ArticleJournal of immunology (Baltimore, Md. : 1950)2021
cAbl Kinase Regulates Inflammasome Activation and Pyroptosis via ASC Phosphorylation.
Article in Journal of immunology (Baltimore, Md. : 1950), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- [Regulatory mechanisms of post-translational modifications in inflammasome signaling: a review].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026Review
- Notch2 Directs aTreg Cell Fate Toward Immunoregulation or Inflammatory Pyroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Pseudorabies Virus UL4 protein promotes the ASC-dependent inflammasome activation and pyroptosis to exacerbate inflammation.PLoS pathogens · 2024Article
- Post-translational control of NLRP3 inflammasome signaling.The Journal of biological chemistry · 2024Review
- Pyroptosis-triggered pathogenesis: New insights on antiphospholipid syndrome.Frontiers in immunology · 2023Review
- The central inflammasome adaptor protein ASC activates the inflammasome after transition from a soluble to an insoluble state.The Journal of biological chemistry · 2022Article
- Inflammasome Activation in an In Vitro Sepsis Model Recapitulates Increased Monocyte Distribution Width Seen in Patients With Sepsis.Critical care explorations · 2022Article
- Posttranslational Regulation of Inflammasomes, Its Potential as Biomarkers and in the Identification of Novel Drugs Targets.Frontiers in cell and developmental biology · 2022Review
- PHOrming the inflammasome: phosphorylation is a critical switch in inflammasome signalling.Biochemical Society transactions · 2021Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Inflammasome activation is regulated in part by the posttranslational modification of inflammasome proteins. Tyrosine phosphorylation is one possible modification. Having previously shown that the protein tyrosine kinase (PTK) inhibitor AG126 greatly inhibits inflammasome activation, we sought to uncover the target kinase. To do this, we screened a commercial tyrosine kinase library for inhibition of inflammasome-dependent IL-18/IL-1β release and pyroptosis. THP-1 cells (human monocyte cell line) were incubated with PTK inhibitors (0.1, 1, and 10 μM) before stimulation with LPS followed by ATP. The PTK inhibitors DCC-2036 (Rebastinib) and GZD824, specific for Bcr-Abl kinase, showed the most severe reduction of IL-18 and lactate dehydrogenase release at all concentrations used. The suggested kinase target, cAbl kinase, was then deleted in THP-1 cells by CRISPR/Cas9 editing and then tested for its role in inflammasome function and potential to phosphorylate the inflammasome adaptor ASC. The cABL knockout not only significantly inhibited inflammasome function but also decreased release of phosphorylated ASC after LPS/ATP stimulation. One predicted target of cAbl kinase is tyrosine 146 in ASC. Complementation of ASC knockout THP-1 cells with mutated Y146A ASC significantly abrogated inflammasome activation and ASC oligomerization as compared with wild-type ASC complementation. Thus, these findings support cAbl kinase as a positive regulator of inflammasome activity and pyroptosis, likely via phosphorylation of ASC.
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