ArticleNature2010
Anthrax toxins cooperatively inhibit endocytic recycling by the Rab11/Sec15 exocyst.
Article in Nature, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 105 citations in OpenAlex.
- Role of Microbial Toxins in Neurodegenerative Diseases: Insights and Future Perspectives.Biomolecules · 2026Review
- Anthrax ET activates Rac1 and RTK signaling to induce F-actin reorganization and endothelial permeability.iScience · 2025Article
- Genome-Wide Identification Analysis of theGenes · 2025Article
- ATP depletion in anthrax edema toxin pathogenesis.PLoS pathogens · 2025Article
- Animal models in biomedical research: Relevance ofHeliyon · 2025Review
- Role of Rab GTPases in Bacteria Escaping from Vesicle Trafficking of Host Cells.Journal of microbiology (Seoul, Korea) · 2024Review
- Notch Signaling in Insect Development: A Simple Pathway with Diverse Functions.International journal of molecular sciences · 2023Review
- A comprehensive Drosophila resource to identify key functional interactions between SARS-CoV-2 factors and host proteins.Cell reports · 2023Article
- Bacterial Nucleotidyl Cyclases Activated by Calmodulin or Actin in Host Cells: Enzyme Specificities and Cytotoxicity Mechanisms Identified to Date.International journal of molecular sciences · 2022Review
- Par-3 family proteins in cell polarity & adhesion.The FEBS journal · 2022Review
- Neuroinflammation in neurodegenerationFrontiers in immunology · 2022Review
- Review
- Nociceptive Sensory Neurons Mediate Inflammation Induced byFrontiers in immunology · 2021Article
- The Endosomal Recycling Pathway-At the Crossroads of the Cell.International journal of molecular sciences · 2020Review
- A Drosophila Model for Clostridium difficile Toxin CDT Reveals Interactions with Multiple Effector Pathways.iScience · 2020Article
- Review
- Article
- Autocrine-paracrine prostaglandin ENature immunology · 2018Article
- Article
- Regulation of Cell Polarity by Exocyst-Mediated Trafficking.Cold Spring Harbor perspectives in biology · 2018Review
4 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Bacillus anthracis is the causative agent of anthrax in humans and other mammals. In lethal systemic anthrax, proliferating bacilli secrete large quantities of the toxins lethal factor (LF) and oedema factor (EF), leading to widespread vascular leakage and shock. Whereas host targets of LF (mitogen-activated protein-kinase kinases) and EF (cAMP-dependent processes) have been implicated in the initial phase of anthrax, less is understood about toxin action during the final stage of infection. Here we use Drosophila melanogaster to identify the Rab11/Sec15 exocyst, which acts at the last step of endocytic recycling, as a novel target of both EF and LF. EF reduces levels of apically localized Rab11 and indirectly blocks vesicle formation by its binding partner and effector Sec15 (Sec15-GFP), whereas LF acts more directly to reduce Sec15-GFP vesicles. Convergent effects of EF and LF on Rab11/Sec15 inhibit expression of and signalling by the Notch ligand Delta and reduce DE-cadherin levels at adherens junctions. In human endothelial cells, the two toxins act in a conserved fashion to block formation of Sec15 vesicles, inhibit Notch signalling, and reduce cadherin expression at adherens junctions. This coordinated disruption of the Rab11/Sec15 exocyst by anthrax toxins may contribute to toxin-dependent barrier disruption and vascular dysfunction during B. anthracis infection.
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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.