Evidence map›Paper›PMID 20045328›Full record

ArticleCurrent biology : CB2010

Transcription-dependent cytosine deamination is a novel mechanism in ultraviolet light-induced mutagenesis.

Giel Hendriks, Fabienne Calléja, Ahmad Besaratinia, Harry Vrieling, Gerd P Pfeifer, Leon H F Mullenders, Jacob G Jansen, Niels de Wind

Open access · bronzeAbstract read
In one paragraph

Article in Current biology : CB, 2010. 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
2.4field-weighted citation impact, top 11% 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, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Transcription-associated mutagenesis.Annual review of genetics · 2014
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Transcription as a source of genome instability.Nature reviews. Genetics · 2012
    Review
  14. The transcript-centric mutations in human genomes.Genomics, proteomics & bioinformatics · 2012
    Article
  15. Article
  16. Article
  17. Article
  18. 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

8 authors at 1 institution in 1 country.

Giel HendriksDepartment of Toxicogenetics, Leiden University Medical Center (LUMC), PO Box 9600, 2300 RC, Leiden, The Netherlands.
Fabienne Calléja
Ahmad Besaratinia
Harry Vrieling
Gerd P Pfeifer
Leon H F Mullenders
Jacob G Jansen
Niels de Wind
City Of Hope National Medical Center · US

Funding

UV damage, repair, and mutagenesisR37ES006070 · NIEHS · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI PFEIFER, GERD P · 2004 to 2013
$3.7M
UV DAMAGE, REPAIR AND MUTAGENESISR01ES006070 · NIEHS · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI PFEIFER, GERD P · 1992 to 2003
$1.1M
NIEHS NIH HHS ES06070NIEHS NIH HHS R01 ES006070NIEHS NIH HHS R37 ES006070
6 · The paper itself

Abstract

Skin cancer is the most ubiquitous cancer type in the Caucasian population, and its incidence is increasing rapidly [1]. Transcribed proliferation-related genes in dermal stem cells are targets for the induction of ultraviolet light (UV)-induced mutations that drive carcinogenesis. We have recently found that transcription of a gene increases its mutability by UV in mammalian stem cells, suggesting a role of transcription in skin carcinogenesis [2]. Here we show that transcription-associated UV-induced nucleotide substitutions are caused by increased deamination of cytosines to uracil within photolesions at the transcribed strand, presumably at sites of stalled transcription complexes. Additionally, via an independent mechanism, transcription of UV-damaged DNA induces the generation of intragenic deletions. We demonstrate that transcription-coupled nucleotide excision repair (TC-NER) provides protection against both classes of transcription-associated mutagenesis. Combined, these results unveil the existence of two mutagenic pathways operating specifically at the transcribed DNA strand of active genes. Moreover, these results uncover a novel role for TC-NER in the suppression of UV-induced genome aberrations and provide a rationale for the efficient induction of apoptosis by stalled transcription complexes.

Indexed as

MutagenesisTranscription, GeneticUltraviolet RaysCytosineDeaminationHypoxanthine PhosphoribosyltransferaseCytosineHypoxanthine Phosphoribosyltransferase

Identifiers

PMID20045328
PMCPMC2818831
OpenAlexW2074858286

What OpenQuestion holds

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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.