Evidence map›Paper›PMID 15456863›Full record

ArticleMolecular and cellular biology2004

Increased sensitivity to UV radiation in mice with a p53 point mutation at Ser389.

Wendy Bruins, Edwin Zwart, Laura D Attardi, Tomoo Iwakuma, Esther M Hoogervorst, Rudolf B Beems, Barbara Miranda, Conny T M van Oostrom, Jolanda van den Berg, Gerard J van den Aardweg and 4 more

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

57 citing papers in PubMed, 120 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Deciphering the PTM codes of the tumor suppressor p53.Journal of molecular cell biology · 2022
    Review
  6. Review
  7. Genomic gain ofScience advances · 2021
    Article
  8. Regulating tumor suppressor genes: post-translational modifications.Signal transduction and targeted therapy · 2020
    Review
  9. Understanding p53 functions through p53 antibodies.Journal of molecular cell biology · 2019
    Review
  10. Evidence for allosteric effects on p53 oligomerization induced by phosphorylation.Protein science : a publication of the Protein Society · 2018
    Article
  11. Article
  12. Review
  13. Review
  14. p53/p63/p73 in the epidermis in health and disease.Cold Spring Harbor perspectives in medicine · 2014
    Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Mechanisms of p53 activation and physiological relevance in the developing kidney.American journal of physiology. Renal physiology · 2012
    Article
  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

14 authors at 6 institutions in 2 countries.

Wendy BruinsLaboratory of Toxicology, Pathology and Genetics, National Institute of Public Health and Environment (RIVM), Bilthoven, The Netherlands.
Edwin Zwart
Laura D Attardi
Tomoo Iwakuma
Esther M Hoogervorst
Rudolf B Beems
Barbara Miranda
Conny T M van Oostrom
Jolanda van den Berg
Gerard J van den Aardweg
Guillermina Lozano
Harry van Steeg
Tyler Jacks
Annemieke de Vries
Cancer Genetics (United States) · USCenter for Cancer Research · USHoward Hughes Medical Institute · USMeertens Institute · NLStanford Medicine · USThe University of Texas MD Anderson Cancer Center · US

Funding

Models for DNA repair and cell cycle control variantsU01ES011044 · NIEHS · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI VIJG, JAN · 2001 to 2006
$5.1M
NIEHS NIH HHS 1U01 ES11044-02NIEHS NIH HHS U01 ES011044
6 · The paper itself

Abstract

Phosphorylation is important for p53 protein stabilization and activation after DNA damage. Serine 389 of p53 is specifically phosphorylated after UV irradiation, whereas gamma radiation activates p53 through a different pathway. To study the in vivo significance of p53 phosphorylation at serine 389, we generated a physiological mouse model in which p53 phosphorylation at serine 389 is abolished by alanine substitution. Homozygous mutant p53.S389A mice are viable and have an apparently normal phenotype. However, cells isolated from these mice are partly compromised in transcriptional activation of p53 target genes and apoptosis after UV irradiation, whereas gamma radiation-induced responses are not affected. Moreover, p53.S389A mice show increased sensitivity to UV-induced skin tumor development, signifying the importance of serine 389 phosphorylation for the tumor-suppressive function of p53.

Indexed as

Point MutationUltraviolet RaysAnimalsAntibiotics, AntineoplasticApoptosisCarcinomaCell CycleCells, CulturedDoxorubicinFibroblastsGamma RaysGene Expression RegulationHumansMiceNeoplasms, Squamous CellPapillomaAntibiotics, AntineoplasticDoxorubicinSerineTumor Suppressor Protein p53

Identifiers

PMID15456863
PMCPMC517897
OpenAlexW2158155127

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.