Abstract
The genes encoding Anthrax Toxin Receptors (ANTXRs) were originally identified based on expression in endothelial cells suggesting a role in angiogenesis. The focus of this review is to discuss what has been learned about the physiological roles of these receptors through evaluation of the Antxr knockout mouse phenotypes. Mice mutant in Antxr genes have defects in extracellular matrix homeostasis. We discuss how knowledge of physiological ANTXR function relates to what is already known about anthrax intoxication.
Highlights
Anthrax Toxin Receptor 1 (ANTXR1) and Anthrax Toxin Receptor 2 (ANTXR2) are the human proteins that serve as receptors for anthrax toxin [1,2], a discovery made ten years ago
We propose that Anthrax Toxin Receptors (ANTXRs) may interact with
Mouse phenotype suggested more widespread expression of Antxr1, as extracellular matrix (ECM) homeostasis defects are seen in tissues and cell types beyond tumor endothelium
Summary
Anthrax Toxin Receptor 1 (ANTXR1) and Anthrax Toxin Receptor 2 (ANTXR2) are the human proteins that serve as receptors for anthrax toxin [1,2], a discovery made ten years ago. Toxins 2013, 5 there has been an intense research effort to tell the story of how toxin interaction with these receptors leads to anthrax intoxication (reviewed in [3,4,5]). The ANTXR proteins evolved for a physiological function, they were eventually hijacked to facilitate entry of a lethal agent produced by the pathogen, Bacillus anthracis. We summarize recent reports on the normal function of anthrax receptors. We discuss studies that uncover the physiological function of ANTXR1 and ANTXR2, with a focus on analysis of the Antxr and Antxr knockout mouse phenotypes
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