ArticleScientific reports2017
Lipopolysaccharide-induced NF-κB nuclear translocation is primarily dependent on MyD88, but TNFα expression requires TRIF and MyD88.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.
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Who cites it
111 citing papers in PubMed, 163 citations in OpenAlex.
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- An immunobiliary single-cell atlas resolves crosstalk between type 2 conventional dendritic cells and γδ T cells in cholangitis.Nature communications · 2026Article
- Toll-like receptor signaling outcome is determined by the stoichiometry of the endogenous TRIFosome.Science advances · 2026Article
- CD163 at the crossroads: a viral-exploited immunomodulator.Virology journal · 2026Review
- The Intestinal Barrier: A Multilayered Gatekeeper Against Systemic Disease.International journal of microbiology · 2026Review
- Pathogenesis and intervention strategies for metabolic dysfunction-associated fatty liver disease from the perspective of the gut-microbiota-liver axis.Frontiers in immunology · 2026Review
- Cannabidiol reduces LPS-induced inflammatory response in the human placenta by reducing NF-κB translocation.Journal of cannabis research · 2025Article
- Type 3 Diabetes: Linking Insulin Resistance to Cognitive Decline.Diseases (Basel, Switzerland) · 2025Review
- Probiotic Pediococcus acidilactici Strains Exert Anti-inflammatory Effects by Regulating Intracellular Signaling Pathways in LPS-Induced RAW 264.7 Cells.Probiotics and antimicrobial proteins · 2025Article
- Evaluating the role of lipopolysaccharides in the joint: fibronectin as a novel protective mechanism.RMD open · 2025Article
- An NF-kB/TNF-alpha signalling feedback loop acts to coordinate tissue regeneration and macrophage behaviour in zebrafish.NPJ Regenerative medicine · 2025Article
51 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
TLR4 signalling through the MyD88 and TRIF-dependent pathways initiates translocation of the transcription factor NF-κB into the nucleus. In cell population studies using mathematical modeling and functional analyses, Cheng et al. suggested that LPS-driven activation of MyD88, in the absence of TRIF, impairs NF-κB translocation. We tested the model proposed by Cheng et al. using real-time single cell analysis in macrophages expressing EGFP-tagged p65 and a TNFα promoter-driven mCherry. Following LPS stimulation, cells lacking TRIF show a pattern of NF-κB dynamics that is unaltered from wild-type cells, but activation of the TNFα promoter is impaired. In macrophages lacking MyD88, there is minimal NF-κB translocation to the nucleus in response to LPS stimulation, and there is no activation of the TNFα promoter. These findings confirm that signalling through MyD88 is the primary driver for LPS-dependent NF-κB translocation to the nucleus. The pattern of NF-κB dynamics in TRIF-deficient cells does not, however, directly reflect the kinetics of TNFα promoter activation, supporting the concept that TRIF-dependent signalling plays an important role in the transcription of this cytokine.
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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.