ArticlePloS one2012
Anthrax lethal factor cleaves mouse nlrp1b in both toxin-sensitive and toxin-resistant macrophages.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
What it found
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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
75 citing papers in PubMed, 123 citations in OpenAlex.
- Molecular mechanisms of NLR proteins in inflammasome activation.Communications biology · 2026Review
- Targeting innate immune sensors for therapeutic strategies in infectious diseases.Journal of microbiology (Seoul, Korea) · 2025Review
- Diverse autoinhibitory mechanisms of FIIND-containing proteins: Insight into regulation of NLRP1 and CARD8 inflammasome.PLoS pathogens · 2025Article
- Conservation and similarity of bacterial and eukaryotic innate immunity.Nature reviews. Microbiology · 2024Review
- The NLR gene family: from discovery to present day.Nature reviews. Immunology · 2023Review
- Species-specific self-DNA detection mechanisms by mammalian cyclic GMP-AMP synthases.Science immunology · 2023Article
- Anthrax toxins regulate pain signaling and can deliver molecular cargoes into ANTXR2Nature neuroscience · 2022Article
- Human NLRP1: From the shadows to center stage.The Journal of experimental medicine · 2022Review
- Activation and regulation mechanisms of NOD-like receptors based on structural biology.Frontiers in immunology · 2022Review
- UVB-Induced Skin Autoinflammation Due toFrontiers in immunology · 2022Article
- NLRP1 Inflammasomes: A Potential Target for the Treatment of Several Types of Brain Injury.Frontiers in immunology · 2022Review
- Focus on the Mechanisms and Functions of Pyroptosis, Inflammasomes, and Inflammatory Caspases in Infectious Diseases.Oxidative medicine and cellular longevity · 2022Review
- Signaling Pathways Regulated by UBR Box-Containing E3 Ligases.International journal of molecular sciences · 2021Review
- Nod-Like Receptors in Host Defence and Disease at the Epidermal Barrier.International journal of molecular sciences · 2021Review
- Article
- Anthrax lethal factor cleaves regulatory subunits of phosphoinositide-3 kinase to contribute to toxin lethality.Nature microbiology · 2020Article
- The NLRP1 and CARD8 inflammasomes.Immunological reviews · 2020Review
- Frontline Science: Anthrax lethal toxin-induced, NLRP1-mediated IL-1β release is a neutrophil and PAD4-dependent event.Journal of leukocyte biology · 2020Article
- Anthrax Toxin Detection: From in Vivo Studies to Diagnostic Applications.Microorganisms · 2020Review
- Characterization of the NLRP1 inflammasome response in bovine species.Innate immunity · 2020Article
15 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
9 authors at 2 institutions in 1 country.
Funding
Abstract
Anthrax lethal factor (LF) is the protease component of anthrax lethal toxin (LT). LT induces pyroptosis in macrophages of certain inbred mouse and rat strains, while macrophages from other inbred strains are resistant to the toxin. In rats, the sensitivity of macrophages to toxin-induced cell death is determined by the presence of an LF cleavage sequence in the inflammasome sensor Nlrp1. LF cleaves rat Nlrp1 of toxin-sensitive macrophages, activating caspase-1 and inducing cell death. Toxin-resistant macrophages, however, express Nlrp1 proteins which do not harbor the LF cleavage site. We report here that mouse Nlrp1b proteins are also cleaved by LF. In contrast to the situation in rats, sensitivity and resistance of Balb/cJ and NOD/LtJ macrophages does not correlate to the susceptibility of their Nlrp1b proteins to cleavage by LF, as both proteins are cleaved. Two LF cleavage sites, at residues 38 and 44, were identified in mouse Nlrp1b. Our results suggest that the resistance of NOD/LtJ macrophages to LT, and the inability of the Nlrp1b protein expressed in these cells to be activated by the toxin are likely due to polymorphisms other than those at the LF cleavage sites.
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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.