ArticleThe Journal of experimental medicine2018
TAK1 restricts spontaneous NLRP3 activation and cell death to control myeloid proliferation.
Article in The Journal of experimental medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 171 papers.
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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.
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Who cites it
171 citing papers in PubMed, 252 citations in OpenAlex.
- Role of PANoptosis in cancer: molecular mechanisms and therapeutic insights.Archives of toxicology · 2026Review
- PANoptosis in the pathogenesis of myelodysplastic syndromes.Molecular oncology · 2026Review
- Pyroptosis: Molecular mechanisms and function.Journal of physiology and biochemistry · 2026Review
- PANoptosis in life and death across cell types: From innate immunity to therapeutic implications.Cell chemical biology · 2026Review
- Decoding PANoptosis: Crosstalk of cell death pathways in immunity and inflammation.Immunologic research · 2026Review
- TGFβ-activated kinase-1 knockdown in hematopoietic stem-progenitor cells causes PANoptosis and myelodysplastic syndrome-like disease in mice.Haematologica · 2026Article
- Prussian blue nanoparticles targeting multiple PANoptosome-mediated PANoptosis for myocardial ischemia-reperfusion injury therapy.Nature communications · 2026Article
- PANoptosis as a Potential Therapeutic Target in Drug-Induced Liver Injury: A Narrative Review.Journal of inflammation research · 2026Review
- Constructing a PANoptosis-based prognostic signature to evaluate the immune landscape and therapeutic response in clear cell renal cell carcinoma.Journal of Zhejiang University. Science. B · 2025Article
- PANoptosis: A novel therapeutic target in kidney disease (Review).International journal of molecular medicine · 2025Review
- Three decades of caspases and RIPKs in life and death.Human molecular genetics · 2025Review
- T3SS effector EseJ in Edwardsiella piscicida inhibits PANoptosis in macrophages.Communications biology · 2025Article
- The molecular mechanisms and therapeutic implications of PANoptosis in ischemic diseases.Apoptosis : an international journal on programmed cell death · 2025Review
- Pentagalloyl glucose inhibits monosodium urate-induced inflammation and NLRP3 inflammasome formation via TAK1.American journal of physiology. Cell physiology · 2025Article
- PANoptosis: a potential target of atherosclerotic cardiovascular disease.Apoptosis : an international journal on programmed cell death · 2025Review
- Innate immune sensor NLRP3 drives PANoptosome formation and PANoptosis.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Caspases: structural and molecular mechanisms and functions in cell death, innate immunity, and disease.Cell discovery · 2025Review
- Roles of PANoptosis and related genes in acute liver failure: neoteric insight from bioinformatics analysis and animal experiment verification.Journal of Zhejiang University. Science. B · 2025Article
- Raver1 linksProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Necroptosis in obesity: a complex cell death event.Apoptosis : an international journal on programmed cell death · 2025Review
111 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The NOD-like receptor (NLR)-P3 inflammasome is a global sensor of infection and stress. Elevated NLRP3 activation levels are associated with human diseases, but the mechanisms controlling NLRP3 inflammasome activation are largely unknown. Here, we show that TGF-β activated kinase-1 (TAK1) is a central regulator of NLRP3 inflammasome activation and spontaneous cell death. Absence of TAK1 in macrophages induced spontaneous activation of the NLRP3 inflammasome without requiring toll-like receptor (TLR) priming and subsequent activating signals, suggesting a distinctive role for TAK1 in maintaining NLRP3 inflammasome homeostasis. Autocrine tumor necrosis factor (TNF) signaling in the absence of TAK1 induced spontaneous RIPK1-dependent NLRP3 inflammasome activation and cell death. We further showed that TAK1 suppressed homeostatic NF-κB and extracellular signal-related kinase (ERK) activation to limit spontaneous TNF production. Moreover, the spontaneous inflammation resulting from TAK1-deficient macrophages drives myeloid proliferation in mice, and was rescued by RIPK1 deficiency. Overall, these studies identify a critical role for TAK1 in maintaining NLRP3 inflammasome quiescence and preserving cellular homeostasis and survival.
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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.