Evidence map›Paper›PMID 26994140›Full record

ArticleThe Journal of biological chemistry2016

The Stress-responsive Gene ATF3 Mediates Dichotomous UV Responses by Regulating the Tip60 and p53 Proteins.

Hongmei Cui, Xingyao Li, Chunhua Han, Qi-En Wang, Hongbo Wang, Han-Fei Ding, Junran Zhang, Chunhong Yan

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Roles of NRF2 in DNA damage repair.Cellular oncology (Dordrecht, Netherlands) · 2023
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. ATF-3 expression inhibits melanoma growth by downregulating ERK and AKT pathways.Laboratory investigation; a journal of technical methods and pathology · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Screening of Long Noncoding RNAs Induced by Radiation Using Microarray.Dose-response : a publication of International Hormesis Society
    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

8 authors at 5 institutions in 2 countries.

Hongmei CuiFrom the Georgia Cancer Center and.
Xingyao LiFrom the Georgia Cancer Center and.
Chunhua Hanthe Department of Radiology, Ohio State University, Columbus, Ohio 43210.
Qi-En Wangthe Department of Radiology, Ohio State University, Columbus, Ohio 43210.
Hongbo Wangthe Key Laboratory of Molecular Pharmacology and Drug Evaluation, School of Pharmacy, Yantai University, Yantai 264005, China, and.
Han-Fei DingFrom the Georgia Cancer Center and Departments of Pathology and.
Junran Zhangthe Department of Radiation Oncology, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106.
Chunhong YanFrom the Georgia Cancer Center and Biochemistry and Molecular Biology, Medical College of Georgia, Augusta University, Augusta, Georgia 30912, cyan@augusta.edu.
Augusta University Health · USThe Ohio State University · USAugusta University · USCase Western Reserve University · USYantai University · CN

Funding

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 R01 CA139107NCI NIH HHS R01 CA164006
6 · The paper itself

Abstract

The response to UV irradiation is important for a cell to maintain its genetic integrity when challenged by environmental genotoxins. An immediate early response to UV irradiation is the rapid induction of activating transcription factor 3 (ATF3) expression. Although emerging evidence has linked ATF3 to stress pathways regulated by the tumor suppressor p53 and the histone acetyltransferase Tip60, the role of ATF3 in the UV response remains largely unclear. Here, we report that ATF3 mediated dichotomous UV responses. Although UV irradiation enhanced the binding of ATF3 to Tip60, knockdown of ATF3 expression decreased Tip60 stability, thereby impairing Tip60 induction by UV irradiation. In line with the role of Tip60 in mediating UV-induced apoptosis, ATF3 promoted the death of p53-defective cells in response to UV irradiation. However, ATF3 could also activate p53 and promote p53-mediated DNA repair, mainly through altering histone modifications that could facilitate recruitment of DNA repair proteins (such as DDB2) to damaged DNA sites. As a result, ATF3 rather protected the p53 wild-type cells from UV-induced apoptosis. Our results thus indicate that ATF3 regulates cell fates upon UV irradiation in a p53-dependent manner.

Indexed as

Activating Transcription Factor 3ApoptosisCell Line, TumorDNA-Binding ProteinsDNA RepairEnzyme StabilityGene Knockdown TechniquesHistone AcetyltransferasesHumansLysine Acetyltransferase 5Tumor Suppressor Protein p53Ultraviolet RaysActivating Transcription Factor 3ATF3 protein, humanDDB2 protein, humanDNA-Binding ProteinsHistone AcetyltransferasesKAT5 protein, humanLysine Acetyltransferase 5TP53 protein, humanTumor Suppressor Protein p53apoptosisATF3DNA damageDNA repairhistone modificationsp53stress responseUV

Identifiers

PMID26994140
PMCPMC4865929
OpenAlexW2413299070

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.