ArticleGenome research2019
Nascent transcript analysis of glucocorticoid crosstalk with TNF defines primary and cooperative inflammatory repression.
Article in Genome research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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.
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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
32 citing papers in PubMed, 47 citations in OpenAlex.
- Balancing inflammation under stress: glucocorticoid regulation of innate immune pathways.Bioscience reports · 2026Review
- Clocks on steroids: how glucocorticoid receptors tell cells the time.The Journal of endocrinology · 2026Review
- Improving calls of differentially transcribed enhancers and their upstream regulators.Bioinformatics advances · 2026Article
- Article
- Differential RELA and GR recruitment to the BIRC3/BIRC2 locus: Molecular insight as to combinatorial regulation by proinflammatory cytokines and glucocorticoid.Molecular pharmacology · 2025Article
- TF Profiler: a transcription factor inference method that broadly measures transcription factor activity and identifies mechanistically distinct networks.Genome biology · 2025Article
- Enhancer RNA transcription pinpoints functional genetic variants linked to asthma.Nature communications · 2025Article
- The Bidirectional Interaction Between NF-Journal of immunology research · 2025Review
- The temporal dynamics of lncRNA Firre-mediated epigenetic and transcriptional regulation.Nature communications · 2024Article
- Multi-tissue transcriptomic and serum metabolomic assessment reveals systemic implications of acute ozone-induced stress response in male Wistar Kyoto rats.Metabolomics : Official journal of the Metabolomic Society · 2023Article
- Differential regulation of BIRC2 and BIRC3 expression by inflammatory cytokines and glucocorticoids in pulmonary epithelial cells.PloS one · 2023Article
- Dark DNA and stress (Review).International journal of molecular medicine · 2023Article
- Induction of natural IgE by glucocorticoids.The Journal of experimental medicine · 2022Article
- Integrated genomics approaches identify transcriptional mediators and epigenetic responses to Afghan desert particulate matter in small airway epithelial cells.Physiological genomics · 2022Article
- Glucocorticoid receptor modulates myeloid-derived suppressor cell function via mitochondrial metabolism in immune thrombocytopenia.Cellular & molecular immunology · 2022Article
- Th1 cytokines synergize to change gene expression and promote corticosteroid insensitivity in pediatric airway smooth muscle.Respiratory research · 2022Article
- Protocol variations in run-on transcription dataset preparation produce detectable signatures in sequencing libraries.BMC genomics · 2022Article
- Monocytes and Macrophages in Spondyloarthritis: Functional Roles and Effects of Current Therapies.Cells · 2022Review
- Article
- Stress sensing within the breast tumor microenvironment: how glucocorticoid receptors live in the moment.Essays in biochemistry · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
The glucocorticoid receptor (NR3C1, also known as GR) binds to specific DNA sequences and directly induces transcription of anti-inflammatory genes that contribute to cytokine repression, frequently in cooperation with NF-kB. Whether inflammatory repression also occurs through local interactions between GR and inflammatory gene regulatory elements has been controversial. Here, using global run-on sequencing (GRO-seq) in human airway epithelial cells, we show that glucocorticoid signaling represses transcription within 10 min. Many repressed regulatory regions reside within "hyper-ChIPable" genomic regions that are subject to dynamic, yet nonspecific, interactions with some antibodies. When this artifact was accounted for, we determined that transcriptional repression does not require local GR occupancy. Instead, widespread transcriptional induction through canonical GR binding sites is associated with reciprocal repression of distal TNF-regulated enhancers through a chromatin-dependent process, as evidenced by chromatin accessibility and motif displacement analysis. Simultaneously, transcriptional induction of key anti-inflammatory effectors is decoupled from primary repression through cooperation between GR and NF-kB at a subset of regulatory regions. Thus, glucocorticoids exert bimodal restraints on inflammation characterized by rapid primary transcriptional repression without local GR occupancy and secondary anti-inflammatory effects resulting from transcriptional cooperation between GR and NF-kB.
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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.