Evidence map›Paper›PMID 20658645›Full record

ReviewEnvironmental and molecular mutagenesis2010

Mammalian nucleotide excision repair proteins and interstrand crosslink repair.

Richard D Wood

Open access · greenAbstract readReview
In one paragraph

Review in Environmental and molecular mutagenesis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% 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

64 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Mechanisms of DNA repair and mutagenesis induced by acetaldehyde, acrolein, aristolochic acids, and vinyl chloride.Journal of environmental science and health. Part C, Toxicology and carcinogenesis · 2025
    Review
  6. Article
  7. Review
  8. When DNA-damage responses meet innate and adaptive immunity.Cellular and molecular life sciences : CMLS · 2024
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Xeroderma Pigmentosum: A Model for Human Premature Aging.The Journal of investigative dermatology · 2021
    Review
  18. Article
  19. Review
  20. Article

4 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Richard D WoodDepartment of Carcinogenesis and The University of Texas Graduate School of Biomedical Sciences at Houston, The University of Texas M. D. Anderson Cancer Center, Science Park-Research Division, Smithville, Texas 78957, USA. rwood@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
Pilot Project ProgramP30ES007784 · NIEHS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI RICHIE, ELLEN R · 1996 to 2011
$16.4M
Recognition and processing of complex lesions by components from multiple DNAP01CA097175 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI NAIRN, RODNEY S · 2004 to 2014
$15.3M
NCI NIH HHS P01 CA097175NCI NIH HHS P30 CA016672NCI NIH HHS P30CA016672NIEHS NIH HHS P30 ES007784NIEHS NIH HHS P30ES007784
6 · The paper itself

Abstract

Although various schemes for interstrand crosslink (ICL) repair incorporate DNA recombination, replication, and double-strand break intermediate steps, action of the nucleotide excision repair (NER) system or some variation of it is a common feature of most models. In the bacterium Escherichia coli, the NER enzyme UvrABC can incise on either side of an ICL to unhook the crosslink, and can proceed via a subsequent recombination step. The relevance of NER to ICL repair in mammalian cells has been challenged. Of all NER mutants, it is clear that ERCC1 and XPF-defective cells show the most pronounced sensitivities to ICL-inducing agents, and defects in ICL repair. However, there is good evidence that cells defective in NER proteins including XPA and XPG are also more sensitive than normal to ICL-inducing agents. These results are summarized here, together with evidence for defective crosslink removal in NER-defective cells. Studies of incision at sites of ICL by cell extracts and purified proteins have been done, but these studies are not all consistent with one another and further research is required.

Indexed as

AnimalsCross-Linking ReagentsDNA RepairHumansCross-Linking Reagents

Identifiers

PMID20658645
PMCPMC3017513
OpenAlexW2166027044

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.