ArticlePloS one2013
Anthrax edema factor toxicity is strongly mediated by the N-end rule.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Anthrax ET activates Rac1 and RTK signaling to induce F-actin reorganization and endothelial permeability.iScience · 2025Article
- ATP depletion in anthrax edema toxin pathogenesis.PLoS pathogens · 2025Article
- Early Circulating Edema Factor in Inhalational Anthrax Infection: Does It Matter?Microorganisms · 2024Article
- Article
- Anthrax toxins regulate pain signaling and can deliver molecular cargoes into ANTXR2Nature neuroscience · 2022Article
- Nociceptive Sensory Neurons Mediate Inflammation Induced byFrontiers in immunology · 2021Article
- Bismaleimide cross-linked anthrax toxin forms functional octamers with high specificity in tumor targeting.Protein science : a publication of the Protein Society · 2019Article
- Zeptomole per milliliter detection and quantification of edema factor in plasma by LC-MS/MS yields insights into toxemia and the progression of inhalation anthrax.Analytical and bioanalytical chemistry · 2019Article
- The Molecular Basis of Toxins' Interactions with Intracellular Signaling via Discrete Portals.Toxins · 2017Review
- Nitric oxide production contributes to Bacillus anthracis edema toxin-associated arterial hypotension and lethality: ex vivo and in vivo studies in the rat.American journal of physiology. Heart and circulatory physiology · 2016Article
- In Silico Genomic Fingerprints of the Bacillus anthracis Group Obtained by Virtual Hybridization.Microarrays (Basel, Switzerland) · 2015Article
- Reductive methylation and mutation of an anthrax toxin fusion protein modulates its stability and cytotoxicity.Scientific reports · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Anthrax edema factor (EF) is a calmodulin-dependent adenylate cyclase that converts adenosine triphosphate (ATP) into 3'-5'-cyclic adenosine monophosphate (cAMP), contributing to the establishment of Bacillus anthracis infections and the resulting pathophysiology. We show that EF adenylate cyclase toxin activity is strongly mediated by the N-end rule, and thus is dependent on the identity of the N-terminal amino acid. EF variants having different N-terminal residues varied by more than 100-fold in potency in cultured cells and mice. EF variants having unfavorable, destabilizing N-terminal residues showed much greater activity in cells when the E1 ubiquitin ligase was inactivated or when proteasome inhibitors were present. Taken together, these results show that EF is uniquely affected by ubiquitination and/or proteasomal degradation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.