Evidence map›Paper›PMID 20713352›Full record

ArticleThe Journal of biological chemistry2010

RB·E2F1 complex mediates DNA damage responses through transcriptional regulation of ZBRK1.

Ching-Chun Liao, Connie Y Tsai, Wen-Chang Chang, Wen-Hwa Lee, Ju-Ming Wang

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  5. Particulate Hexavalent Chromium Inhibits E2F1 Leading to Reduced RAD51 Nuclear Foci Formation in Human Lung Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2021
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  11. Dynamic coregulatory complex containing BRCA1, E2F1 and CtIP controls ATM transcription.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2012
    Article
  12. Article
  13. Review
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 3 institutions in 2 countries.

Ching-Chun LiaoFrom the Institute of Basic Medical Sciences, Tainan, Taiwan.
Connie Y TsaiDepartment of Biological Chemistry, University of California, Irvine, California 92697.
Wen-Chang ChangInstitute of Pharmacology, College of Medicine, Tainan, Taiwan; Center for Gene Regulation and Signal Transduction Research, National Cheng Kung University, Tainan, Taiwan.
Wen-Hwa LeeDepartment of Biological Chemistry, University of California, Irvine, California 92697. Electronic address: whlee@uci.edu.
Ju-Ming WangCenter for Gene Regulation and Signal Transduction Research, National Cheng Kung University, Tainan, Taiwan; Institute of Biosignal Transduction, Tainan, Taiwan. Electronic address: yumingw@mail.ncku.edu.tw.
National Cheng Kung University · TWUniversity of California, Irvine · USChina Medical University · TW

Funding

Transcriptional Role of BRCA1 in Breast CancerR01CA094170 · NCI · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI LEE, WEN-HWA · 2002 to 2012
$2.7M
NCI NIH HHS CA94170NCI NIH HHS R01 CA094170
6 · The paper itself

Abstract

RB plays an essential role in DNA damage-induced growth arrest and regulates the expression of several factors essential for DNA repair machinery. However, how RB coordinates DNA damage response through transcriptional regulation of genes involved in growth arrest remains largely unexplored. We examined whether RB can mediate the response to DNA damage through modulation of ZBRK1, a zinc finger-containing transcriptional repressor that can modulate the expression of GADD45A, a DNA damage response gene, to induce cell cycle arrest in response to DNA damage. We found that the ZBRK1 promoter contains an authentic E2F-recognition sequence that specifically binds E2F1, but not E2F4 or E2F6, together with chromatin remodeling proteins CtIP and CtBP to form a repression complex that suppresses ZBRK1 transcription. Furthermore, loss of RB-mediated transcriptional repression led to an increase in ZBRK1 transcript levels, correlating with increased sensitivity to ultraviolet (UV) and methyl methanesulfonate-induced DNA damage. Taken together, these results suggest that the RB·CtIP (CtBP interacting protein)/CtBP (C terminus-binding protein) /E2F1 complex plays a critical role in ZBRK1 transcriptional repression, and loss of this repression may contribute to cellular sensitivity of DNA damage, ultimately leading to carcinogenesis.

Indexed as

Carrier ProteinsCell CycleCell Cycle ProteinsCell Line, TumorChromatin Assembly and DisassemblyDNA DamageE2F1 Transcription FactorEndodeoxyribonucleasesGADD45 ProteinsHumansMesylatesMultiprotein ComplexesNuclear ProteinsRepressor ProteinsResponse ElementsRetinoblastoma ProteinCarrier ProteinsCell Cycle ProteinsE2F1 protein, humanE2F1 Transcription FactorEndodeoxyribonucleasesGADD45A protein, humanGADD45 ProteinsMesylatesmethanesulfonic acidMultiprotein ComplexesNuclear ProteinsRBBP8 protein, humanRepressor ProteinsRetinoblastoma ProteinZNF350 protein, human

Identifiers

PMID20713352
PMCPMC2963368
OpenAlexW1548623780

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.