus, and precedes several other events normally associated with this mode of cell death.
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