ReviewThe FEBS journal2020
Control of the inflammasome by the ubiquitin system.
Review in The FEBS journal, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
91 citing papers in PubMed.
- Pathogenic NLRP3 mutants form constitutively active inflammasomes resulting in immune-metabolic limitation of IL-1β production.Nature communications · 2024Trial
- Serum EV-Derived rno-let-7b-5p Is Associated with Lung-Adipose Alterations in Allergic Asthma.International journal of molecular sciences · 2026Article
- Targeting Cathepsin B with p-coumaric acid rescues WWP1-dependent proteasomal degradation of NLRP3 in hyperuricemic nephropathy.Molecular medicine (Cambridge, Mass.) · 2026Article
- Ubiquitination and autophagy in host-pathogen interactions: from immune surveillance to therapeutic targeting.Nature reviews. Immunology · 2026Review
- Siah2 is a lipid-mediated metabolic sensor in adipose tissue macrophage.Journal of lipid research · 2026Article
- Novel Therapeutic Targets of Endothelial Inflammation in Acute Lung Injury and Acute Respiratory Distress Syndrome.Journal of respiratory biology and translational medicine · 2026Article
- Article
- Jinbei Decoction Attenuates LPS-Induced Acute Lung Injury via Suppression of TRAF6-Dependent Inflammatory Response in Macrophage.Journal of cellular and molecular medicine · 2025Article
- Adipocyte FMO3-derived TMAO induces WAT dysfunction and metabolic disorders by promoting inflammasome activation in ageing.Nature communications · 2025Article
- Rictor Ameliorates Acute Antibody-Mediated Rejection Following Kidney Transplantation by Suppressing Macrophage M1 Polarization Through p65-NLRP3 Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Research and development prospects of TRIM65.Journal of cancer research and clinical oncology · 2025Review
- Research and development prospects of TRIM65.Journal of cancer research and clinical oncology · 2025Review
- Mechanism of action of the nucleotide-binding oligomerization domain-like receptor protein 3 inflammasome and its regulation in liver injury.Chinese medical journal · 2025Review
- Ubiquitination of gasdermin D N-terminal domain directs its membrane translocation and pore formation during pyroptosis.Cell death & disease · 2025Article
- The NLRP3 inflammasome in urogenital cancers: structure, dual function, and therapeutic potential.Frontiers in oncology · 2025Review
- Chronic Exposure to Cigarette Smoke Induces Pyroptosis in Pulmonary Epithelial Cells via EGR1/USP44/TRAF6 Axis in COPD.Journal of inflammation research · 2025Article
- Targeting Caspase-1 in osteoarthritis: multi-omics insights into the effects of VX-765 on human chondrocyte function and phenotype.Frontiers in immunology · 2025Article
- Research Progress of A20 in Acute Leukemia: A20 in Acute Leukemia.Galen medical journal · 2025Review
- IL-1β and CXCR4 as Potential Therapeutic Targets for Alzheimer's Disease.Combinatorial chemistry & high throughput screening · 2025Article
- NLRP3 inflammasome in Alzheimer's disease: molecular mechanisms and emerging therapies.Frontiers in immunology · 2025Review
31 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
Inflammation is the body's response to danger. One of the first immune cell types to encounter danger is the macrophage. Macrophages sense danger signals such as extracellular ATP or bacterial toxins, derived from tissue damage or infection, and initiate the activation of an intracellular molecular complex called the inflammasome. The inflammasome consists of a cytosolic pattern recognition receptor, an adaptor molecule ASC (apoptosis-associated speck-like protein containing a CARD) and the protease caspase-1. Assembly of the complex leads to the cleavage and activation of caspase-1 that triggers processing and release of the cytokines interleukin (IL)-1β and IL-18, and ultimately cell death via the process of pyroptosis. The ability to sense and respond to danger appropriately is critical for maintaining immune homeostasis. Dysregulation of inflammasomes contributes to the progression of chronic diseases prevalent in the ageing population, such as Alzheimer's disease, COPD and metabolic disease; hence, it is critical that activation of the inflammatory response and inflammasome activation are tightly regulated. Post-translational modifications (PTMs) such as ubiquitination have recently emerged as important regulators of inflammasome assembly. However, the mechanisms by which PTMs regulate the inflammasome are still not understood. This review aims to summarize our knowledge to date on how the ubiquitin system controls inflammasome activation and where this area of research is heading.
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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.