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Detection of Toxin Translocation into the Host Cytosol by Surface Plasmon Resonance
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Receptors of anthrax toxin and cell entry

Gisou van der Goot1, John A T Young

  • 1Global Health Institute, Ecole Polytechnique Fédérale de Lausanne, SV-AI Extension, Station 15, 1015 Lausanne, Switzerland. gisou.vandergoot@epfl.ch

Molecular Aspects of Medicine
|September 8, 2009
PubMed

Insights

Anthrax toxin entry relies on interactions between protective antigen (PA) and its receptors, ANTXR1/ANTXR2. Receptor type influences PA pore formation pH, with cellular factors regulating toxin-receptor complex endocytosis.

Area of Science:

  • Microbiology
  • Cell Biology
  • Biochemistry

Background:

  • Anthrax toxin requires host cell entry for toxicity.
  • Protective antigen (PA) is the cell-binding and pore-forming subunit of anthrax toxin.
  • Cellular receptors ANTXR1 and ANTXR2 mediate PA binding.

Purpose of the Study:

  • To review the molecular mechanisms of PA interaction with ANTXR1 and ANTXR2.
  • To elucidate how receptor choice affects the pH-dependent pore formation of PA.
  • To discuss the role of cellular factors in the endocytosis of PA-receptor complexes.

Main Methods:

  • Literature review of existing studies on anthrax toxin-receptor interactions.
  • Analysis of molecular details of PA binding to ANTXR1 and ANTXR2.
  • Examination of the influence of receptor type on PA pore formation pH threshold.
  • Review of cellular factors involved in endocytosis regulation.

Main Results:

  • PA interacts with both ANTXR1 and ANTXR2, but receptor binding kinetics and affinity may differ.
  • The specific receptor (ANTXR1 or ANTXR2) influences the acidic pH required for PA conformational change and pore formation.
  • Cellular factors, including accessory proteins and membrane dynamics, play a crucial role in the internalization of the PA-receptor complex.
  • Understanding these interactions is key to developing targeted interventions.

Conclusions:

  • Anthrax toxin cell entry is a complex process involving specific receptor interactions.
  • Receptor-mediated regulation of PA pore formation pH is a critical determinant of toxin activity.
  • Cellular factors are essential regulators of toxin endocytosis, offering potential therapeutic targets.

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