Evidence map›Paper›PMID 27146783›Full record

ArticleBMC genomics2016

The common stress responsive transcription factor ATF3 binds genomic sites enriched with p300 and H3K27ac for transcriptional regulation.

Jonathan Zhao, Xingyao Li, Mingxiong Guo, Jindan Yu, Chunhong Yan

Open access · goldAbstract read
In one paragraph

Article in BMC genomics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
4.7field-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

75 citing papers in PubMed, 118 citations in OpenAlex.

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  13. [ATF3 regulates inflammatory response in atherosclerotic plaques in mice through the NF-κB signaling pathway].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
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15 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

5 authors at 4 institutions in 1 country.

Jonathan ZhaoDepartment of Medicine, Division of Hematology and Oncology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Xingyao LiGeorgia Cancer Center, Augusta University, Augusta, GA, USA.
Mingxiong GuoCenter for Cell Biology and Cancer Research, Albany Medical College, Albany, NY, USA.
Jindan YuDepartment of Medicine, Division of Hematology and Oncology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA. jindan-yu@northwestern.edu.
Chunhong YanGeorgia Cancer Center, Augusta University, Augusta, GA, USA. cyan@augusta.edu.
Northwestern University · USAlbany Medical Center Hospital · USAugusta University · USAugusta University Health · US

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
The Role of ATF3 in the DNA Damage ResponseR01CA139107 · NCI · AUGUSTA UNIVERSITY · PI YAN, CHUNHONG · 2010 to 2015
$1.2M
Screening Assays for Small Molecules Targeting Oncogenic eIF4E ExpressionR01CA164006 · NCI · AUGUSTA UNIVERSITY · PI YAN, CHUNHONG · 2012 to 2014
$832k
NCI NIH HHS P30 CA060553NCI NIH HHS R01 CA139107NCI NIH HHS R01 CA164006
6 · The paper itself

Abstract

backgroundDysregulation of the common stress responsive transcription factor ATF3 has been causally linked to many important human diseases such as cancer, atherosclerosis, infections, and hypospadias. Although it is believed that the ATF3 transcription activity is central to its cellular functions, how ATF3 regulates gene expression remains largely unknown. Here, we employed ATF3 wild-type and knockout isogenic cell lines to carry out the first comprehensive analysis of global ATF3-binding profiles in the human genome under basal and stressed (DNA damage) conditions.

resultsAlthough expressed at a low basal level, ATF3 was found to bind a large number of genomic sites that are often associated with genes involved in cellular stress responses. Interestingly, ATF3 appears to bind a large portion of genomic sites distal to transcription start sites and enriched with p300 and H3K27ac. Global gene expression profiling analysis indicates that genes proximal to these genomic sites were often regulated by ATF3. While DNA damage elicited by camptothecin dramatically altered the ATF3 binding profile, most of the genes regulated by ATF3 upon DNA damage were pre-bound by ATF3 before the stress. Moreover, we demonstrated that ATF3 was co-localized with the major stress responder p53 at genomic sites, thereby collaborating with p53 to regulate p53 target gene expression upon DNA damage.

conclusionsThese results suggest that ATF3 likely bookmarks genomic sites and interacts with other transcription regulators to control gene expression.

Indexed as

Activating Transcription Factor 3Binding SitesCamptothecinCell Line, TumorDNAGene Expression ProfilingGene Expression RegulationGene Knockout TechniquesHCT116 CellsHEK293 CellsHistonesHumansp300-CBP-Associated Factorp300-CBP Transcription FactorsTumor Suppressor Protein p53Activating Transcription Factor 3ATF3 protein, humanCamptothecinDNAHistonesp300-CBP-Associated Factorp300-CBP Transcription FactorsTP53 protein, humanTumor Suppressor Protein p53ATF3ChIP-seqEnhancerH3K27acp300p53

Identifiers

PMID27146783
PMCPMC4857411
OpenAlexW2347116954

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.