Evidence map›Paper›PMID 20047468›Full record

ArticleZebrafish2009

Zebrafish have a competent p53-dependent nucleotide excision repair pathway to resolve ultraviolet B-induced DNA damage in the skin.

Zhiqiang Zeng, Jennifer Richardson, Daniel Verduzco, David L Mitchell, E Elizabeth Patton

Open access · greenAbstract read
In one paragraph

Article in Zebrafish, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

18 citing papers in PubMed, 45 citations in OpenAlex.

  1. Early ultraviolet exposure disrupts late dorsal fin skeletal development in zebrafish.Developmental dynamics : an official publication of the American Association of Anatomists · 2026
    Article
  2. Article
  3. Article
  4. Rapid recruitment of p53 to DNA damage sites directs DNA repair choice and integrity.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  5. Review
  6. Medaka (International journal of molecular sciences · 2020
    Article
  7. UVB Irradiation Induced Cell Damage and Early Onset ofAnimals : an open access journal from MDPI · 2020
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Genetic and environmental melanoma models in fish.Pigment cell & melanoma research · 2010
    Review
  18. A novel method to assess photobiomodulation in stimulating regenerative capacity and vascularization in zebrafish.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair 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

5 authors at 4 institutions in 2 countries.

Zhiqiang ZengInstitute of Genetics and Molecular Medicine, MRC Human Genetics Unit, Edinburgh Cancer Research Centre, The University of Edinburgh, Edinburgh, UK.
Jennifer Richardson
Daniel Verduzco
David L Mitchell
E Elizabeth Patton
Edinburgh Cancer Research · GBInstitute of Genetics and Cancer · GBThe University of Texas MD Anderson Cancer Center · USThe University of Texas Southwestern Medical Center · US

Funding

Pilot Project ProgramP30ES007784 · NIEHS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI RICHIE, ELLEN R · 1996 to 2011
$16.4M
The Etiology of UV-Induced MelanomaR01CA113671 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI MITCHELL, DAVID L · 2006 to 2010
$1.2M
Medical Research Council G120/875Medical Research Council MC_PC_U127585840Medical Research Council MC_U127585840NCI NIH HHS CA113671NCI NIH HHS R01 CA113671NIEHS NIH HHS ES07784Worldwide Cancer Research 07-0421
6 · The paper itself

Abstract

Ultraviolet (UV) light is a primary environmental risk factor for melanoma, a deadly form of skin cancer derived from the pigmented cells called melanocytes. UVB irradiation causes DNA damage, mainly in the form of pyrimidine dimers (cis-syn cyclobutane pyrimidine dimers and pyrimidine (6-4) pyrimidone photoproducts), and organisms have developed complex multiprotein repair processes to cope with the DNA damage. Zebrafish is becoming an important model system to study the effects of UV light in animals, in part because the embryos are easily treated with UV irradiation, and the DNA damage repair pathways appear to be conserved in zebrafish and mammals. We are interested in exploring the effects of UV irradiation in young adult zebrafish, so that we can apply them to the study of gene-environment interactions in models of skin cancer. Using the Xiphophorus UV melanoma model as a starting point, we have developed a UV irradiation treatment chamber, and established UV treatment conditions at different ages of development. By translating the Xiphophorus UV treatment methodology to the zebrafish system, we show that the adult zebrafish skin is competent for nucleotide excision DNA damage repair, and that like in mammalian cells, UV treatment promotes phosphorylation of H2AX and a p53-dependent response. These studies provide the groundwork for exploring the role of UV light in melanoma development in zebrafish.

Indexed as

DNA DamageDNA RepairAnimalsApoptosisDisease Models, AnimalEmbryo, NonmammalianGene Expression Regulation, DevelopmentalHistonesMelanomaPhosphorylationSkinSkin NeoplasmsTumor Suppressor Protein p53Ultraviolet RaysZebrafishHistonesTumor Suppressor Protein p53

Identifiers

PMID20047468
PMCPMC2804931
OpenAlexW2122532602

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.