ReviewFrontiers in immunology2019
Signaling Crosstalk Mechanisms That May Fine-Tune Pathogen-Responsive NFκB.
Review in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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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.
The trial behind it
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
34 citing papers in PubMed, 52 citations in OpenAlex.
- Immunomodulatory Effects of Lidocaine: Mechanisms of Actions and Therapeutic Applications.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Proanthocyanidins in immune-mediated inflammatory diseases: molecular mechanisms and therapeutic potential.Frontiers in pharmacology · 2026Review
- Multifaceted regulation of thymic tolerance by pattern recognition cascades.Frontiers in immunology · 2026Review
- Effects of laser regulation on anti-inflammatory and osteogenic differentiation of periodontal ligament stem cells though NF-κB signaling pathway.BMC oral health · 2025Article
- Onboard, tethered IL-12 boosts potency of the Tmod NOT gate and preserves selectivity.Journal for immunotherapy of cancer · 2025Article
- The NF-κB signaling network in the life of T cells.Frontiers in immunology · 2025Review
- Molecular Mechanisms Linking Omega-3 Fatty Acids and the Gut-Brain Axis.Molecules (Basel, Switzerland) · 2024Review
- Single-cell stimulus-response gene expression trajectories reveal the stimulus specificities of dynamic responses by single macrophages.Molecular cell · 2024Article
- Biophysical characterization of RelA-p52 NF-κB dimer-A link between the canonical and the non-canonical NF-κB pathway.Protein science : a publication of the Protein Society · 2024Article
- Genetic overlap between Alzheimer's disease and immune-mediated diseases: an atlas of shared genetic determinants and biological convergence.Molecular psychiatry · 2024Article
- DDX5 inhibits inflammation by modulating m6A levels of TLR2/4 transcripts during bacterial infection.EMBO reports · 2024Article
- Detecting and dissecting signaling crosstalk via the multilayer network integration of signaling and regulatory interactions.Nucleic acids research · 2024Article
- Anti-inflammatory and protective effects ofFrontiers in pharmacology · 2024Article
- Genetic overlap between Alzheimer's disease and immune-mediated diseases: An atlas of shared genetic determinants and biological convergence.Research square · 2023Article
- Article
- NFκB signaling in T cell memory.Frontiers in immunology · 2023Review
- Anterior Cruciate Ligament Reconstruction Surgery: Creating a Permissive Healing Phenotype in Military Personnel and Civilians for Faster Recovery.Military medicine · 2022Article
- Anti-Colitic Effect of an Exopolysaccharide Fraction fromPolymers · 2022Article
- Allostery, and how to define and measure signal transduction.Biophysical chemistry · 2022Review
- DAMPs/PAMPs induce monocytic TLR activation and tolerance in COVID-19 patients; nucleic acid binding scavengers can counteract such TLR agonists.Biomaterials · 2022Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Precise control of inflammatory gene expression is critical for effective host defense without excessive tissue damage. The principal regulator of inflammatory gene expression is nuclear factor kappa B (NFκB), a transcription factor. Nuclear NFκB activity is controlled by IκB proteins, whose stimulus-responsive degradation and re-synthesis provide for transient or dynamic regulation. The IκB-NFκB signaling module receives input signals from a variety of pathogen sensors, such as toll-like receptors (TLRs). The molecular components and mechanisms of NFκB signaling are well-understood and have been reviewed elsewhere in detail. Here we review the molecular mechanisms that mediate cross-regulation of TLR-IκB-NFκB signal transduction by signaling pathways that do not activate NFκB themselves, such as interferon signaling pathways. We distinguish between potential regulatory crosstalk mechanisms that (i) occur proximal to TLRs and thus may have stimulus-specific effects, (ii) affect the core IκB-NFκB signaling module to modulate NFκB activation in response to several stimuli. We review some well-documented examples of molecular crosstalk mechanisms and indicate other potential mechanisms whose physiological roles require further study.
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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.