Evidence map›Paper›PMID 19783230›Full record

ArticleDNA repair2009

Polk mutant mice have a spontaneous mutator phenotype.

J Nicole Kosarek Stancel, Lisa D McDaniel, Susana Velasco, James Richardson, Caixia Guo, Errol C Friedberg

Abstract read
In one paragraph

Article in DNA repair, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

38 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Mitomycin C-induced DNA double-strand breaks are enhanced by catalytical inactivation of DNA polymerase κ in mice.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. RIP140 regulatesCancer drug resistance (Alhambra, Calif.) · 2022
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. DNA polymerase kappa protects human cells against MMC-induced genotoxicity through error-free translesion DNA synthesis.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2017
    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

6 authors at 1 institution in 1 country.

J Nicole Kosarek StancelLaboratory of Molecular Pathology, Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9072, USA.
Lisa D McDaniel
Susana Velasco
James Richardson
Caixia Guo
Errol C Friedberg
The University of Texas Southwestern Medical Center · US

Funding

MOUSE MODELS OF DNA REPAIR - DEFECTIVE HUMAN DISEASESR01ES011344 · NIEHS · UT SOUTHWESTERN MEDICAL CENTER · PI FRIEDBERG, ERROL · 2001 to 2011
$3.3M
NIEHS NIH HHS R01 ES011344NIEHS NIH HHS R01-ES011344
6 · The paper itself

Abstract

Mice defective for the Polk gene, which encodes DNA polymerase kappa, are viable and do not manifest obvious phenotypes. The present studies document a spontaneous mutator phenotype in Polk(-/-) mice. The initial indication of enhanced spontaneous mutations in these mice came from the serendipitous observation of a postulated founder mutation that manifested in multiple disease states among a cohort of mice comprising all three possible Polk genotypes. Polk(-/-) and isogenic wild-type controls carrying a reporter transgene (the lambda-phage cII gene) were used for subsequent quantitative and qualitative studies on mutagenesis in various tissues. We observed significantly increased mutation frequencies in the kidney, liver, and lung of Polk(-/-) mice, but not in the spleen or testis. G:C base pairs dominated the mutation spectra of the kidney, liver, and lung. These results are consistent with the notion that Pol kappa is required for accurate translesion DNA synthesis past naturally occurring polycyclic guanine adducts, possibly generated by cholesterol and/or its metabolites.

Indexed as

DNA DamageMutationPhenotypeAnimalsBase PairingCell LineDNA-Directed DNA PolymeraseGenes, ReporterMiceMice, KnockoutY-Family DNA PolymerasesDNA-Directed DNA PolymerasePolk protein, mouseY-Family DNA Polymerases

Identifiers

PMID19783230
PMCPMC2787749
OpenAlexW2065458842

What OpenQuestion holds

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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.