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A caspase-activated DNase that degrades DNA during apoptosis, and its inhibitor ICAD

Author

Listed:
  • Masato Enari

    (Osaka University Medical School)

  • Hideki Sakahira

    (Osaka University Medical School)

  • Hideki Yokoyama

    (Osaka University Medical School)

  • Katsuya Okawa

    (Central Laboratories for Key Technology, Kirin Brewery Co.)

  • Akihiro Iwamatsu

    (Central Laboratories for Key Technology, Kirin Brewery Co.)

  • Shigekazu Nagata

    (Osaka University Medical School
    Osaka Bioscience Institute)

Abstract

The homeostasis of animals is regulated not only by the growth and differentiation of cells, but also by cell death through a process known as apoptosis. Apoptosis is mediated by members of the caspase family of proteases, and eventually causes the degradation of chromosomal DNA. A caspase-activated deoxyribonuclease (CAD) and its inhibitor (ICAD) have now been identified in the cytoplasmic fraction of mouse lymphoma cells. CAD is a protein of 343 amino acids which carries a nuclear-localization signal; ICAD exists in a long and a short form. Recombinant ICAD specifically inhibits CAD-induced degradation of nuclear DNA and its DNase activity. When CAD is expressed with ICAD in COS cells or in a cell-free system, CAD is produced as a complex with ICAD: treatment with caspase 3 releases the DNase activity which causes DNA fragmentation in nuclei. ICAD therefore seems to function as a chaperone for CAD during its synthesis, remaining complexed with CAD to inhibit its DNase activity; caspases activated by apoptotic stimuli then cleave ICAD, allowing CAD to enter the nucleus and degrade chromosomal DNA.

Suggested Citation

  • Masato Enari & Hideki Sakahira & Hideki Yokoyama & Katsuya Okawa & Akihiro Iwamatsu & Shigekazu Nagata, 1998. "A caspase-activated DNase that degrades DNA during apoptosis, and its inhibitor ICAD," Nature, Nature, vol. 391(6662), pages 43-50, January.
    • Handle: RePEc:nat:nature:v:391:y:1998:i:6662:d:10.1038_34112
    DOI: 10.1038/34112
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    Cited by:

    1. Avner Schlessinger & Jinfeng Liu & Burkhard Rost, 2007. "Natively Unstructured Loops Differ from Other Loops," PLOS Computational Biology, Public Library of Science, vol. 3(7), pages 1-12, July.
    2. Leire Valcárcel-Ocete & Gorka Alkorta-Aranburu & Mikel Iriondo & Asier Fullaondo & María García-Barcina & José Manuel Fernández-García & Elena Lezcano-García & José María Losada-Domingo & Javier Ruiz-, 2015. "Exploring Genetic Factors Involved in Huntington Disease Age of Onset: E2F2 as a New Potential Modifier Gene," PLOS ONE, Public Library of Science, vol. 10(7), pages 1-14, July.

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