ArticleThe Journal of biological chemistry2019
TRAF3-interacting JNK-activating modulator promotes inflammation by stimulating translocation of Toll-like receptor 4 to lipid rafts.
Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Structural and functional characterization of the New Delhi metallo beta-lactamase-1 (NDM-1) D254A mutant: a biochemical, microbiological and bioinformatics study.World journal of microbiology & biotechnology · 2025Article
- Artesunate Ameliorates SLE Atherosclerosis Through PPARγ-Driven Cholesterol Efflux Restoration and Disruption of Lipid Raft-Organized TLR9/MyD88 Signaling Pathway.Biomolecules · 2025Article
- Neuroprotective effects ofFrontiers in pharmacology · 2024Article
- TRAF3IP3 Is Cleaved by EV71 3C Protease and Exhibits Antiviral Activity.Frontiers in microbiology · 2022Article
- Diabetes Mellitus and Periodontitis Share Intracellular Disorders as the Main Meeting Point.Cells · 2021Review
- Article
- Alpinia oxyphylla Miq extract reduces cerebral infarction by downregulating JNK-mediated TLR4/T3JAM- and ASK1-related inflammatory signaling in the acute phase of transient focal cerebral ischemia in rats.Chinese medicine · 2021Article
- Mannose Receptor Mediates the Activation of Chitooligosaccharides on Blunt Snout Bream (Frontiers in immunology · 2021Article
- STAT3 Differentially Regulates TLR4-Mediated Inflammatory Responses in Early or Late Phases.International journal of molecular sciences · 2020Article
- Sphingomyelin Synthase 2 Promotes Endothelial Dysfunction by Inducing Endoplasmic Reticulum Stress.International journal of molecular sciences · 2019Article
- Simvastatin Attenuates HMolecules (Basel, Switzerland) · 2019Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toll-like receptors (TLRs) are key players of the innate immune system and contribute to inflammation and pathogen clearance. Although TLRs have been extensively studied, it remains unclear how exactly bacterial lipopolysaccharide (LPS)-induced conformational changes of the extracellular domain of the TLRs trigger the dimerization of their intracellular domain across the plasma membrane and thereby stimulate downstream signaling. Here, using LPS-stimulated THP-1-derived macrophages and murine macrophages along with immunoblotting and immunofluorescence and quantitative analyses, we report that in response to inflammatory stimuli, the coiled-coil protein TRAF3-interacting JNK-activating modulator (T3JAM) associates with TLR4, promotes its translocation to lipid rafts, and thereby enhances macrophage-mediated inflammation. T3JAM overexpression increased and T3JAM depletion decreased TLR4 signaling through both the MyD88-dependent pathway and TLR4 endocytosis. Importantly, deletion or mutation of T3JAM to disrupt its coiled-coil-mediated homoassociation abrogated TLR4 recruitment to lipid rafts. Consistently, T3JAM depletion in mice dampened TLR4 signaling and alleviated LPS-induced inflammatory damage. Collectively, our findings reveal an additional molecular mechanism by which TLR4 activity is regulated and suggest that T3JAM may function as a molecular clamp to "tighten up" TLR4 and facilitate its translocation to lipid rafts.
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