ArticleLife science alliance2018
Dimerization and auto-processing induce caspase-11 protease activation within the non-canonical inflammasome.
Article in Life science alliance, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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The trial behind it
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Who cites it
53 citing papers in PubMed, 75 citations in OpenAlex.
- Innate immune sensors of inflammasomes and PANoptosomes: structural-mechanistic insights and therapeutic implications.Cell research · 2026Review
- Induced pluripotent stem cell-derived macrophages enable broad modeling of human inflammasome signaling.Cell reports methods · 2026Article
- How to recognize if a cell dies from pyroptosis?Molecular biology reports · 2026Review
- LPS-induced structural reorganization and polymerization drive noncanonical inflammasome activation.Science advances · 2026Article
- Advances of Caspase-11 for veterinary respiratory infections.Frontiers in veterinary science · 2026Review
- NLRP3-mediated pyroptosis in cardiovascular disease: from molecular mechanisms to therapeutic targets.Frontiers in pharmacology · 2026Review
- Molecular mechanisms and regulation of inflammasome activation and signaling: sensing of pathogens and damage molecular patterns.Cellular & molecular immunology · 2025Review
- Cardiolipin inhibits the non-canonical inflammasome by preventing LPS binding to caspase-4/11.The EMBO journal · 2025Article
- New insights into the noncanonical inflammasome point to caspase-4 as a druggable target.Nature reviews. Immunology · 2025Review
- LPS binding caspase activation and recruitment domains (CARDs) are bipartite lipid binding modules.Science advances · 2025Article
- The NLRP3 inflammasome in urogenital cancers: structure, dual function, and therapeutic potential.Frontiers in oncology · 2025Review
- Inflammasome-mediated pyroptosis in defense against pathogenic bacteria.Immunological reviews · 2025Review
- Inflammasome components as new therapeutic targets in inflammatory disease.Nature reviews. Immunology · 2025Review
- Pyroptotic cell corpses are crowned with F-actin-rich filopodia that engage CLEC9A signaling in incoming dendritic cells.Nature immunology · 2025Article
- LPS binding caspase activation and recruitment domains (CARDs) are bipartite lipid binding modules.bioRxiv : the preprint server for biology · 2024Article
- Review
- Mechanistic insights from inflammasome structures.Nature reviews. Immunology · 2024Review
- Evolution of Caspases and the Invention of Pyroptosis.International journal of molecular sciences · 2024Review
- Harnessing Pyroptosis for Cancer Immunotherapy.Cells · 2024Review
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Caspase-11 is a cytosolic sensor and protease that drives innate immune responses to the bacterial cell wall component, LPS. Caspase-11 provides defence against cytosolic Gram-negative bacteria; however, excessive caspase-11 responses contribute to murine endotoxic shock. Upon sensing LPS, caspase-11 assembles a higher order structure called the non-canonical inflammasome that enables the activation of caspase-11 protease function, leading to gasdermin D cleavage and cell death. The mechanism by which caspase-11 acquires protease function is, however, poorly defined. Here, we show that caspase-11 dimerization is necessary and sufficient for eliciting basal caspase-11 protease function, such as the ability to auto-cleave. We further show that during non-canonical inflammasome signalling, caspase-11 self-cleaves at site (D285) within the linker connecting the large and small enzymatic subunits. Self-cleavage at the D285 site is required to generate the fully active caspase-11 protease (proposed here to be p32/p10) that mediates gasdermin D cleavage, macrophage death, and NLRP3-dependent IL-1β production. This study provides a detailed molecular mechanism by which LPS induces caspase-11-driven inflammation and cell death to provide host defence against cytosolic bacterial infection.
Identifiers
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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.