Evidence map›Paper›PMID 28115629›Full record

ArticleNucleic acids research2017

A novel role for transcription-coupled nucleotide excision repair for the in vivo repair of 3,N4-ethenocytosine.

Isaac A Chaim, Alycia Gardner, Jie Wu, Teruaki Iyama, David M Wilson, Leona D Samson

Abstract read
In one paragraph

Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Article
  2. The aflatoxin BNAR cancer · 2025
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Etheno adducts: from tRNA modifications to DNA adducts and back to miscoding ribonucleotides.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Fluorescent Probes of DNA Repair.ACS chemical biology · 2018
    Review
  16. Review
  17. In vivo measurements of interindividual differences in DNA glycosylases and APE1 activities.Proceedings of the National Academy of Sciences of the United States of America · 2017
    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.

Isaac A ChaimDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Alycia GardnerCenter for Environmental Health Sciences, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Jie WuThe Barbara K. Ostrom (1978) Bioinformatics and Computing Facility in the Swanson Biotechnology Center, Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Teruaki IyamaLaboratory of Molecular Gerontology, National Institute on Aging, Intramural Research Program, National Institutes of Health, 251 Bayview Boulevard, Suite 100, Baltimore, MD 21224, USA.
David M WilsonLaboratory of Molecular Gerontology, National Institute on Aging, Intramural Research Program, National Institutes of Health, 251 Bayview Boulevard, Suite 100, Baltimore, MD 21224, USA.
Leona D SamsonDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.

Funding

TOXICOLOGY CORE UNITP30ES002109 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI YAFFE, MICHAEL B · 1985 to 2020
$25.6M
Oxidative DNA Damage Repair in Premature Aging and NeurodegenerationZIAAG000751 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 2009 to 2019
$5.3M
EUKARYTIC DNA ALKYLATION REPAIRR01CA055042 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SAMSON, LEONA D. · 1991 to 2010
$4.8M
Eukaryotic DNA Alkylation RepairR01ES022872 · NIEHS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI SAMSON, LEONA D. · 2013 to 2017
$1.7M
NCI NIH HHS R01 CA055042NIEHS NIH HHS P30 ES002109NIEHS NIH HHS R01 ES022872
6 · The paper itself

Abstract

Etheno (ε) DNA base adducts are highly mutagenic lesions produced endogenously via reactions with lipid peroxidation (LPO) products. Cancer-promoting conditions, such as inflammation, can induce persistent oxidative stress and increased LPO, resulting in the accumulation of ε-adducts in different tissues. Using a recently described fluorescence multiplexed host cell reactivation assay, we show that a plasmid reporter bearing a site-specific 3,N4-ethenocytosine (εC) causes transcriptional blockage. Notably, this blockage is exacerbated in Cockayne Syndrome and xeroderma pigmentosum patient-derived lymphoblastoid and fibroblast cells. Parallel RNA-Seq expression analysis of the plasmid reporter identifies novel transcriptional mutagenesis properties of εC. Our studies reveal that beyond the known pathways, such as base excision repair, the process of transcription-coupled nucleotide excision repair plays a role in the removal of εC from the genome, and thus in the protection of cells and tissues from collateral damage induced by inflammatory responses.

Indexed as

DNA RepairTranscription, GeneticAdenineAnimalsCell LineCells, CulturedCockayne SyndromeCytosineDNA AdductsDNA Repair EnzymesHumansMiceMice, KnockoutMutagenesisRNA Polymerase IIXeroderma Pigmentosum1,N(6)-ethenoadenine3,N(4)-ethenocytosineAdenineCytosineDNA AdductsDNA Repair EnzymesRNA Polymerase II

Identifiers

PMID28115629
PMCPMC5389632

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.