Evidence map›Paper›PMID 31167905›Full record

ArticleJournal of virology2019

TAF Family Proteins and MEF2C Are Essential for Epstein-Barr Virus Super-Enhancer Activity.

Chong Wang, Sizun Jiang, Luyao Zhang, Difei Li, Jun Liang, Yohei Narita, Isabella Hou, Qian Zhong, Benjamin E Gewurz, Mingxiang Teng and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of virology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

15 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Chromatin Control of EBV Infection and Latency.Current topics in microbiology and immunology · 2025
    Article
  4. Viral oncogenesis in cancer: from mechanisms to therapeutics.Signal transduction and targeted therapy · 2025
    Review
  5. Review
  6. Review
  7. Review
  8. IPiScience · 2022
    Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. CRISPR screen in cancer: status quo and future perspectives.American journal of cancer research · 2021
    Review
  14. Article
  15. 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

11 authors at 2 institutions in 1 country.

Chong WangDivision of Infectious Disease, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Sizun JiangDivision of Infectious Disease, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Luyao ZhangDivision of Infectious Disease, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Difei LiDivision of Infectious Disease, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Jun LiangDivision of Infectious Disease, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Yohei NaritaDivision of Infectious Disease, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.ORCID 0000-0002-8867-3669
Isabella HouDivision of Infectious Disease, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Qian ZhongDivision of Infectious Disease, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Benjamin E GewurzDivision of Infectious Disease, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Mingxiang TengDepartment of Biostatistics & Bioinformatics, H. Lee Moffitt Cancer Center & Research Institute, Tampa, Florida, USA Mingxiang.teng@moffitt.org bzhao@bwh.harvard.edu.ORCID 0000-0002-8536-8941
Bo ZhaoDivision of Infectious Disease, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA Mingxiang.teng@moffitt.org bzhao@bwh.harvard.edu.
Brigham and Women's Hospital · USMoffitt Cancer Center · US

Funding

TRANSLATIONAL RESEARCHP30CA076292 · NCI · UNIVERSITY OF SOUTH FLORIDA · PI KENNETH Lynn WRIGHT · 1998 to 2026
$93.5M
Epstein-Barr Virus Nuclear Proteins in B Cell Growth TransformationR01CA047006 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI ZHAO, BO · 2002 to 2021
$12.1M
Targeting Epstein-Barr Virus super-enhancersR01AI123420 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI Bo Zhao · 2016 to 2026
$5.1M
Metabolic Network Remodeling in Epstein-Barr Virus LymphomagenesisR01AI137337 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI GEWURZ, BENJAMIN ELISON · 2018 to 2022
$2.2M
MOLECULAR BIOLOGY OF EPSTEIN-BARR VIRUS INFECTIONR35CA047006 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI KIEFF, ELLIOTT D · 1987 to 2000
$1.6M
NCI NIH HHS P30 CA076292NCI NIH HHS R01 CA047006NCI NIH HHS R35 CA047006NIAID NIH HHS R01 AI123420NIAID NIH HHS R01 AI137337
6 · The paper itself

Abstract

Super-enhancers (SEs) are clusters of enhancers marked by extraordinarily high and broad chromatin immunoprecipitation followed by deep sequencing (ChIP-seq) signals for H3K27ac or other transcription factors (TFs). SEs play pivotal roles in development and oncogenesis. Epstein-Barr virus (EBV) super-enhancers (ESEs) are co-occupied by all essential EBV oncogenes and EBV-activated NF-κB subunits. Perturbation of ESEs stops lymphoblastoid cell line (LCL) growth. To further characterize ESEs and identify proteins critical for ESE function, MYC ESEs were cloned upstream of a green fluorescent protein (GFP) reporter. Reporters driven by MYC ESEs 525 kb and 428 kb upstream of MYC (525ESE and 428ESE) had very high activities in LCLs but not in EBV-negative BJAB cells. EBNA2 activated MYC ESE-driven luciferase reporters. CRISPRi targeting 525ESE significantly decreased MYC expression. Genome-wide CRISPR screens identified factors essential for ESE activity. TBP-associated factor (TAF) family proteins, including TAF8, TAF11, and TAF3, were essential for the activity of the integrated 525ESE-driven reporter in LCLs. TAF8 and TAF11 knockout significantly decreased 525ESE activity and MYC transcription. MEF2C was also identified to be essential for 525ESE activity. Depletion of MEF2C decreased 525ESE reporter activity, MYC expression, and LCL growth. MEF2C cDNA resistant to CRIPSR cutting rescued MEF2C knockout and restored 525ESE reporter activity and MYC expression. MEF2C depletion decreased IRF4, EBNA2, and SPI1 binding to 525ESE in LCLs. MEF2C depletion also affected the expression of other ESE target genes, including the ETS1 and BCL2 genes. These data indicated that in addition to EBNA2, TAF family members and MEF2C are essential for ESE activity, MYC expression, and LCL growth.

Indexed as

Gene Expression Regulation, ViralCell Line, TumorCell SurvivalCRISPR-Cas SystemsEnhancer Elements, GeneticEpstein-Barr Virus InfectionsGene EditingGene ExpressionGene Knockout TechniquesGenes, mycHerpesvirus 4, HumanHistonesHost-Pathogen InteractionsHumansMEF2 Transcription FactorsTATA-Binding Protein Associated FactorsHistonesMEF2C protein, humanMEF2 Transcription FactorsTATA-Binding Protein Associated FactorsCRISPREBVMEF2CMYCsuper-enhancertranscription factors

Identifiers

PMID31167905
PMCPMC6675876
OpenAlexW2948418818

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.