Evidence map›Paper›PMID 28475868›Full record

ArticleMolecular cell2017

Glucocorticoid Receptor:MegaTrans Switching Mediates the Repression of an ERα-Regulated Transcriptional Program.

Feng Yang, Qi Ma, Zhijie Liu, Wenbo Li, Yuliang Tan, Chunyu Jin, Wubin Ma, Yiren Hu, Jia Shen, Kenneth A Ohgi and 3 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
5.3field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 68 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Epigenetic Modulation of Estrogen Receptor Signaling in Ovarian Cancer.International journal of molecular sciences · 2024
    Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. HDAC-driven mechanisms in anticancer resistance: epigenetics and beyond.Cancer drug resistance (Alhambra, Calif.) · 2024
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

13 authors at 3 institutions in 2 countries.

Feng YangHoward Hughes Medical Institute, Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Qi MaHoward Hughes Medical Institute, Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Zhijie LiuDepartment of Molecular Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA.
Wenbo LiDepartment of Biochemistry and Molecular Biology, University of Texas McGovern Medical School, Houston, TX 77030, USA.
Yuliang TanHoward Hughes Medical Institute, Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Chunyu JinHoward Hughes Medical Institute, Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Wubin MaHoward Hughes Medical Institute, Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Yiren HuHoward Hughes Medical Institute, Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA; Biological Sciences Graduate Program, University of California, San Diego, La Jolla, CA 92093, USA.
Jia ShenHoward Hughes Medical Institute, Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Kenneth A OhgiHoward Hughes Medical Institute, Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Francesca TeleseHoward Hughes Medical Institute, Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
Wen LiuSchool of Pharmaceutical Sciences, Fujian Provincial Key Laboratory of Innovative Drug Target Research, Xiamen University, Xiamen, Fujian 361102, China.
Michael G RosenfeldHoward Hughes Medical Institute, Department of Medicine, School of Medicine, University of California, San Diego, La Jolla, CA 92093, USA. Electronic address: mrosenfeld@ucsd.edu.
Howard Hughes Medical Institute · USThe University of Texas Health Science Center at San Antonio · USXiamen University · CN

Funding

HORMONAL AND DEVELOPMENTAL REGULATION OF GENE EXPRESSIONR01DK018477 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ROSENFELD, MICHAEL G · 1986 to 2025
$12.7M
REGULATION OF NEUROENDOCRINE SWITCHING EVENTSR37DK039949 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ROSENFELD, MICHAEL G · 1987 to 2020
$12.3M
Ligand Regulated Epigenetic/Nuclear Architectural Strategies and Human DiseaseR01NS034934 · NINDS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ROSENFELD, MICHAEL G · 1995 to 2013
$6.8M
Enhancer TherapyR01CA173903 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GLASS, CHRISTOPHER K · 2012 to 2016
$6.3M
MOLECULAR MECHANISMS OF AORTIC AND PULMONARY DEFECTSR01HL065445 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ROSENFELD, MICHAEL G · 2000 to 2014
$5.3M
REGULATION OF NEUROENDOCRINE SWITCHING EVENTSR01DK039949 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ROSENFELD, MICHAEL G · 1996 to 2024
$2.4M
Repressive Transcriptional Programs in Breast CancerR01CA213371 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ROSENFELD, MICHAEL G · 2017 to 2021
$755k
Howard Hughes Medical InstituteNCI NIH HHS R01 CA173903NCI NIH HHS R01 CA213371NHLBI NIH HHS R01 HL065445NIDDK NIH HHS R01 DK018477NIDDK NIH HHS R01 DK039949NIDDK NIH HHS R37 DK039949NINDS NIH HHS R01 NS034934
6 · The paper itself

Abstract

The molecular mechanisms underlying the opposing functions of glucocorticoid receptors (GRs) and estrogen receptor α (ERα) in breast cancer development remain poorly understood. Here we report that, in breast cancer cells, liganded GR represses a large ERα-activated transcriptional program by binding, in trans, to ERα-occupied enhancers. This abolishes effective activation of these enhancers and their cognate target genes, and it leads to the inhibition of ERα-dependent binding of components of the MegaTrans complex. Consistent with the effects of SUMOylation on other classes of nuclear receptors, dexamethasone (Dex)-induced trans-repression of the estrogen E

Indexed as

Gene Expression Regulation, NeoplasticReceptor Cross-TalkTranscription, GeneticBinding SitesBreast NeoplasmsDexamethasoneDown-RegulationEnhancer Elements, GeneticEstradiolEstrogen Receptor alphaFemaleHEK293 CellsHistone Deacetylase 3Histone DeacetylasesHumansMCF-7 CellsDexamethasoneESR1 protein, humanEstradiolEstrogen Receptor alphaHistone Deacetylase 3Histone DeacetylasesMultiprotein ComplexesNCOR1 protein, humanNCOR2 protein, humanNuclear Receptor Co-Repressor 1Nuclear Receptor Co-Repressor 2Receptors, Glucocorticoidenhancersnuclear receptorstranscriptional regulationtransrepression

Identifiers

PMID28475868
PMCPMC5510478
OpenAlexW2611886390

What OpenQuestion holds

Textmetadata
LicenceTDM
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.