Evidence map›Paper›PMID 21173222›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2011

Epstein-Barr virus nuclear antigen 3C regulated genes in lymphoblastoid cell lines.

Bo Zhao, Jessica C Mar, Seiji Maruo, Sungwook Lee, Benjamin E Gewurz, Eric Johannsen, Kristina Holton, Renee Rubio, Kenzo Takada, John Quackenbush and 1 more

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

35 citing papers in PubMed, 48 citations in OpenAlex.

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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

11 authors at 4 institutions in 2 countries.

Bo ZhaoDepartment of Medicine and Microbiology and Molecular Genetics, Channing Laboratory, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.
Jessica C Mar
Seiji Maruo
Sungwook Lee
Benjamin E Gewurz
Eric Johannsen
Kristina Holton
Renee Rubio
Kenzo Takada
John Quackenbush
Elliott Kieff
Harvard University · USBrigham and Women's Hospital · USDana-Farber Cancer Institute · USHokkaido University · JP

Funding

Genomic Analysis of Network Perturbations in Human DiseaseP50HG004233 · NHGRI · DANA-FARBER CANCER INST · PI VIDAL, MARC · 2007 to 2017
$31.6M
Epstein-Barr Virus Nuclear Proteins in B Cell Growth TransformationR01CA047006 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI ZHAO, BO · 2002 to 2021
$12.1M
NCI NIH HHS R01 CA047006NCI NIH HHS R01CA047006NHGRI NIH HHS P50 HG004233
6 · The paper itself

Abstract

EBV nuclear antigen 3C (EBNA3C) is an essential transcription factor for EBV transformed lymphoblast cell line (LCL) growth. To identify EBNA3C-regulated genes in LCLs, microarrays were used to measure RNA abundances in each of three different LCLs that conditionally express EBNA3C fused to a 4-OH-Tamoxifen-dependent estrogen receptor hormone binding domain (EBNA3CHT). At least three RNAs were assayed for each EBNA3CHT LCL under nonpermissive conditions, permissive conditions, and nonpermissive conditions with wild-type EBNA3C transcomplementation. Using a two-way ANOVA model of EBNA3C levels, we identified 550 regulated genes that were at least 1.5-fold up- or down-regulated with false discovery rates < 0.01. EBNA3C-regulated genes overlapped significantly with genes regulated by EBNA2 and EBNA3A consistent with coordinated effects on cell gene transcription. Of the 550 EBNA3C-regulated genes, 106 could be placed in protein networks. A seeded Bayesian network analysis of the 80 most significant EBNA3C-regulated genes suggests that RAC1, LYN, and TNF are upstream of other EBNA3C-regulated genes. Gene set enrichment analysis found enrichment for MAP kinase signaling, cytokine-cytokine receptor interactions, JAK-STAT signaling, and cell adhesion molecules, implicating these pathways in EBNA3C effects on LCL growth or survival. EBNA3C significantly up-regulated the CXCL12 ligand and its CXCR4 receptor and increased LCL migration. CXCL12 up-regulation depended on EBNA3C's interaction with the cell transcription factor, RBPJ, which is essential for LCL growth. EBNA3C also up-regulated MYC 1.3-fold and down-regulated CDKN2A exons 2 and 3, shared by p16 and p14, 1.4-fold, with false discovery rates < 5 × 10(-4).

Indexed as

Analysis of VarianceAntigens, ViralBayes TheoremCell Line, TumorCluster AnalysisEpstein-Barr Virus Nuclear AntigensGene Expression ProfilingGene Expression Regulation, NeoplasticGenesHumansImmunoglobulin J Recombination Signal Sequence-Binding ProteinLymphocyte ActivationMicroarray AnalysisReceptors, EstrogenReverse Transcriptase Polymerase Chain ReactionTranscription FactorsAntigens, ViralEBNA-3C, epstein-barr virusEpstein-Barr Virus Nuclear AntigensImmunoglobulin J Recombination Signal Sequence-Binding ProteinRBPJ protein, humanReceptors, EstrogenTranscription Factors

Identifiers

PMID21173222
PMCPMC3017193
OpenAlexW2071385685

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.