Evidence map›Paper›PMID 29263365›Full record

ArticleNature communications2017

Brd4 binds to active enhancers to control cell identity gene induction in adipogenesis and myogenesis.

Ji-Eun Lee, Young-Kwon Park, Sarah Park, Younghoon Jang, Nicholas Waring, Anup Dey, Keiko Ozato, Binbin Lai, Weiqun Peng, Kai Ge

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 142 papers.

0numbers the graph read from it
0cells of the map it votes in
142citing papers in PubMed
7.8field-weighted citation impact, top 2% 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

142 citing papers in PubMed, 200 citations in OpenAlex.

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  14. Many faces of mammalian NSD methyltransferases.Cellular & molecular biology letters · 2026
    Review
  15. Article
  16. Article
  17. Article
  18. Inhibition of triglyceride metabolism-associated enhancers alters lipid deposition during adipocyte differentiation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  19. Review
  20. Epigenetics-targeted drugs: current paradigms and future challenges.Signal transduction and targeted therapy · 2024
    Review

82 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

10 authors at 2 institutions in 1 country.

Ji-Eun LeeAdipocyte Biology and Gene Regulation Section, Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.ORCID http://orcid.org/0000-0002-3768-7016
Young-Kwon ParkAdipocyte Biology and Gene Regulation Section, Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.
Sarah ParkAdipocyte Biology and Gene Regulation Section, Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.
Younghoon JangAdipocyte Biology and Gene Regulation Section, Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.
Nicholas WaringAdipocyte Biology and Gene Regulation Section, Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.
Anup DeyProgram in Genomics of Differentiation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, 20892, USA.
Keiko OzatoProgram in Genomics of Differentiation, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, 20892, USA.
Binbin LaiAdipocyte Biology and Gene Regulation Section, Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.
Weiqun PengDepartments of Physics and Anatomy and Regenerative Biology, The George Washington University, Washington, DC, 20052, USA.
Kai GeAdipocyte Biology and Gene Regulation Section, Laboratory of Endocrinology and Receptor Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA. kai.ge@nih.gov.ORCID http://orcid.org/0000-0002-7442-5138
National Institutes of Health · USGeorge Washington University · US

Funding

Regulation of PPARgamma Expression and Adipogenesis by PTIP-Associated FactorsZIADK075003 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI GE, KAI · 2009 to 2025
$17.6M
Genomics Core FacilityZICDK071001 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI HANOVER, JOHN A. · 2009 to 2023
$16.6M
Chromatin and epigenetic memory ZIAHD008815 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI OZATO, KEIKO · 2009 to 2025
$16.2M
Epigenomic Regulation of PPARgamma and AdipogenesisZIADK075017 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI GE, KAI · 2009 to 2025
$12.4M
6 · The paper itself

Abstract

The epigenomic reader Brd4 is an important drug target for cancers. However, its role in cell differentiation and animal development remains largely unclear. Using two conditional knockout mouse strains and derived cells, we demonstrate that Brd4 controls cell identity gene induction and is essential for adipogenesis and myogenesis. Brd4 co-localizes with lineage-determining transcription factors (LDTFs) on active enhancers during differentiation. LDTFs coordinate with H3K4 mono-methyltransferases MLL3/MLL4 (KMT2C/KMT2D) and H3K27 acetyltransferases CBP/p300 to recruit Brd4 to enhancers activated during differentiation. Brd4 deletion prevents the enrichment of Mediator and RNA polymerase II transcription machinery, but not that of LDTFs, MLL3/MLL4-mediated H3K4me1, and CBP/p300-mediated H3K27ac, on enhancers. Consequently, Brd4 deletion prevents enhancer RNA production, cell identity gene induction and cell differentiation. Interestingly, Brd4 is dispensable for maintaining cell identity genes in differentiated cells. These findings identify Brd4 as an enhancer epigenomic reader that links active enhancers with cell identity gene induction in differentiation.

Indexed as

AdipogenesisAnimalsBromodomain Containing ProteinsCell DifferentiationCell LineageDNA-Binding ProteinsEnhancer Elements, GeneticEpigenesis, GeneticGene Expression RegulationHistone CodeHistone-Lysine N-MethyltransferaseMiceMice, KnockoutMuscle DevelopmentNuclear Proteinsp300-CBP Transcription FactorsBrd4 protein, mouseBromodomain Containing ProteinsDNA-Binding ProteinsHistone-Lysine N-MethyltransferaseKmt2c protein, mouseMLL4 protein, mouseNuclear Proteinsp300-CBP Transcription FactorsRNA Polymerase IITranscription Factors

Identifiers

PMID29263365
PMCPMC5738375
OpenAlexW2775398039

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.