ArticleCell2016
Direct GR Binding Sites Potentiate Clusters of TF Binding across the Human Genome.
Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 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
118 citing papers in PubMed, 194 citations in OpenAlex.
- Glucocorticoids elevate clear cell renal cell carcinoma sensitivity to HIF-2α inhibitors by suppressing H4K12 lactylation.Signal transduction and targeted therapy · 2026Article
- Alpha-1 antitrypsin-glucocorticoid receptor axis: a new pathway in immune modulation.Molecular medicine (Cambridge, Mass.) · 2026Article
- Genome-wide dynamic nascent transcript profiles reveal that most paused RNA polymerases terminate.Nucleic acids research · 2026Article
- ChIP happens: from biochemical origins to the modern omics toolbox for understanding steroid hormone receptors.The Biochemical journal · 2026Review
- Molecular Mechanisms of Transcription Factors with Dual Activator and Repressor Functions.Molecular and cellular biology · 2026Review
- Article
- SMARCA2 is an essential and potent cofactor for a specific subset of the glucocorticoid response in A549 cells.bioRxiv : the preprint server for biology · 2025Article
- Applications of high-throughput reporter assays to gene regulation studies.Current opinion in structural biology · 2025Review
- Serum- and glucocorticoid-induced kinase 3 orchestrates glucocorticoid signaling to facilitate chromatin remodeling during murine adipogenesis.The Journal of clinical investigation · 2025Article
- Article
- Comprehensive functional annotation of ESR1-driven enhancers in breast cancer reveals hierarchical activity independent of genomic and epigenomic contexts.Genome research · 2025Article
- The glucocorticoid receptor is affected by its target ZBTB16 in a dissociated manner.The Journal of endocrinology · 2025Article
- Auricular malformations are driven by copy number variations in a hierarchical enhancer cluster and a dominant enhancer recapitulates human pathogenesis.Nature communications · 2025Article
- Variant-to-function approaches for adipose tissue: Insights into cardiometabolic disorders.Cell genomics · 2025Review
- An evolutionarily conserved constellation of functional cis-elements programs the virus-responsive fate of the human (epi)genome.Nucleic acids research · 2025Article
- Inhibiting EZH2 complements steroid effects in Duchenne muscular dystrophy.Science advances · 2025Article
- Unraveling the Genetics of Shared Clinical and Serological Manifestations in Patients With Systemic Inflammatory Autoimmune Diseases.Arthritis & rheumatology (Hoboken, N.J.) · 2025Article
- PU.1 eviction at lymphocyte-specific chromatin domains mediates glucocorticoid response in acute lymphoblastic leukemia.Nature communications · 2024Article
- DNA-binding factor footprints and enhancer RNAs identify functional non-coding genetic variants.Genome biology · 2024Article
- Review
58 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
8 authors at 1 institution in 1 country.
Funding
Abstract
The glucocorticoid receptor (GR) binds the human genome at >10,000 sites but only regulates the expression of hundreds of genes. To determine the functional effect of each site, we measured the glucocorticoid (GC) responsive activity of nearly all GR binding sites (GBSs) captured using chromatin immunoprecipitation (ChIP) in A549 cells. 13% of GBSs assayed had GC-induced activity. The responsive sites were defined by direct GR binding via a GC response element (GRE) and exclusively increased reporter-gene expression. Meanwhile, most GBSs lacked GC-induced reporter activity. The non-responsive sites had epigenetic features of steady-state enhancers and clustered around direct GBSs. Together, our data support a model in which clusters of GBSs observed with ChIP-seq reflect interactions between direct and tethered GBSs over tens of kilobases. We further show that those interactions can synergistically modulate the activity of direct GBSs and may therefore play a major role in driving gene activation in response to GCs.
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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.