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Identification of the cellular receptor for anthrax toxin

Author

Listed:
  • Kenneth A. Bradley

    (McArdle Laboratory for Cancer Research, University of Wisconsin—Madison
    Biological and Biomedical Sciences Graduate Program)

  • Jeremy Mogridge

    (Harvard Medical School
    University of Toronto)

  • Michael Mourez

    (Harvard Medical School)

  • R. John Collier

    (Harvard Medical School)

  • John A. T. Young

    (McArdle Laboratory for Cancer Research, University of Wisconsin—Madison)

Abstract

The tripartite toxin secreted by Bacillus anthracis, the causative agent of anthrax, helps the bacterium evade the immune system and can kill the host during a systemic infection. Two components of the toxin enzymatically modify substrates within the cytosol of mammalian cells: oedema factor (OF) is an adenylate cyclase that impairs host defences through a variety of mechanisms including inhibiting phagocytosis1,2; lethal factor (LF) is a zinc-dependent protease that cleaves mitogen-activated protein kinase kinase and causes lysis of macrophages3,4,5. Protective antigen (PA), the third component, binds to a cellular receptor and mediates delivery of the enzymatic components to the cytosol. Here we describe the cloning of the human PA receptor using a genetic complementation approach. The receptor, termed ATR (anthrax toxin receptor), is a type I membrane protein with an extracellular von Willebrand factor A domain that binds directly to PA. In addition, a soluble version of this domain can protect cells from the action of the toxin.

Suggested Citation

  • Kenneth A. Bradley & Jeremy Mogridge & Michael Mourez & R. John Collier & John A. T. Young, 2001. "Identification of the cellular receptor for anthrax toxin," Nature, Nature, vol. 414(6860), pages 225-229, November.
  • Handle: RePEc:nat:nature:v:414:y:2001:i:6860:d:10.1038_n35101999
    DOI: 10.1038/n35101999
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    Cited by:

    1. Kuo-Sheng Hsu & James M. Dunleavey & Christopher Szot & Liping Yang & Mary Beth Hilton & Karen Morris & Steven Seaman & Yang Feng & Emily M. Lutz & Robert Koogle & Francesco Tomassoni-Ardori & Saurabh, 2022. "Cancer cell survival depends on collagen uptake into tumor-associated stroma," Nature Communications, Nature, vol. 13(1), pages 1-18, December.

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