Evidence map›Paper›PMID 29126175›Full record

ArticleNucleic acids research2018

Conventional and pioneer modes of glucocorticoid receptor interaction with enhancer chromatin in vivo.

Thomas A Johnson, Razvan V Chereji, Diana A Stavreva, Stephanie A Morris, Gordon L Hager, David J Clark

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% 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

62 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

  1. Pooled it
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  13. The glucocorticoid receptor potentiates aldosterone-induced transcription by the mineralocorticoid receptor.Proceedings of the National Academy of Sciences of the United States of America · 2024
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2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Thomas A JohnsonLaboratory of Receptor Biology and Gene Expression, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
Razvan V CherejiDivision of Developmental Biology, Eunice Kennedy Shriver National Institute for Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.
Diana A StavrevaLaboratory of Receptor Biology and Gene Expression, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
Stephanie A MorrisOffice of Cancer Nanotechnology Research, Center for Strategic Scientific Initiatives, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
Gordon L HagerLaboratory of Receptor Biology and Gene Expression, National Cancer Institute, NIH, Bethesda, MD 20892, USA.
David J ClarkDivision of Developmental Biology, Eunice Kennedy Shriver National Institute for Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892, USA.
National Cancer Institute · USNational Institutes of Health · US

Funding

Chromatin Structure and Gene ExpressionZIABC005450 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HAGER, GORDON L · 2009 to 2025
$35.2M
Chromatin Remodeling and Gene ActivationZIAHD008775 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI CLARK, DAVID J · 2009 to 2025
$20.1M
Chromatin Remodeling ProteinsZIABC010646 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HAGER, GORDON L · 2009 to 2021
$4.0M
6 · The paper itself

Abstract

Glucocorticoid hormone plays a major role in metabolism and disease. The hormone-bound glucocorticoid receptor (GR) binds to a specific set of enhancers in different cell types, resulting in unique patterns of gene expression. We have addressed the role of chromatin structure in GR binding by mapping nucleosome positions in mouse adenocarcinoma cells. Before hormone treatment, GR-enhancers exist in one of three chromatin states: (i) Nucleosome-depleted enhancers that are DNase I-hypersensitive, associated with the Brg1 chromatin remodeler and flanked by nucleosomes incorporating histone H2A.Z. (ii) Nucleosomal enhancers that are DNase I-hypersensitive, marked by H2A.Z and associated with Brg1. (iii) Nucleosomal enhancers that are inaccessible to DNase I, incorporate little or no H2A.Z and lack Brg1. Hormone-induced GR binding results in nucleosome shifts at all types of GR-enhancer, coinciding with increased recruitment of Brg1. We propose that nucleosome-depleted GR-enhancers are formed and maintained by other transcription factors which recruit Brg1 whereas, at nucleosomal enhancers, GR behaves like a pioneer factor, interacting with nucleosomal sites and recruiting Brg1 to remodel the chromatin.

Indexed as

Enhancer Elements, GeneticAnimalsCell LineCell Line, TumorChromatinChromatin Assembly and DisassemblyDexamethasoneDNA HelicasesGlucocorticoidsHistonesMiceNuclear ProteinsNucleosomesProtein BindingReceptors, GlucocorticoidTranscriptional ActivationChromatinDexamethasoneDNA HelicasesGlucocorticoidsH2az1 protein, mouseHistonesNuclear ProteinsNucleosomesReceptors, GlucocorticoidSmarca4 protein, mouseTranscription Factors

Identifiers

PMID29126175
PMCPMC5758879
OpenAlexW2767948671

What OpenQuestion holds

Textmetadata
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.