ArticleScientific reports2016
LPS-induced NFκB enhanceosome requires TonEBP/NFAT5 without DNA binding.
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 43 papers.
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Who cites it
43 citing papers in PubMed, 58 citations in OpenAlex.
- TonEBP as a key regulator of hypothalamic leptin signaling and resistance.Cellular and molecular life sciences : CMLS · 2026Article
- Hepatocyte TonEBP promotes metabolic stress-induced hepatic fibroinflammation involving transcriptional activation of ELR⁺ CXC chemokines.Cell death discovery · 2026Article
- The miR-1260b-NFAT5 axis regulates inflammasome priming and M1 macrophage polarization in periodontitis.Frontiers in immunology · 2026Article
- NFAT5 Regulates IL8 to Promote Cell Growth and Migration in Non-Small Cell Lung Cancer.Thoracic cancer · 2025Article
- Cerulenin partially corrects the disrupted developmental transcriptomic signature in Huntington's disease striatal medium spiny neurons.Stem cells (Dayton, Ohio) · 2025Article
- Noradrenaline Synergistically EnhancesInternational journal of molecular sciences · 2025Article
- NFAT5: a stress-related transcription factor with multiple functions in health and disease.Cell stress · 2025Review
- Adequate post-ischemic reperfusion of the mouse brain requires endothelial NFAT5.Acta neuropathologica communications · 2024Article
- HES1 potentiates high salt stress response as an enhancer of NFAT5-DNA binding.Communications biology · 2024Article
- A comparative analysis of TonEBP conditional knockout mouse models reveals inter-dependency between compartments of the intervertebral disc.Development (Cambridge, England) · 2024Article
- DendroX: multi-level multi-cluster selection in dendrograms.BMC genomics · 2024Article
- TonEBP: A Key Transcription Factor in Microglia Following Intracerebral Hemorrhage Induced-Neuroinflammation.International journal of molecular sciences · 2024Article
- Tissue Sodium Accumulation Induces Organ Inflammation and Injury in Chronic Kidney Disease.International journal of molecular sciences · 2023Review
- NLRC3 expression in macrophage impairs glycolysis and host immune defense by modulating the NF-κB-NFAT5 complex during septic immunosuppression.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- TonEBP expression is essential in the IL-1β-induced migration and invasion of human A549 lung cancer cells.Oncology research · 2023Article
- TonEBP in Myeloid Cells Promotes Obesity-Induced Insulin Resistance and Inflammation Through Adipose Tissue Remodeling.Diabetes · 2022Article
- Tonicity-responsive enhancer-binding protein promotes diabetic neuroinflammation and cognitive impairment via upregulation of lipocalin-2.Journal of neuroinflammation · 2021Article
- Article
- NFAT5 Amplifies Antipathogen Responses by Enhancing Chromatin Accessibility, H3K27 Demethylation, and Transcription Factor Recruitment.Journal of immunology (Baltimore, Md. : 1950) · 2021Article
- TonEBP recognizes R-loops and initiates m6A RNA methylation for R-loop resolution.Nucleic acids research · 2021Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NFκB is a central mediator of inflammation. Present inhibitors of NFκB are mostly based on inhibition of essential machinery such as proteasome and protein kinases, or activation of nuclear receptors; as such, they are of limited therapeutic use due to severe toxicity. Here we report an LPS-induced NFκB enhanceosome in which TonEBP is required for the recruitment of p300. Increased expression of TonEBP enhances the NFκB activity and reduced TonEBP expression lowers it. Recombinant TonEBP molecules incapable of recruiting p300 do not stimulate NFκB. Myeloid-specific deletion of TonEBP results in milder inflammation and sepsis. We discover that a natural small molecule cerulenin specifically disrupts the enhanceosome without affecting the activation of NFκB itself. Cerulenin suppresses the pro-inflammatory activation of macrophages and sepsis without detectable toxicity. Thus, the NFκB enhanceosome offers a promising target for useful anti-inflammatory agents.
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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.