ArticleNucleic acids research2023
p38-mediated FOXN3 phosphorylation modulates lung inflammation and injury through the NF-κB signaling pathway.
Article in Nucleic acids research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 44 citations in OpenAlex.
- miR-182-5p regulates proliferation and senescence in chicken Leydig cells via the Wnt/β-catenin pathway by targeting FOXN3.Poultry science · 2026Article
- SKP2 Regulates Pulmonary Inflammatory Injury Triggered by Bacterial Infection Through p27-Mediated Degradation of FOXN3.MedComm · 2026Article
- Maternal Inflammation Alters Nuclear and Mitochondrial DNA Methylation Patterns in Neonatal Brain Monocytes.Cells · 2026Article
- Chinese cobra (Naja atra) SVPLACommunications biology · 2026Article
- Copper-rhein nanozymes induce bacterial activation-exhaustion death for the treatment of bacterial pneumonia and infected wounds.Journal of nanobiotechnology · 2026Article
- Foxn3 is part of a transcriptional network that regulates primary cilia in the developing retina.Development (Cambridge, England) · 2026Article
- FOXN3 integrates the KU70/KU80/SREBP-1 complex to regulate lipid metabolism in non-alcoholic fatty liver disease.Nucleic acids research · 2026Article
- PARP1 stabilizes FOXN3 to suppress pulmonary fibrosis through p38-related feedback regulation.Science advances · 2026Article
- Quorum sensing geneFrontiers in microbiology · 2026Article
- Investigating the impact of Sprouty-related EVH1 domain-containing protein 3 on gastric cancer prognosis and tumor microenvironments.Frontiers in oncology · 2026Article
- Protocadherin 1 (PCDH1) Promotes Pancreatic Cancer Metastasis by Regulating Epithelial-Mesenchymal Transition (EMT) Progression Through the NF-κB Pathway.Cancer management and research · 2026Article
- B-cell DNA methylation signature in response to hepatitis B virus vaccination in females and males.Frontiers in immunology · 2026Article
- Capsaicin diet drives gut inflammation and exosomal miR-17-3p elevation in idiopathic short stature.Nature communications · 2025Article
- Homeostasis of Gut Microbiota Protects against Susceptibility to Fungal Pneumonia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Multidimensional integrated lung protection measures attenuate pulmonary inflammation and improve lung function by inhibiting the NF-κB signaling pathway in elderly patients with lung dysfunction.Clinical and experimental medicine · 2025Article
- Tumor Immunosenescence Driven by Chronic Inflammation: Mechanisms, Microenvironment Remodeling and Therapeutic Strategies.Aging and disease · 2025Review
- Vitamin C in Cardiovascular Disease: From Molecular Mechanisms to Clinical Evidence and Therapeutic Applications.Antioxidants (Basel, Switzerland) · 2025Review
- Mucous Permeable Nanoparticle for Inducing Cuproptosis-Like Death In Broad-Spectrum Bacteria for Nebulized Treatment of Acute Pneumonia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Phosphorylation of FOXN3 by NEK6 promotes pulmonary fibrosis through Smad signaling.Nature communications · 2025Article
- Modulation of pain sensitivity by Ascl1- and Lhx6-dependent GABAergic neuronal function in streptozotocin diabetic mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
Corrections and comments
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Authors and funding
14 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
NF-κB activates the primary inflammatory response pathway responsible for methicillin-resistant Staphylococcus aureus (MRSA)-induced lung inflammation and injury. Here, we report that the Forkhead box transcription factor FOXN3 ameliorates MRSA-induced pulmonary inflammatory injury by inactivating NF-κB signaling. FOXN3 competes with IκBα for binding to heterogeneous ribonucleoprotein-U (hnRNPU), thereby blocking β-TrCP-mediated IκBα degradation and leading to NF-κB inactivation. FOXN3 is directly phosphorylated by p38 at S83 and S85 residues, which induces its dissociation from hnRNPU, thus promoting NF-κB activation. After dissociation, the phosphorylated FOXN3 becomes unstable and undergoes proteasomal degradation. Additionally, hnRNPU is essential for p38-mediated FOXN3 phosphorylation and subsequent phosphorylation-dependent degradation. Functionally, genetic ablation of FOXN3 phosphorylation results in strong resistance to MRSA-induced pulmonary inflammatory injury. Importantly, FOXN3 phosphorylation is clinically positively correlated with pulmonary inflammatory disorders. This study uncovers a previously unknown regulatory mechanism underpinning the indispensable role of FOXN3 phosphorylation in the inflammatory response to pulmonary infection.
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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.