Evidence map›Paper›PMID 12697828›Full record

ArticleMolecular and cellular biology2003

Regulation of E2F1 by BRCT domain-containing protein TopBP1.

Kang Liu, Fang-Tsyr Lin, J Michael Ruppert, Weei-Chin Lin

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
4.2field-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

83 citing papers in PubMed, 133 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. A small-molecule inhibitor of TopBP1 exerts anti-MYC activity and synergy with PARP inhibitors.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. E2F1 sumoylation as a protective cellular mechanism in oxidative stress response.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  13. Article
  14. Article
  15. Therapeutic Targeting ofAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2019
    Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Review

23 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

4 authors at 1 institution in 1 country.

Kang LiuDivision of Hematology and Oncology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama 35294-3300, USA.
Fang-Tsyr Lin
J Michael Ruppert
Weei-Chin Lin
University of Alabama at Birmingham · US

Funding

The ATM/E2F1 Pathway in DNA Damage and Growth ControlR01CA100857 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI LIN, WEEI-CHIN · 2004 to 2019
$4.8M
Therapeutic Targeting of Oncogenic Stress in Cancer TreatmentR01CA138641 · NCI · BAYLOR COLLEGE OF MEDICINE · PI LIN, WEEI-CHIN · 2010 to 2014
$1.5M
CLINICAL ONCOLOGY RESEARCH CAREER DEVELOPMENT PROGRAMK12CA076937 · NCI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI RINEHART, JOHN · 1997 to 2002
$1.2M
NCI NIH HHS K12 CA 7693705NCI NIH HHS R01 CA100857NCI NIH HHS R01 CA138641
6 · The paper itself

Abstract

The E2F transcription factor integrates cellular signals and coordinates cell cycle progression. Our prior studies demonstrated selective induction and stabilization of E2F1 through ATM-dependent phosphorylation in response to DNA damage. Here we report that DNA topoisomerase IIbeta binding protein 1 (TopBP1) regulates E2F1 during DNA damage. TopBP1 contains eight BRCT (BRCA1 carboxyl-terminal) motifs and upon DNA damage is recruited to stalled replication forks, where it participates in a DNA damage checkpoint. Here we demonstrated an interaction between TopBP1 and E2F1. The interaction depended on the amino terminus of E2F1 and the sixth BRCT domain of TopBP1. It was specific to E2F1 and was not observed in E2F2, E2F3, or E2F4. This interaction was induced by DNA damage and phosphorylation of E2F1 by ATM. Through this interaction, TopBP1 repressed multiple activities of E2F1, including transcriptional activity, induction of S-phase entry, and apoptosis. Furthermore, TopBP1 relocalized E2F1 from diffuse nuclear distribution to discrete punctate nuclear foci, where E2F1 colocalized with TopBP1 and BRCA1. Thus, the specific interaction between TopBP1 and E2F1 during DNA damage inhibits the known E2F1 activities but recruits E2F1 to a BRCA1-containing repair complex, suggesting a direct role of E2F1 in DNA damage checkpoint/repair at stalled replication forks.

Indexed as

Cell Cycle ProteinsDNA-Binding ProteinsGene Expression RegulationApoptosisAtaxia Telangiectasia Mutated ProteinsBRCA1 ProteinCarrier ProteinsCell NucleusCells, CulturedDNA DamageDNA ReplicationDoxorubicinE2F1 Transcription FactorE2F2 Transcription FactorE2F3 Transcription FactorE2F4 Transcription FactorAtaxia Telangiectasia Mutated ProteinsATM protein, humanBRCA1 ProteinCarrier ProteinsCell Cycle ProteinsDNA-Binding ProteinsDoxorubicinE2F1 protein, humanE2F1 Transcription FactorE2F2 protein, humanE2F2 Transcription FactorE2F3 Transcription FactorE2F4 protein, humanE2F4 Transcription FactorE2F Transcription FactorsNuclear ProteinsProtein Serine-Threonine KinasesRecombinant ProteinsTOPBP1 protein, humanTranscription FactorsTumor Suppressor Proteins

Identifiers

PMID12697828
PMCPMC153207
OpenAlexW2116258646

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.