Evidence map›Paper›PMID 12483511›Full record

ReviewOncogene2002

Subpathways of nucleotide excision repair and their regulation.

Philip C Hanawalt

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 175 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
175citing papers in PubMed, 2 pooled it
8.2field-weighted citation impact, top 2% 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

175 citing papers in PubMed, 2 syntheses or guidelines pooled it, 444 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Review
  5. Article
  6. The Influence of Circadian Rhythms on DNA Damage Repair in Skin Photoaging.International journal of molecular sciences · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Oxidative stress drives mutagenesis through transcription-coupled repair in bacteria.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Molecular Interactions between Dietary Lipids and Bone Tissue during Aging.International journal of molecular sciences · 2021
    Review
  18. Article
  19. Review
  20. Article

115 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.

Philip C HanawaltDepartment of Biological Sciences, Stanford University, Stanford, California, CA 94305-5020, USA. hanawalt@stanford.edu
Stanford University · US

Funding

Role of transcription in genomic stabilityR01CA077712 · NCI · STANFORD UNIVERSITY · PI HANAWALT, PHILIP COURTLAND · 1998 to 2016
$5.6M
Transcription Coupled DNA Repair and Human DiseaseR01CA091456 · NCI · STANFORD UNIVERSITY · PI HANAWALT, PHILIP COURTLAND · 2002 to 2006
$1.3M
Transcription coupled DNA repair in E. ColiR01CA090915 · NCI · STANFORD UNIVERSITY · PI HANAWALT, PHILIP COURTLAND · 2002 to 2006
$1.1M
CELULAR PROCESSING OF DAMAGED DNA--ROLE IN ONCOGENESISR35CA044349 · NCI · STANFORD UNIVERSITY · PI HANAWALT, PHILIP C · 1987 to 2000
$959k
Role of transcription in genomic stabilityR56CA077712 · NCI · STANFORD UNIVERSITY · PI HANAWALT, PHILIP COURTLAND · 2008 to 2008
$328k
NCI NIH HHS CA 44349NCI NIH HHS CA77712NCI NIH HHS CA90915NCI NIH HHS CA91456NCI NIH HHS R01 CA077712
6 · The paper itself

Abstract

Nucleotide excision repair provides an important cellular defense against a large variety of structurally unrelated DNA alterations. Most of these alterations, if unrepaired, may contribute to mutagenesis, oncogenesis, and developmental abnormalities, as well as cellular lethality. There are two subpathways of nucleotide excision repair; global genomic repair (GGR) and transcription coupled repair (TCR), that is selective for the transcribed DNA strand in expressed genes. Some of the proteins involved in the recognition of DNA damage (including RNA polymerase) are also responsive to natural variations in the secondary structural features of DNA. Gratuitous repair events in undamaged DNA might then contribute to genomic instability. However, damage recognition enzymes for GGR are normally maintained at very low levels unless the cells are genomically stressed. GGR is controlled through the SOS stress response in E. coli and through the activated p53 tumor suppressor in human cells. These inducible responses in human cells are important, as they have been shown to operate upon chemical carcinogen DNA damage at levels to which humans are environmentally exposed. Interestingly, most rodent tissues are deficient in the p53-dependent GGR pathway. Since rodents are used as surrogates for environmental cancer risk assessment, it is essential that we understand how they differ from humans with respect to DNA repair and oncogenic responses to environmental genotoxins. In the case of terminally differentiated mammalian cells, a new paradigm has appeared in which GGR is attenuated but both strands of expressed genes are repaired efficiently.

Indexed as

AnimalsCell DifferentiationDNA DamageDNA RepairEscherichia coliGene Expression Regulation, BacterialHumansNeuronsOncogenic VirusesSpecies SpecificityTumor Suppressor Protein p53Tumor Suppressor Protein p53

Identifiers

PMID12483511
OpenAlexW1979123830

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.