Evidence map›Paper›PMID 25051172›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2014

Transient estrogen receptor binding and p300 redistribution support a squelching mechanism for estradiol-repressed genes.

Michael J Guertin, Xuesen Zhang, Scott A Coonrod, Gordon L Hager

Open access · hybridAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed, 1 pooled it
3.3field-weighted citation impact, top 7% 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

54 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

  1. Pooled it
  2. Review
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  7. Article
  8. p300 KAT regulates SOX10 stability and function in human melanoma.bioRxiv : the preprint server for biology · 2024
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  16. Integrative analysis reveals multiple modes of LXR transcriptional regulation in liver.Proceedings of the National Academy of Sciences of the United States of America · 2022
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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

4 authors at 3 institutions in 2 countries.

Michael J GuertinLaboratory of Receptor Biology and Gene Expression (M.J.G., G.L.H.), National Cancer Institute, Bethesda, Maryland 20892; State Key Laboratory of Reproductive Medicine (X.Z.), Nanjing Medical University, Nanjing 210029, China; and Baker Institute for Animal Health (X.Z., S.A.C.), College of Veterinary Medicine, Cornell University, Ithaca, New York 14853.
Xuesen Zhang
Scott A Coonrod
Gordon L Hager
National Cancer Institute · USCornell University · USNanjing Medical University · CN

Funding

Function of Steroid Receptors in Subcellular CompartmentsZIABC010027 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI HAGER, GORDON L · 2009 to 2025
$8.7M
Intramural NIH HHS
6 · The paper itself

Abstract

Proper gene regulation is essential for proper organismal development and appropriate responses to external stimuli. Specialized factors, termed master regulators, are often responsible for orchestrating the molecular events that result from signaling cascades. Master regulators coordinate the activation and repression of specific gene classes. Estrogen receptor α (ER) precipitates the signaling cascade that results from endogenous or exogenous estrogen hormones. ER is a classic transcriptional activator and the mechanisms by which ER coordinates gene activation are well characterized. However, it remains unclear how ER coordinates the immediate repression of genes. We integrated genomic transcription, chromosome looping, transcription factor binding, and chromatin structure data to analyze the molecular cascade that results from estradiol (E2)-induced signaling in human MCF-7 breast cancer cells and addressed the context-specific nature of gene regulation. We defined a class of genes that are immediately repressed upon estrogen stimulation, and we compared and contrasted the molecular characteristics of these repressed genes vs activated and unregulated genes. The most striking and unique feature of the repressed gene class is transient binding of ER at early time points after estrogen stimulation. We also found that p300, a coactivator and acetyltransferase, quantitatively redistributes from non-ER enhancers to ER enhancers after E2 treatment. These data support an extension of the classic physiological squelching model, whereby ER hijacks coactivators from repressed genes and redistributes the coactivators to ER enhancers that activate transcription.

Indexed as

Binding SitesBreast NeoplasmsE1A-Associated p300 ProteinEnhancer Elements, GeneticEstradiolEstrogen Receptor alphaEstrogensFemaleGene Expression Regulation, NeoplasticGenomeHumansLigandsMCF-7 CellsProtein BindingResponse ElementsSequence Analysis, DNAE1A-Associated p300 ProteinEP300 protein, humanESR1 protein, humanEstradiolEstrogen Receptor alphaEstrogensLigands

Identifiers

PMID25051172
PMCPMC4154243
OpenAlexW2010136675

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.