Evidence map›Paper›PMID 29514270›Full record

ArticleNucleic acids research2018

Cytotoxic and mutagenic properties of alkyl phosphotriester lesions in Escherichia coli cells.

Jiabin Wu, Pengcheng Wang, Yinsheng Wang

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

16 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Formation of Carboxymethyl-Phosphotriester Adducts in DNA.Chemical research in toxicology · 2025
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Metabolism and DNA Adduct Formation of Tobacco-SpecificInternational journal of molecular sciences · 2022
    Review
  8. Metabolic Activation and DNA Interactions of CarcinogenicInternational journal of molecular sciences · 2022
    Review
  9. Article
  10. The complexity and regulation of repair of alkylation damage to nucleic acids.Critical reviews in biochemistry and molecular biology · 2021
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
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

3 authors at 1 institution in 1 country.

Jiabin WuEnvironmental Toxicology Graduate Program and Department of Chemistry, University of California Riverside, Riverside, CA 92521-0403, USA.
Pengcheng WangEnvironmental Toxicology Graduate Program and Department of Chemistry, University of California Riverside, Riverside, CA 92521-0403, USA.
Yinsheng WangEnvironmental Toxicology Graduate Program and Department of Chemistry, University of California Riverside, Riverside, CA 92521-0403, USA.
University of California, Riverside · US

Funding

Repair and Biological Consequences of Alkylated Thymidine LesionsR01ES025121 · NIEHS · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI WANG, YINSHENG · 2015 to 2019
$2.2M
NIEHS NIH HHS R01 ES025121
6 · The paper itself

Abstract

Exposure to many endogenous and exogenous agents can give rise to DNA alkylation, which constitutes a major type of DNA damage. Among the DNA alkylation products, alkyl phosphotriesters have relatively high frequencies of occurrence and are resistant to repair in mammalian tissues. However, little is known about how these lesions affect the efficiency and fidelity of DNA replication in cells or how the replicative bypass of these lesions is modulated by translesion synthesis DNA polymerases. In this study, we synthesized oligodeoxyribonucleotides containing four pairs (Sp and Rp) of alkyl phosphotriester lesions at a defined site, and examined how these lesions are recognized by DNA replication machinery in Escherichia coli cells. We found that the Sp diastereomer of the alkyl phosphotriester lesions could be efficiently bypassed, whereas the Rp counterparts moderately blocked DNA replication. Moreover, the Sp-methyl phosphotriester induced TT→GT and TT→GC mutations at the flanking TT dinucleotide site, and the induction of these mutations required Ada protein, which is known to remove efficiently the methyl group from the Sp-methyl phosphotriester. Together, our study provided a comprehensive understanding about the recognition of alkyl phosphotriester lesions by DNA replication machinery in cells, and revealed for the first time the Ada-dependent induction of mutations at the Sp-methyl phosphotriester site.

Indexed as

DNA DamageDNA ReplicationMutationAlkylationDNA, BacterialDNA-Directed DNA PolymeraseDNA RepairEscherichia coliEscherichia coli ProteinsMutagenesisO(6)-Methylguanine-DNA MethyltransferaseStereoisomerismTranscription FactorsAda protein, E coliDNA, BacterialDNA-Directed DNA PolymeraseEscherichia coli ProteinsO(6)-Methylguanine-DNA MethyltransferaseTranscription Factors

Identifiers

PMID29514270
PMCPMC5934668
OpenAlexW2793104416

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.