Evidence map›Paper›PMID 24741006›Full record

ArticleCancer research2014

E2F1 responds to ultraviolet radiation by directly stimulating DNA repair and suppressing carcinogenesis.

Anup Kumar Biswas, David L Mitchell, David G Johnson

Abstract read
In one paragraph

Article in Cancer research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-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

24 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  5. Review
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  7. Review
  8. Review
  9. 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
  10. Article
  11. Article
  12. Article
  13. The broken cycle: E2F dysfunction in cancer.Nature reviews. Cancer · 2019
    Review
  14. Article
  15. Article
  16. Review
  17. Article
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  20. 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

3 authors at 1 institution in 1 country.

Anup Kumar BiswasAuthors' Affiliations: Department of Molecular Carcinogenesis, University of Texas MD Anderson Cancer Center, Science Park; and The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, Texas.
David L MitchellAuthors' Affiliations: Department of Molecular Carcinogenesis, University of Texas MD Anderson Cancer Center, Science Park; and The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TexasAuthors' Affiliations: Department of Molecular Carcinogenesis, University of Texas MD Anderson Cancer Center, Science Park; and The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, Texas.
David G JohnsonAuthors' Affiliations: Department of Molecular Carcinogenesis, University of Texas MD Anderson Cancer Center, Science Park; and The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, TexasAuthors' Affiliations: Department of Molecular Carcinogenesis, University of Texas MD Anderson Cancer Center, Science Park; and The University of Texas Graduate School of Biomedical Sciences at Houston, Houston, Texas djohnson@mdanderson.org.
The University of Texas MD Anderson Cancer Center · US

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
DUAL ROLE OF E2F1 IN TUMORIGENESISR01CA079648 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI JOHNSON, DAVID G. · 1999 to 2014
$4.7M
NCI NIH HHS CA016672NCI NIH HHS CA079648NCI NIH HHS P30 CA016672NCI NIH HHS R01 CA079648
6 · The paper itself

Abstract

In response to DNA damage, the E2F1 transcription factor is phosphorylated at serine 31 (serine 29 in mouse) by the ATM or ATR kinases, which promotes E2F1 protein stabilization. Phosphorylation of E2F1 also leads to the recruitment of E2F1 to sites of DNA damage, where it functions to enhance DNA repair. To study the role of this E2F1 phosphorylation event in vivo, a knock-in mouse model was generated, in which serine 29 was mutated to alanine. The S29A mutation impairs E2F1 stabilization in response to ultraviolet (UV) radiation and doxorubicin treatment, but has little effect on the expression of E2F target genes. The apoptotic and proliferative responses to acute UV radiation exposure are also similar between wild-type and E2f1(S29A/) (S29A) mice. As expected, the S29A mutation prevents E2F1 association with damaged DNA and reduces DNA repair efficiency. Moreover, E2f1(S29A/) (S29A) mice display increased sensitivity to UV-induced skin carcinogenesis. This knock-in mouse model thus links the ability of E2F1 to directly promote DNA repair with the suppression of tumor development.

Indexed as

DNA RepairUltraviolet RaysAmino Acid SubstitutionAnimalsCarcinogenesisCells, CulturedDNA DamageE2F1 Transcription FactorGene Knock-In TechniquesGenes, Tumor SuppressorMiceMice, TransgenicPhosphorylationPrimary Cell CultureProtein Processing, Post-TranslationalProtein StabilityE2f1 protein, mouseE2F1 Transcription Factor

Identifiers

PMID24741006
PMCPMC4083823
OpenAlexW2172194086

What OpenQuestion holds

Textmetadata
LicenceTDM
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.