ArticleThe Journal of biological chemistry2017
A Disease-associated Mutant of NLRC4 Shows Enhanced Interaction with SUG1 Leading to Constitutive FADD-dependent Caspase-8 Activation and Cell Death.
Article in The Journal of biological chemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 48 citations in OpenAlex.
- Innate immune sensors of inflammasomes and PANoptosomes: structural-mechanistic insights and therapeutic implications.Cell research · 2026Review
- Dysregulation of innate immune sensors and autoinflammation: insights from an NLRC4 mouse AIFEC model.Cellular & molecular immunology · 2026Article
- Caspase-8 in inflammatory diseases: a potential therapeutic target.Cellular & molecular biology letters · 2024Review
- Regulation of the Inflammasome Activation by Ubiquitination Machinery.Advances in experimental medicine and biology · 2024Review
- LNCGM1082 in Gut Epithelial Cells Promotes Expulsion of Infected Epithelial Cells and Release of IL-18.ImmunoHorizons · 2024Article
- Review
- LNCGM1082-mediated NLRC4 activation drives resistance to bacterial infection.Cellular & molecular immunology · 2023Article
- Time‑dependent changes in NLRP3 and Nrf2 levels in lipopolysaccharide‑induced acute lung injury.International journal of molecular medicine · 2022Article
- [Autoinflammation-A clinical and genetic challenge].Der Hautarzt; Zeitschrift fur Dermatologie, Venerologie, und verwandte Gebiete · 2022Article
- [Autoinflammation-A clinical and genetic challenge].Zeitschrift fur Rheumatologie · 2021Article
- Molecular mechanisms of phenotypic variability in monogenic autoinflammatory diseases.Nature reviews. Rheumatology · 2021Review
- Techniques to Study Inflammasome Activation and Inhibition by Small Molecules.Molecules (Basel, Switzerland) · 2021Review
- A Novel Mutation in the NBD Domain ofFrontiers in immunology · 2021Article
- Article
- Updating the NLRC4 Inflammasome: from Bacterial Infections to Autoimmunity and Cancer.Frontiers in immunology · 2021Review
- Inflammasomes in the pathophysiology of autoinflammatory syndromes.Journal of leukocyte biology · 2020Review
- Control of the inflammasome by the ubiquitin system.The FEBS journal · 2020Review
- HSC70 regulates cold-induced caspase-1 hyperactivation by an autoinflammation-causing mutant of cytoplasmic immune receptor NLRC4.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Human Hyperekplexic Mutations in Glycine Receptors Disinhibit the Brainstem by Hijacking GABAiScience · 2019Article
- Ubiquitination-Mediated Inflammasome Activation during Bacterial Infection.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nod-like receptor family card containing 4 (NLRC4)/Ipaf is involved in recognition of pathogen-associated molecular patterns leading to caspase-1 activation and cytokine release, which mediate protective innate immune response. Point mutations in NLRC4 cause autoinflammatory syndromes. Although all the mutations result in constitutive caspase-1 activation, their phenotypic presentations are different, implying that these mutations cause different alterations in properties of NLRC4. NLRC4 interacts with SUG1 and induces caspase-8-mediated cell death. Here, we show that one of the autoinflammatory syndrome-causing mutants of NLRC4, H443P, but not T337A and V341A, constitutively activates caspase-8 and induces apoptotic cell death in human lung epithelial cells. Compared with wild type NLRC4, the H443P mutant shows stronger interaction with SUG1 and with ubiquitinated cellular proteins. Phosphorylation of NLRC4 at Ser
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