Abstract
Anthrax is caused by the gram-positive bacterium Bacillus anthracis. The pathogenesis of this disease is dependent on the presence of two binary toxins, edema toxin (EdTx) and lethal toxin (LeTx). LeTx, the major virulence factor contributing to anthrax, contains the effector moiety lethal factor (LF), a zinc-dependent metalloprotease specific for targeting mitogen-activated protein kinase kinases. This review will focus on the protease-specific activity and function of LF, and will include a discussion on the implications and consequences of this activity, both in terms of anthrax disease, and how this activity can be exploited to gain insight into other pathologic conditions.
Highlights
Over the last decade there has been a renewed interest in understanding anthrax due to the recent use of anthrax as a biological weapon
These MAPKKs are in turn activated by different MAPKK kinases (MAPKKKs), which are differentially activated by extracellular stimuli, including growth factors, inflammatory signals, and environmental stresses
Expression in tumor cells, a different picture emerged from in vivo studies in which it was noted that tumors deficient in anthrax toxin receptor expression were still sensitive to lethal toxin (LeTx) treatment, resulting in decreased tumor growth in vivo [83]
Summary
Over the last decade there has been a renewed interest in understanding anthrax due to the recent use of anthrax as a biological weapon. While the mechanism by which anthrax kills its host is still unclear, the lethality of the disease was attributed to the production of anthrax toxin more than 50 years ago [1]. Following this seminal discovery by Smith and Keppie, it has been determined that. EF is a calmodulin-dependent adenylate cyclase that upon activation increases the conversion of intracellular ATP to cyclic AMP (cAMP) This results in the disruption of water homeostasis followed by edema [10]. B. anthracis strains deficient in EF production were shown to still be lethal in mice [11], EF does play a role in anthrax pathogenesis. We will explore the utility of exploiting this activity to further our understanding of the mechanism of LeTx action, and as a tool to evaluate the role of MEK signaling pathways in neovascular disease
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