ArticlePloS one2009
Anthrax lethal toxin induced lysosomal membrane permeabilization and cytosolic cathepsin release is Nlrp1b/Nalp1b-dependent.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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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.
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Who cites it
34 citing papers in PubMed, 67 citations in OpenAlex.
- Advances in the research of gasdermin-dependent pyroptosis mechanisms and therapeutic targets in inflammatory diseases.Apoptosis : an international journal on programmed cell death · 2026Review
- Gasdermins: multifunctional effectors of membrane permeabilization across cellular compartments.The FEBS journal · 2025Review
- Article
- Molecular mechanisms of gasdermin D pore-forming activity.Nature immunology · 2023Review
- Molecular biology of autoinflammatory diseases.Inflammation and regeneration · 2021Review
- Molecular dissection of box jellyfish venom cytotoxicity highlights an effective venom antidote.Nature communications · 2019Article
- The Lysosome Signaling Platform: Adapting With the Times.Frontiers in cell and developmental biology · 2019Review
- The Outcome of theJournal of immunology (Baltimore, Md. : 1950) · 2018Article
- Review
- E3 ubiquitin ligases Pellinos as regulators of pattern recognition receptor signaling and immune responses.Immunological reviews · 2015Review
- Programmed cell death and its role in inflammation.Military Medical Research · 2015Article
- The acidic transformed nano-VOToxicology reports · 2015Article
- Distinct cathepsins control necrotic cell death mediated by pyroptosis inducers and lysosome-destabilizing agents.Cell cycle (Georgetown, Tex.) · 2015Article
- Regulated necrosis: the expanding network of non-apoptotic cell death pathways.Nature reviews. Molecular cell biology · 2014Review
- Selective inhibitor of endosomal trafficking pathways exploited by multiple toxins and viruses.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Review
- Cytosolic flagellin-induced lysosomal pathway regulates inflammasome-dependent and -independent macrophage responses.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Role of lysosome rupture in controlling Nlrp3 signaling and necrotic cell death.Cell cycle (Georgetown, Tex.) · 2013Article
- The endolysosomal system in cell death and survival.Cold Spring Harbor perspectives in biology · 2013Review
- Cellular adaptation to anthrax lethal toxin-induced mitochondrial cholesterol enrichment, hyperpolarization, and reactive oxygen species generation through downregulating MLN64 in macrophages.Molecular and cellular biology · 2012Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
NOD-like receptors (NLRs) are a group of cytoplasmic molecules that recognize microbial invasion or 'danger signals'. Activation of NLRs can induce rapid caspase-1 dependent cell death termed pyroptosis, or a caspase-1 independent cell death termed pyronecrosis. Bacillus anthracis lethal toxin (LT), is recognized by a subset of alleles of the NLR protein Nlrp1b, resulting in pyroptotic cell death of macrophages and dendritic cells. Here we show that LT induces lysosomal membrane permeabilization (LMP). The presentation of LMP requires expression of an LT-responsive allele of Nlrp1b, and is blocked by proteasome inhibitors and heat shock, both of which prevent LT-mediated pyroptosis. Further the lysosomal protease cathepsin B is released into the cell cytosol and cathepsin inhibitors block LT-mediated cell death. These data reveal a role for lysosomal membrane permeabilization in the cellular response to bacterial pathogens and demonstrate a shared requirement for cytosolic relocalization of cathepsins in pyroptosis and pyronecrosis.
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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.