ArticleScientific reports2016
Pyk2 activates the NLRP3 inflammasome by directly phosphorylating ASC and contributes to inflammasome-dependent peritonitis.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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58 citing papers in PubMed, 87 citations in OpenAlex.
- Aurora A exacerbates antibiotic-resistant Staphylococcus aureus infection through ASC phosphorylation.EMBO reports · 2026Article
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- Lactic acid drives NLRP3 inflammasome activation and caspase-1-like cytokine cleavage via intracellular acidification.Cell death & disease · 2026Article
- Molecular mechanisms of NLRP3 inflammasome activation.Experimental & molecular medicine · 2026Review
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- The role of autoantibodies in Alzheimer's disease: Pathogenetic connections or epiphenomena?Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Thermal Proteome Profiling Reveals Meltome Upon NLRP3 Inflammasome Activation.Molecular & cellular proteomics : MCP · 2025Article
- Construction of a PANoptosis-Related Gene Signature for Diabetic Nephropathy.Kidney & blood pressure research · 2025Article
- LBH589 reduces oxidized mitochondrial DNA and suppresses NLRP3 inflammasome activation to relieve pulmonary inflammation.PloS one · 2025Article
- Chemical screens for particle-induced macrophage death identifies kinase inhibitors of phagocytosis as targets for toxicity.Journal of nanobiotechnology · 2024Article
- Pseudorabies Virus UL4 protein promotes the ASC-dependent inflammasome activation and pyroptosis to exacerbate inflammation.PLoS pathogens · 2024Article
- ADP as a novel stimulus for NLRP3-inflammasome activation in mice fails to translate to humans.Purinergic signalling · 2024Article
- Post-translational control of NLRP3 inflammasome signaling.The Journal of biological chemistry · 2024Review
- Pas de deux of NLRP3 and ASC with CD63 on mast cell granules.Nature immunology · 2024Article
- Anaphylactic degranulation by mast cells requires the mobilization of inflammasome components.Nature immunology · 2024Article
- Cellular Dynamics of Fas-Associated Death Domain in the Regulation of Cancer and Inflammation.International journal of molecular sciences · 2024Review
- Inflammasomes as regulators of mechano-immunity.EMBO reports · 2024Review
- PTK2B promotes TBK1 and STING oligomerization and enhances the STING-TBK1 signaling.Nature communications · 2023Article
- SARS-CoV-2 Papain-like Protease Negatively Regulates the NLRP3 Inflammasome Pathway and Pyroptosis by Reducing the Oligomerization and Ubiquitination of ASC.Microorganisms · 2023Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inflammasome adaptor protein, ASC, contributes to both innate immune responses and inflammatory diseases via self-oligomerization, which leads to the activation of the protease, caspase-1. Here, we report that the cytosolic tyrosine kinases, FAK and Pyk2, are differentially involved in NLRP3 and AIM2 inflammasome activation. The inhibition of FAK and Pyk2 with RNA interference or chemical inhibitors dramatically abolished ASC oligomerization, caspase-1 activation, and IL-1β secretion in response to NLRP3 or AIM2 stimulation. Pyk2 is phosphorylated by the kinase Syk and relocalizes to the ASC specks upon NLRP3 inflammasome activation. Pyk2, but not FAK, could directly phosphorylate ASC at Tyr146, and only the phosphorylated ASC could participate in speck formation and trigger IL-1β secretion. Moreover, the clinical-trial-tested Pyk2/FAK dual inhibitor PF-562271 reduced monosodium urate-mediated peritonitis, a disease model used for studying the consequences of NLRP3 activation. Our results suggest that although Pyk2 and FAK are involved in inflammasome activation, only Pyk2 directly phosphorylates ASC and brings ASC into an oligomerization-competent state by allowing Tyr146 phosphorylation to participate ASC speck formation and subsequent NLRP3 inflammation.
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