ArticleNature2013
Key tissue targets responsible for anthrax-toxin-induced lethality.
Article in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
79 citing papers in PubMed.
- Infectious bacteria as biological warfare agents: mechanisms, epidemiological threats, and defense strategies.Frontiers in bioengineering and biotechnology · 2026Review
- Targeting virulence to disarm the pathogen: Enzyme-activated-substrate inhibition of Anthrax edema factor.Bioorganic & medicinal chemistry letters · 2025Article
- Anthrax ET activates Rac1 and RTK signaling to induce F-actin reorganization and endothelial permeability.iScience · 2025Article
- ERK pathway reactivation prevents anthrax toxin lethality in mice.Nature microbiology · 2025Article
- ATP depletion in anthrax edema toxin pathogenesis.PLoS pathogens · 2025Article
- Review
- Identification of Potential Therapeutic Targets Against Anthrax-Toxin-Induced Liver and Heart Damage.Toxins · 2025Article
- Article
- Anthrax lethal toxin and tumor necrosis factor-α synergize on intestinal epithelia to induce mouse death.Protein & cell · 2024Article
- Early Circulating Edema Factor in Inhalational Anthrax Infection: Does It Matter?Microorganisms · 2024Article
- ERK and c-Myc signaling in host-derived tumor endothelial cells is essential for solid tumor growth.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Inflammasome activation by Gram-positive bacteria: Mechanisms of activation and regulation.Frontiers in immunology · 2023Review
- Article
- Categorizing Sequences of Concern by Function To Better Assess Mechanisms of Microbial Pathogenesis.Infection and immunity · 2022Review
- Anthrax toxins regulate pain signaling and can deliver molecular cargoes into ANTXR2Nature neuroscience · 2022Article
- Antibiotic Discovery and Resistance: The Chase and the Race.Antibiotics (Basel, Switzerland) · 2022Review
- Article
- Multiple stages of evolutionary change in anthrax toxin receptor expression in humans.Nature communications · 2021Article
- The secretome mouse provides a genetic platform to delineate tissue-specific in vivo secretion.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Nociceptive Sensory Neurons Mediate Inflammation Induced byFrontiers in immunology · 2021Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Bacillus anthracis, the causative agent of anthrax disease, is lethal owing to the actions of two exotoxins: anthrax lethal toxin (LT) and oedema toxin (ET). The key tissue targets responsible for the lethal effects of these toxins are unknown. Here we generated cell-type-specific anthrax toxin receptor capillary morphogenesis protein-2 (CMG2)-null mice and cell-type-specific CMG2-expressing mice and challenged them with the toxins. Our results show that lethality induced by LT and ET occurs through damage to distinct cell types; whereas targeting cardiomyocytes and vascular smooth muscle cells is required for LT-induced mortality, ET-induced lethality occurs mainly through its action in hepatocytes. Notably, and in contradiction to what has been previously postulated, targeting of endothelial cells by either toxin does not seem to contribute significantly to lethality. Our findings demonstrate that B. anthracis has evolved to use LT and ET to induce host lethality by coordinately damaging two distinct vital systems.
Indexed as
Identifiers
What OpenQuestion holds
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.