ReviewNucleic acids research2019
Genome reading by the NF-κB transcription factors.
Review in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 119 citations in OpenAlex.
- Clinical, Immunological, and Genetic Features in Patients with NFKB1 and NFKB2 Mutations: a Systematic Review.Journal of clinical immunology · 2024Pooled it
- Nuclear factor κB signalling in breast cancer: mechanisms, crosstalk and therapeutic targeting.Molecular biology reports · 2026Review
- Synergistic targeting of NF-κB by cinnamic and p-coumaric acids: computational and DPPH radical scavenging assessment.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Epigenetic Landscape of H3K27ac, H3K27me3, H3K4me1, and H3K4me3 Marks in Channel Catfish Following Βeta Glucan Exposure.International journal of molecular sciences · 2026Article
- Role Shift of Glial Cells from Physiology to Pathology in Alzheimer's Disease: The Regulatory Impact of Exercise.Neuroscience bulletin · 2026Review
- SARS-CoV-2 Nsp1 suppresses the canonical NF-κB pathway by promoting ubiquitin-dependent degradation of TAK1 kinase.PLoS pathogens · 2026Article
- Article
- Orientia tsutsugamushi targets lamin A using Ank effectors and alters chromatin to inhibit NF-κB.Communications biology · 2026Article
- NEMO/IKKγ: Emerging player in the NF-κB pathway and potential therapeutic target in inflammation.Inflammation · 2026Review
- Regulatory roles of microRNAs in signaling pathways and their biomarker potential in prostate cancer.Cancer cell international · 2026Review
- Small heterodimer partner protects against osteoarthritis by inhibiting IKKβ/NF-κB-mediated matrix-degrading enzymes in chondrocytes.Nature communications · 2026Article
- A multi-grained symmetric differential equation model for learning protein-ligand binding dynamics.Nature communications · 2025Article
- Cytokine-independent induction of LGP2/DHX58 in viral infection.The Journal of general virology · 2025Article
- Teamwork of clustered low-affinity κB sites and accessory factors regulates transcriptional strength of NF-κB RelA dimers.Nucleic acids research · 2025Article
- Relationship of S100 Proteins with Neuroinflammation.Biomolecules · 2025Review
- Experimental Models and Their Applicability in Inflammation Studies: Rodents, Fish, and Nematodes.International journal of molecular sciences · 2025Review
- An evolutionarily conserved constellation of functional cis-elements programs the virus-responsive fate of the human (epi)genome.Nucleic acids research · 2025Article
- The NF-κB signaling network in the life of T cells.Frontiers in immunology · 2025Review
- Multi-omics analysis reveals Jianpi formula-derived bioactive peptide-YG-22 potentially inhibited colorectal cancer via regulating epigenetic reprogram and signal pathway regulation.Frontiers in genetics · 2025Article
- Epigenetic regulation of transcription factors involved in NLRP3 inflammasome and NF-kB signaling pathways.Frontiers in immunology · 2025Review
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
The NF-κB family of dimeric transcription factors regulates transcription by selectively binding to DNA response elements present within promoters or enhancers of target genes. The DNA response elements, collectively known as κB sites or κB DNA, share the consensus 5'-GGGRNNNYCC-3' (where R, Y and N are purine, pyrimidine and any nucleotide base, respectively). In addition, several DNA sequences that deviate significantly from the consensus have been shown to accommodate binding by NF-κB dimers. X-ray crystal structures of NF-κB in complex with diverse κB DNA have helped elucidate the chemical principles that underlie target selection in vitro. However, NF-κB dimers encounter additional impediments to selective DNA binding in vivo. Work carried out during the past decades has identified some of the barriers to sequence selective DNA target binding within the context of chromatin and suggests possible mechanisms by which NF-κB might overcome these obstacles. In this review, we first highlight structural features of NF-κB:DNA complexes and how distinctive features of NF-κB proteins and DNA sequences contribute to specific complex formation. We then discuss how native NF-κB dimers identify DNA binding targets in the nucleus with support from additional factors and how post-translational modifications enable NF-κB to selectively bind κB sites in vivo.
Indexed as
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What OpenQuestion holds
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.