Evidence map›Paper›PMID 32479598›Full record

ArticleNucleic acids research2020

Regulatory sharing between estrogen receptor α bound enhancers.

Julia B Carleton, Matthew Ginley-Hidinger, Kristofer C Berrett, Ryan M Layer, Aaron R Quinlan, Jason Gertz

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

11 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Serine starvation silences estrogen receptor signaling through histone hypoacetylation.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  8. The power of the (imperfect) palindrome: Sequence-specific roles of palindromic motifs in gene regulation.BioEssays : news and reviews in molecular, cellular and developmental biology · 2022
    Review
  9. Review
  10. Article
  11. Article
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.

Julia B CarletonHuntsman Cancer Institute, University of Utah, Salt Lake City, UT, USA.
Matthew Ginley-HidingerHuntsman Cancer Institute, University of Utah, Salt Lake City, UT, USA.
Kristofer C BerrettHuntsman Cancer Institute, University of Utah, Salt Lake City, UT, USA.
Ryan M LayerBioFrontiers Institute, University of Colorado, Boulder, CO, USA.
Aaron R QuinlanDepartments of Human Genetics and Biomedical Informatics, University of Utah, Salt Lake City, UT, USA.
Jason GertzHuntsman Cancer Institute, University of Utah, Salt Lake City, UT, USA.
University of Utah · USUniversity of Colorado Boulder · US

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Jared P Rutter · 1986 to 2026
$72.6M
Utah Center for Clinical and Translational ScienceUL1TR002538 · NCATS · UNIVERSITY OF UTAH · PI HESS, RACHEL, MAJERSIK, JENNIFER JUHL · 2018 to 2022
$26.0M
TRAINING PROGRAM IN GENETICST32GM007464 · NIGMS · UNIVERSITY OF UTAH · PI GRUNWALD, DAVID J., STANFIELD, GILLIAN · 1985 to 2020
$6.1M
In situ evaluation of combinatorial gene regulation in the human genomeR01HG008974 · NHGRI · UNIVERSITY OF UTAH · PI GERTZ, JASON · 2017 to 2021
$3.2M
NCATS NIH HHS UL1 TR002538NCI NIH HHS P30 CA042014NHGRI NIH HHS R01 HG008974NIGMS NIH HHS T32 GM007464
6 · The paper itself

Abstract

The human genome encodes an order of magnitude more gene expression enhancers than promoters, suggesting that most genes are regulated by the combined action of multiple enhancers. We have previously shown that neighboring estrogen-responsive enhancers exhibit complex synergistic contributions to the production of an estrogenic transcriptional response. Here we sought to determine the molecular underpinnings of this enhancer cooperativity. We generated genetic deletions of four estrogen receptor α (ER) bound enhancers that regulate two genes and found that enhancers containing full estrogen response element (ERE) motifs control ER binding at neighboring sites, while enhancers with pre-existing histone acetylation/accessibility confer a permissible chromatin environment to the neighboring enhancers. Genome engineering revealed that two enhancers with half EREs could not compensate for the lack of a full ERE site within the cluster. In contrast, two enhancers with full EREs produced a transcriptional response greater than the wild-type locus. By swapping genomic sequences, we found that the genomic location of a full ERE strongly influences enhancer activity. Our results lead to a model in which a full ERE is required for ER recruitment, but the presence of a pre-existing permissible chromatin environment can also be needed for estrogen-driven gene regulation to occur.

Indexed as

Transcription, GeneticAcetylationChromatinDNA-Binding ProteinsEnhancer Elements, GeneticEstrogen Receptor alphaGene Expression RegulationGenome, HumanHumansNucleotide MotifsPromoter Regions, GeneticChromatinDNA-Binding ProteinsESR1 protein, humanEstrogen Receptor alpha

Identifiers

PMID32479598
PMCPMC7337896
OpenAlexW3029837782

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.