ArticleCellular microbiology2008
Anthrax lethal toxin-induced inflammasome formation and caspase-1 activation are late events dependent on ion fluxes and the proteasome.
Article in Cellular microbiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
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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.
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Who cites it
75 citing papers in PubMed, 115 citations in OpenAlex.
- NEKfla: A Genetically Encoded Förster Resonance Energy Transfer Biosensor for Live-Cell Monitoring of Early NIMA-Related Kinase 7-NLR Family Pyrin Domain Containing 3 Inflammasome Signaling.Biomaterials research · 2026Article
- The gasdermin family: emerging therapeutic targets in diseases.Signal transduction and targeted therapy · 2024Review
- Special Issue: Gram-Positive Bacterial Toxins.Microorganisms · 2023Article
- The subversion of toll-like receptor signaling by bacterial and viral proteases during the development of infectious diseases.Molecular aspects of medicine · 2022Review
- Inflammasomes and Pyroptosis of Liver Cells in Liver Fibrosis.Frontiers in immunology · 2022Review
- NLRP7: From inflammasome regulation to human disease.Immunology · 2021Review
- Article
- Frontline Science: Anthrax lethal toxin-induced, NLRP1-mediated IL-1β release is a neutrophil and PAD4-dependent event.Journal of leukocyte biology · 2020Article
- Therapeutic modulation of inflammasome pathways.Immunological reviews · 2020Review
- The NLRP1 Inflammasome in Human Skin and Beyond.International journal of molecular sciences · 2020Review
- The NLRP1 inflammasome: new mechanistic insights and unresolved mysteries.Current opinion in immunology · 2019Review
- The N-end rule ubiquitin ligase UBR2 mediates NLRP1B inflammasome activation by anthrax lethal toxin.The EMBO journal · 2019Article
- Functional degradation: A mechanism of NLRP1 inflammasome activation by diverse pathogen enzymes.Science (New York, N.Y.) · 2019Article
- A Membrane Potential- and Calpain-Dependent Reversal of Caspase-1 Inhibition Regulates Canonical NLRP3 Inflammasome.Cell reports · 2018Article
- [The function of NLRP1 in noninfectious pulmonary injury following allogeneic hematopoietic stem cell transplantation].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2017Article
- Article
- Bithionol blocks pathogenicity of bacterial toxins, ricin, and Zika virus.Scientific reports · 2016Article
- Sulforaphane inhibits multiple inflammasomes through an Nrf2-independent mechanism.Journal of leukocyte biology · 2016Article
- Identification of agents effective against multiple toxins and viruses by host-oriented cell targeting.Scientific reports · 2015Article
- The cyclopentenone prostaglandin 15d-PGJ2 inhibits the NLRP1 and NLRP3 inflammasomes.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Anthrax lethal toxin (LT) is cytotoxic to macrophages from certain inbred mouse strains. The gene controlling macrophage susceptibility to LT is Nalp1b. Nalp1b forms part of the inflammasome, a multiprotein complex involved in caspase-1 activation and release of interleukin (IL)-1beta and IL-18. We confirm the role of caspase-1 in LT-mediated death by showing that caspase inhibitors differentially protected cells against LT, with the degree of protection corresponding to each compound's ability to inhibit caspase-1. Caspase-1 activation and cytokine processing and release were late events inhibited by elevated levels of KCl and sucrose, by potassium channel blockers, and by proteasome inhibitors, suggesting that inflammasome formation requires a protein-degradation event and occurs downstream of LT-mediated potassium efflux. In addition, IL-18 and IL-1beta release was dependent on cell death, indicating that caspase-1-mediated cytotoxicity is independent of these cytokines. Finally, inducing NALP3-inflammasome formation in LT-resistant macrophages did not sensitize cells to LT, suggesting that general caspase-1 activation cannot account for sensitivity to LT and that a Nalp1b-mediated event is specifically required for death. Our data indicate that inflammasome formation is a contributing, but not initiating, event in LT-mediated cytotoxicity and that earlier LT-mediated events leading to ion fluxes are required for death.
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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.