ArticleScience signaling2015
Distinct single-cell signaling characteristics are conferred by the MyD88 and TRIF pathways during TLR4 activation.
Article in Science signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.
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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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
81 citing papers in PubMed, 1 synthesis or guideline pooled it, 115 citations in OpenAlex.
- Contribution of TLR4 to colorectal tumor microenvironment, etiology and prognosis.Journal of cancer research and clinical oncology · 2023Pooled it
- Macrophage-Specific NF-κB Activation Dynamics Can Segregate Inflammatory Bowel Disease Patients.Frontiers in immunology · 2019Trial
- Macrophage polarization plasticity in pulmonary fibrosis: a review from pathogenesis to therapeutic targeting.Inflammopharmacology · 2026Review
- Macrophage response specificity to ligand mixtures is improved by signaling pathway antagonism.Molecular systems biology · 2026Article
- Curcumin blocks Fusobacterium nucleatum-driven tumor progression and carcinogenesis in ESCC via inhibiting the TLR4/MYD88/TRIF/STAT3 axis.Journal of gastroenterology · 2026Article
- Salmonella Typhimurium hijacks a host glucose transporter for intravacuolar proliferation.Cell communication and signaling : CCS · 2026Article
- Pro-inflammatory LPS drives production and release of the chemokine MCP-1 in human coronary artery smooth muscle cells.Molecular and cellular biochemistry · 2026Article
- Pathogenesis and intervention strategies for metabolic dysfunction-associated fatty liver disease from the perspective of the gut-microbiota-liver axis.Frontiers in immunology · 2026Review
- Irisin-Loaded Cerium-Containing Mesoporous Bioactive Glass for Effective Immunomodulation and Odontogenesis of Dental Pulp Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Computational modelling of aggressive B-cell lymphoma.Biochemical Society transactions · 2025Review
- Synergy and antagonism in the integration of BCR and CD40 signals that control B-cell population expansion.Molecular systems biology · 2025Article
- NF-κB: master regulator of cellular responses in health and disease.Immunity & inflammation · 2025Review
- Article
- Dynamical and combinatorial coding by MAPK p38 and NFκB in the inflammatory response of macrophages.Molecular systems biology · 2024Article
- Article
- TLR4 sensing of IsdB ofmBio · 2024Article
- Immune Homeostasis Maintenance Through Advanced Immune Therapeutics to Target Atherosclerosis.Methods in molecular biology (Clifton, N.J.) · 2024Article
- QMrebind: incorporating quantum mechanical force field reparameterization at the ligand binding site for improved drug-target kinetics through milestoning simulations.Chemical science · 2023Article
- Review
- Tonic TNF conditioning of macrophages safeguards stimulus-specific inflammatory responses.EMBO reports · 2023Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Toll-like receptors (TLRs) recognize specific pathogen-associated molecular patterns and initiate innate immune responses through signaling pathways that depend on the adaptor proteins MyD88 (myeloid differentiation marker 88) or TRIF (TIR domain-containing adaptor protein-inducing interferon-β). TLR4, in particular, uses both adaptor proteins to activate the transcription factor nuclear factor κB (NF-κB); however, the specificity and redundancy of these two pathways remain to be elucidated. We developed a mathematical model to show how each pathway encodes distinct dynamical features of NF-κB activity and makes distinct contributions to the high variability observed in single-cell measurements. The assembly of a macromolecular signaling platform around MyD88 associated with receptors at the cell surface determined the timing of initial responses to generate a reliable, digital NF-κB signal. In contrast, ligand-induced receptor internalization into endosomes produced noisy, delayed, yet sustained NF-κB signals through TRIF. With iterative mathematical model development, we predicted the molecular mechanisms by which the MyD88- and TRIF-mediated pathways provide ligand concentration-dependent signaling dynamics that transmit information about the pathogen threat.
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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.