ArticleJournal of immunology (Baltimore, Md. : 1950)2014
Inflammasome priming by lipopolysaccharide is dependent upon ERK signaling and proteasome function.
Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers.
What it found
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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.
The trial behind it
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Who cites it
114 citing papers in PubMed, 199 citations in OpenAlex.
- Comparative Analysis of LPS/IFN-γ and LPS/ATP-Induced Inflammatory Models in BV2 Microglia.Neurochemical research · 2026Article
- Maternal High Fat Diet and Acute Viral Mimic Exposure Impact Placental Inflammation, Lipid Peroxidation and Cellular Proliferation-to-Death Ratio Across Mouse Pregnancy.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026Article
- Streptococcus anginosus activates the NLRP3 inflammasome to promote inflammatory responses from macrophages.Journal of leukocyte biology · 2026Article
- Chemotherapy-derived DAMPs drive reprogramming of tumor-associated macrophages toward a pro-inflammatory phenotype in hepatocellular carcinoma.Scientific reports · 2026Article
- Article
- Prunetin ameliorates myocardial pyroptosis after myocardial infarction by inhibiting the TNF-α/p38 MAPK/ERK pathway.Frontiers in cardiovascular medicine · 2026Article
- Evaluating antioxidant treatment approaches for eosinophilic chronic sinusitis.Frontiers in immunology · 2026Review
- Soyeom-Jetong mixture attenuates NLRP3 inflammasome-mediated inflammation.Frontiers in pharmacology · 2026Article
- A combined AI and cell biology approach surfaces targets and mechanistically distinct Inflammasome inhibitors.iScience · 2024Article
- Aripiprazole, but Not Olanzapine, Alters the Response to Oxidative Stress in Fao Cells by Reducing the Activation of Mitogen-Activated Protein Kinases (MAPKs) and Promoting Cell Survival.International journal of molecular sciences · 2024Article
- NLRP3 Negative Regulation Mechanisms in the Resting State and Its Implications for Therapeutic Development.International journal of molecular sciences · 2024Review
- Deciphering the molecular mechanism of NLRP3 in BPA-mediated toxicity: Implications for targeted therapies.Heliyon · 2024Review
- Nuclear receptor coactivator 6 is a critical regulator of NLRP3 inflammasome activation and gouty arthritis.Cellular & molecular immunology · 2024Article
- Investigation of sex-based differences in the immunotoxicity of silver nanoparticles.Nanotoxicology · 2024Article
- DNA hypomethylation promotes the expression of CASPASE-4 which exacerbates inflammation and amyloid-β deposition in Alzheimer's disease.Alzheimer's research & therapy · 2024Article
- Establishment of prognostic model of bladder cancer based on apoptosis-related genes, in which P4HB promotes BLCA progression.BMC urology · 2023Article
- Systems Biology and Cytokines Potential Role in Lung Cancer Immunotherapy Targeting Autophagic Axis.Biomedicines · 2023Review
- Characterization of Electrospun BDMC-Loaded PLA Nanofibers with Drug Delivery Function and Anti-Inflammatory Activity.International journal of molecular sciences · 2023Article
- Article
- Integrin Mac1 mediates paraquat and maneb-induced learning and memory impairments in mice through NADPH oxidase-NLRP3 inflammasome axis-dependent microglial activation.Journal of neuroinflammation · 2023Article
54 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
Caspase-1 activation is a central event in innate immune responses to many pathogenic infections and tissue damage. The NLRP3 inflammasome, a multiprotein scaffolding complex that assembles in response to two distinct steps, priming and activation, is required for caspase-1 activation. However, the detailed mechanisms of these steps remain poorly characterized. To investigate the process of LPS-mediated NLRP3 inflammasome priming, we used constitutively present pro-IL-18 as the caspase-1-specific substrate to allow study of the early events. We analyzed human monocyte caspase-1 activity in response to LPS priming, followed by activation with ATP. Within minutes of endotoxin priming, the NLRP3 inflammasome is licensed for ATP-induced release of processed IL-18, apoptosis-associated speck-forming complex containing CARD, and active caspase-1, independent of new mRNA or protein synthesis. Moreover, extracellular signal-regulated kinase 1 (ERK1) phosphorylation is central to the priming process. ERK inhibition and small interfering RNA-mediated ERK1 knockdown profoundly impair priming. In addition, proteasome inhibition prevents ERK phosphorylation and blocks priming. Scavenging reactive oxygen species with diphenylene iodonium also blocks both priming and ERK phosphorylation. These findings suggest that ERK1-mediated posttranslational modifications license the NLRP3 inflammasome to respond to the second signal ATP by inducing posttranslational events that are independent of new production of pro-IL-1β and NOD-like receptor components.
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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.