Evidence map›Paper›PMID 29241532›Full record

ArticleCell reports2017

Glucocorticoid Receptor Binding Induces Rapid and Prolonged Large-Scale Chromatin Decompaction at Multiple Target Loci.

Alasdair W Jubb, Shelagh Boyle, David A Hume, Wendy A Bickmore

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.2field-weighted citation impact, top 12% of its field
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

33 citing papers in PubMed, 49 citations in OpenAlex.

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  15. Article
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  18. Transcriptional enhancers and their communication with gene promoters.Cellular and molecular life sciences : CMLS · 2021
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 2 countries.

Alasdair W JubbMRC Human Genetics Unit, Institute of Genetics and Molecular Medicine, The University of Edinburgh, Crewe Road, Edinburgh EH4 2XU, UK; The Roslin Institute and Royal (Dick) School of Veterinary Studies, The University of Edinburgh, Easter Bush, Midlothian EH25 9RG, UK; Department of Medicine, University of Cambridge, Box 93, Addenbrookes Hospital, Hills Road, Cambridge CB2 2QQ, UK.
Shelagh BoyleMRC Human Genetics Unit, Institute of Genetics and Molecular Medicine, The University of Edinburgh, Crewe Road, Edinburgh EH4 2XU, UK.
David A HumeThe Roslin Institute and Royal (Dick) School of Veterinary Studies, The University of Edinburgh, Easter Bush, Midlothian EH25 9RG, UK; Mater Research-University of Queensland, Translational Research Institute, 37 Kent Street, Woolloongabba, QLD 4102, Australia. Electronic address: david.hume@roslin.ed.ac.uk.
Wendy A BickmoreMRC Human Genetics Unit, Institute of Genetics and Molecular Medicine, The University of Edinburgh, Crewe Road, Edinburgh EH4 2XU, UK. Electronic address: wendy.bickmore@igmm.ed.ac.uk.
University of Edinburgh · GBMater Research · AUUniversity of Cambridge · GB

Funding

Medical Research Council MC_PC_U127527202Wellcome Trust
6 · The paper itself

Abstract

Glucocorticoids act by binding to the glucocorticoid receptor (GR), which binds to specific motifs within enhancers of target genes to activate transcription. Previous studies have suggested that GRs can promote interactions between gene promoters and distal elements within target loci. In contrast, we demonstrate here that glucocorticoid addition to mouse bone-marrow-derived macrophages produces very rapid chromatin unfolding detectable by fluorescence in situ hybridization (FISH) at loci associated with GR binding. Rapid chromatin decompaction was generally not dependent on transcription at those loci that are known to be inducible in both mouse and human macrophages and was sustained for up to 5 days following ligand removal. Chromatin decompaction was not dependent upon persistent GR binding, which decayed fully after 24 hr. We suggest that sustained large-scale chromatin reorganization forms an important part of the response to glucocorticoid and might contribute to glucocorticoid sensitivity and resistance.

Indexed as

AnimalsBinding SitesChromatinChromatin Assembly and DisassemblyDexamethasoneDNA-Binding ProteinsGene Expression RegulationHumansIn Situ Hybridization, FluorescenceKineticsKruppel-Like Factor 4Kruppel-Like Transcription FactorsMacrophagesMaleMiceMice, Inbred C57BLChromatinDexamethasoneDNA-Binding ProteinsHIVEP2 protein, humanKruppel-Like Factor 4Kruppel-Like Transcription FactorsNCOA5 protein, humanNuclear Receptor CoactivatorsProto-Oncogene Proteins c-fosReceptors, GlucocorticoidTranscription Factorschromatin remodelingenhancerfluorescence in situ hybridizationglucocorticoid receptormacrophage

Identifiers

PMID29241532
PMCPMC5745231
OpenAlexW2772149037

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.