ArticleImmunity2024
N4BP1 coordinates ubiquitin-dependent crosstalk within the IκB kinase family to limit Toll-like receptor signaling and inflammation.
Article in Immunity, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Mechanism of Kushen Tongguan Pill on benign prostatic hyperplasia: roles of TLR4/NF-κB pathway and macrophage M1 polarization.Journal of molecular histology · 2026Article
- cFLIP suppresses caspase-1- and MLKL-independent perinatal lethality driven by auto-processing impaired caspase-8 D387A.Cell death and differentiation · 2026Article
- Poxvirus attack of antiviral defense pathways unleashes an effector-triggered NF-κB response.Science (New York, N.Y.) · 2026Article
- Byakangelicol Alleviates Ischemic Brain Injury by Inhibiting Microglial Activation and Oxidative Stress.Molecular neurobiology · 2026Article
- N4BP1 acts as a potent negative regulator of IL-17 signaling by blocking the translation of Act1 mRNA.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Solution structure of mouse HBS1L/SKI7-specific UBA domain in complex with ubiquitin: Implications for stalled ribosome recognition.PloS one · 2026Article
- Toll-like receptors in innate immunity and inflammation: from fundamental biology to clinic insights.Immunity & inflammation · 2026Review
- Dual role of N4BP1 in neutrophil-epithelial crosstalk in periodontitis.Frontiers in immunology · 2026Article
- Article
- FLIPProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Enteroviral 3C protease cleaves N4BP1 to impair the host inflammatory response.Journal of virology · 2025Article
- NRF2 Deficiency in Bladder Epithelial Cells Owing to Ubiquitination by N6-Methyladenosine-Modified TRIM21 Induces Oxidative Stress and Inflammation to Aggravate IC/BPS.Journal of inflammation research · 2025Article
- Functional anatomy of zinc finger antiviral protein complexes.Nature communications · 2024Article
- TLR3 Knockdown Attenuates Pressure-Induced Neuronal Damage In Vitro.Journal of cellular and molecular medicine · 2024Article
- TBK1-associated adapters TANK and AZI2 protect mice against TNF-induced cell death and severe autoinflammatory diseases.Nature communications · 2024Article
- Leveraging Therapeutic Proteins and Peptides fromInternational journal of molecular sciences · 2024Article
- Adaptor-Mediated Trafficking of Tank Binding Kinase 1 During Diverse Cellular Processes.Traffic (Copenhagen, Denmark)Review
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13 authors.
Funding
Abstract
The ubiquitin-binding endoribonuclease N4BP1 potently suppresses cytokine production by Toll-like receptors (TLRs) that signal through the adaptor MyD88 but is inactivated via caspase-8-mediated cleavage downstream of death receptors, TLR3, or TLR4. Here, we examined the mechanism whereby N4BP1 limits inflammatory responses. In macrophages, deletion of N4BP1 prolonged activation of inflammatory gene transcription at late time points after TRIF-independent TLR activation. Optimal suppression of inflammatory cytokines by N4BP1 depended on its ability to bind polyubiquitin chains, as macrophages and mice-bearing inactivating mutations in a ubiquitin-binding motif in N4BP1 displayed increased TLR-induced cytokine production. Deletion of the noncanonical IκB kinases (ncIKKs), Tbk1 and Ikke, or their adaptor Tank phenocopied N4bp1 deficiency and enhanced macrophage responses to TLR1/2, TLR7, or TLR9 stimulation. Mechanistically, N4BP1 acted in concert with the ncIKKs to limit the duration of canonical IκB kinase (IKKα/β) signaling. Thus, N4BP1 and the ncIKKs serve as an important checkpoint against over-exuberant innate immune responses.
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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.