ArticlePLoS pathogens2019
Gasdermin-D and Caspase-7 are the key Caspase-1/8 substrates downstream of the NAIP5/NLRC4 inflammasome required for restriction of Legionella pneumophila.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 105 citations in OpenAlex.
- The NLRP3 inflammasome in physiological and dysfunctional host response in human sepsis and critical illness: a narrative review.Critical care (London, England) · 2026Review
- Diverse infection models demonstrate robust resistance ofbioRxiv : the preprint server for biology · 2026Article
- Human non-canonical inflammasomes activate CASP3 to limit intracellular Salmonella replication in macrophages.PLoS pathogens · 2026Article
- Molecular evolution and adaptations ofFrontiers in cellular and infection microbiology · 2026Review
- Molecular mechanisms and regulation of inflammasome activation and signaling: sensing of pathogens and damage molecular patterns.Cellular & molecular immunology · 2025Review
- Innate detection ofbioRxiv : the preprint server for biology · 2025Article
- Article
- Mechanistic insights into gasdermin-mediated pyroptosis.Nature reviews. Molecular cell biology · 2025Review
- Pyroptosis: molecular mechanisms and roles in disease.Cell research · 2025Review
- Innate immune mechanisms of infection: what we know and potential conserved mechanisms affecting sleep during infection.Neurobiology of sleep and circadian rhythms · 2025Article
- Activation of the conserved Hippo kinases by inflammasome-triggered proteolytic cleavage controls programmed cell death in macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Executioner caspases degrade essential mediators of pathogen-host interactions to inhibit growth of intracellular Listeria monocytogenes.Cell death & disease · 2025Article
- NLRC4, inflammation and colorectal cancer (Review).International journal of oncology · 2024Review
- Distinct sequential death complexes regulate pyroptosis and IL-1β release in response toScience advances · 2024Article
- The gasdermin family: emerging therapeutic targets in diseases.Signal transduction and targeted therapy · 2024Review
- Hope for vascular cognitive impairment: Ac-YVAD-cmk as a novel treatment against white matter rarefaction.PloS one · 2024Article
- Article
- Apoptotic signaling clears engineeredeLife · 2023Article
- Article
- Bucket lists must be completed during cell death.Trends in cell biology · 2023Review
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Inflammasomes are cytosolic multi-protein complexes that detect infection or cellular damage and activate the Caspase-1 (CASP1) protease. The NAIP5/NLRC4 inflammasome detects bacterial flagellin and is essential for resistance to the flagellated intracellular bacterium Legionella pneumophila. The effectors required downstream of NAIP5/NLRC4 to restrict bacterial replication remain unclear. Upon NAIP5/NLRC4 activation, CASP1 cleaves and activates the pore-forming protein Gasdermin-D (GSDMD) and the effector caspase-7 (CASP7). However, Casp1-/- (and Casp1/11-/-) mice are only partially susceptible to L. pneumophila and do not phenocopy Nlrc4-/-mice, because NAIP5/NLRC4 also activates CASP8 for restriction of L. pneumophila infection. Here we show that CASP8 promotes the activation of CASP7 and that Casp7/1/11-/- and Casp8/1/11-/- mice recapitulate the full susceptibility of Nlrc4-/- mice. Gsdmd-/- mice exhibit only mild susceptibility to L. pneumophila, but Gsdmd-/-Casp7-/- mice are as susceptible as the Nlrc4-/- mice. These results demonstrate that GSDMD and CASP7 are the key substrates downstream of NAIP5/NLRC4/CASP1/8 required for resistance to L. pneumophila.
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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.