In order for the anthrax toxin to enter a cell, its receptor-binding subunit must heptamerize, thus allowing the two enzymatic subunits to join prior to endocytosis. Laurence Abrami and colleagues at the University of Geneva and the National Institute of Allergy and Infectious Diseases recently revealed that endocytosis is regulated by counteracting posttranslational modifications in the receptor itself. Palmitoylation of the receptor's cytoplasmic tail facilitates endocytosis of the toxin and receptor by preventing the receptor from being prematurely incorporated into lipid rafts, ubiquitinated, and degraded. 1












