ArticleCellular signalling2021
The deubiquitinase STAMBP modulates cytokine secretion through the NLRP3 inflammasome.
Article in Cellular signalling, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 1 of them a synthesis that pooled it.
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Who cites it
41 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Mitochondrial dysfunction gene expression, DNA methylation, and inflammatory cytokines interaction activate Alzheimer's disease: a multi-omics Mendelian randomization study.Journal of translational medicine · 2024Pooled it
- USP13 ameliorates diabetic cardiomyopathy via deubiquitinating NLRP3 and inhibiting pyroptosis in cardiomyocytes.Cell death and differentiation · 2026Article
- STAMBP drives colorectal cancer progression via CXCR4 deubiquitination and bone marrow-derived suppressor cell recruitment.Genes and immunity · 2026Article
- Molecular mechanisms of NLRP3 inflammasome activation.Experimental & molecular medicine · 2026Review
- From concept to application: Exploring the evolution and potential of DUBTAC technology.Acta pharmaceutica Sinica. B · 2026Review
- FBXL8 Stabilizes IκBα and Negatively Regulated NF-κB Activation to Suppress Pancreatic Cancer Progression.International journal of biological sciences · 2026Article
- Deubiquitinase MoAMSH inhibits autophagy by targeting MoAtg6 in Magnaporthe oryzae.Cell communication and signaling : CCS · 2025Article
- STAMBP Accelerates Progression and Tamoxifen Resistance of Breast Cancer Through Deubiquitinating ERα.Biomolecules · 2025Article
- Cardiomyocyte USP20 alleviates septic cardiomyopathy by deubiquitinating and inhibiting NLRP3 activity.Clinical and translational medicine · 2025Article
- Cross-Sectional and Longitudinal Immunoprofiling of Oligoarticular Juvenile Idiopathic Arthritis Reveals Different Patterns in Synovial Fluid and Plasma.Scandinavian journal of immunology · 2025Article
- Updated insights into the molecular networks for NLRP3 inflammasome activation.Cellular & molecular immunology · 2025Review
- The Role of Caspase-1 and Caspase-4 in Modulating Gingival Epithelial Cell Responses toPathogens (Basel, Switzerland) · 2025Article
- Article
- Exploring Gut Microbe-Host Genes in Postpartum Depression: Mendelian Randomization and Transcriptomic Analysis.International journal of women's health · 2025Article
- Ubiquitin-proteasome system: a potential participant and therapeutic target in antiphospholipid syndrome.Frontiers in immunology · 2025Review
- Inflammatory cytokines and their potential role in kidney stone disease: a Mendelian randomization study.International urology and nephrology · 2024Article
- Identification of STAM-binding protein as a target for the treatment of gemcitabine resistance pancreatic cancer in a nutrient-poor microenvironment.Cell death & disease · 2024Article
- YOD1 protects against MRSA sepsis-induced DIC through Lys33-linked deubiquitination of NLRP3.Cell death & disease · 2024Article
- The roles of ubiquitination and deubiquitination of NLRP3 inflammasome in inflammation-related diseases: A review.Biomolecules & biomedicine · 2024Review
- Distinct inflammation-related proteins associated with T cell immune recovery during chronic HIV-1 infection.Emerging microbes & infections · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome is a multimeric, cytoplasmic, protein complex that regulates maturation and secretion of interleukin (IL)-1β, a potent pro-inflammatory cytokine. Critical to host defense against pathogens, IL-1β amplifies early innate immune responses by activating transcription of numerous other cytokines and chemokines. Excessive IL-1β is associated with poor outcomes in inflammatory illnesses, such as sepsis and the acute respiratory distress syndrome (ARDS). Tight regulation of this signaling axis is vital, but little is known about mechanisms to limit excessive inflammasome activity. Here we identify the deubiquitinase STAM-binding protein (STAMBP) as a negative regulator of the NLRP3 inflammasome. In monocytes, knockout of STAMBP by CRISPR/Cas9 gene editing increased expression of numerous cytokines and chemokines in response to Toll-like receptor (TLR) agonists or bacterial lipopolysaccharide (LPS). This exaggerated inflammatory response was dependent on IL-1β signaling, and STAMBP knockout directly increased release of IL-1β with TLR ligation. While STAMBP does not modulate NLRP3 protein abundance, cellular depletion of the deubiquitinase increased NLRP3 K63 chain polyubiquitination resulting in increased NLRP3 inflammasome activation. These findings describe a unique mechanism of non-degradative ubiquitination of NLRP3 by STAMBP to limit excessive inflammasome activation and to reduce injurious IL-1β signaling.
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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.