ArticleScientific reports2016
p58(IPK) suppresses NLRP3 inflammasome activation and IL-1β production via inhibition of PKR in macrophages.
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 29 papers.
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Who cites it
29 citing papers in PubMed, 35 citations in OpenAlex.
- The molecular mechanisms of pyroptosis and its implications in tumor immunotherapy.Molecular cancer · 2026Review
- Gastrointestinal inflammation and cancer: viral and bacterial interplay.Gut microbes · 2025Review
- Corticosterone effects induced by stress and immunity and inflammation: mechanisms of communication.Frontiers in endocrinology · 2025Review
- Cellular Stress: Modulator of Regulated Cell Death.Biology · 2023Review
- Neuronal p58Cells · 2023Article
- Signaling plasticity in the integrated stress response.Frontiers in cell and developmental biology · 2023Review
- Cell deaths: Involvement in the pathogenesis and intervention therapy of COVID-19.Signal transduction and targeted therapy · 2022Review
- Korean Red Ginseng, a regulator of NLRP3 inflammasome, in the COVID-19 pandemic.Journal of ginseng research · 2022Review
- Interactions between NLRP3 inflammasome and glycolysis in macrophages: New insights into chronic inflammation pathogenesis.Immunity, inflammation and disease · 2022Review
- NLRP3-Mediated Inflammation in Atherosclerosis and Associated Therapeutics.Frontiers in cell and developmental biology · 2022Review
- A tale of two proteins: PACT and PKR and their roles in inflammation.The FEBS journal · 2021Review
- The NLRP3 inflammasome and COVID-19: Activation, pathogenesis and therapeutic strategies.Cytokine & growth factor reviews · 2021Review
- Promise of the NLRP3 Inflammasome Inhibitors in In Vivo Disease Models.Molecules (Basel, Switzerland) · 2021Review
- Dual topology of co-chaperones at the membrane of the endoplasmic reticulum.Cell death discovery · 2021Review
- Relevant mediators involved in and therapies targeting the inflammatory response induced by activation of the NLRP3 inflammasome in ischemic stroke.Journal of neuroinflammation · 2021Review
- Double-Stranded RNA Dependent Kinase R Regulates Antibacterial Immunity in Sepsis.Journal of innate immunity · 2021Article
- Peroxynitrite/PKR Axis Modulates the NLRP3 Inflammasome of Cardiac Fibroblasts.Frontiers in immunology · 2020Article
- NLRP3 Inflammasome: The Stormy Link Between Obesity and COVID-19.Frontiers in immunology · 2020Review
- The complement receptor C5aR2 promotes protein kinase R expression and contributes to NLRP3 inflammasome activation and HMGB1 release from macrophages.The Journal of biological chemistry · 2019Article
- Opioid Tolerance in Critical Illness.The New England journal of medicine · 2019Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The NLRP3 inflammasome activation is a key signaling event for activation and secretion of pro-inflammatory cytokines such as IL-1β from macrophages. p58(IPK) is a molecular chaperone that regulates protein homeostasis through inhibiting eIF-2α kinases including double-stranded RNA-dependent protein kinase (PKR), which has been recently implicated in inflammasome activation. Herein we investigate the role of p58(IPK) in TLR4 signaling and inflammasome activation in macrophages. Primary bone marrow-derived macrophages (BMDM) was isolated from p58(IPK) knockout (KO) and wildtype (WT) mice and treated with lipopolysaccharide (LPS) and ATP to activate TLR4 signaling and stimulate inflammasome activation. Compared to WT macrophages, p58(IPK) deficient cells demonstrated significantly stronger activation of PKR, NF-κB, and JNK and higher expression of pro-inflammatory genes TNF-α and IL-1β. Coincidently, p58(IPK) deletion intensified NLRP3-inflammasome activation indicated by enhanced caspase 1 cleavage and increased IL-1β maturation and secretion. Pretreatment with specific PKR inhibitor or overexpression of p58(IPK) largely abolished the changes in inflammasome activation and IL-1β secretion in p58(IPK) null macrophages. Furthermore, immunoprecipitation assay confirmed the binding of p58(IPK) with PKR, but not other TLR4 downstream signaling molecules. Collectively, these results suggest a novel and crucial role of p58(IPK) in regulation of inflammasome activation and IL-1β secretion in macrophages.
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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.