Evidence map›Paper›PMID 26400162›Full record

ArticleNucleic acids research2015

Cytotoxic and mutagenic properties of O4-alkylthymidine lesions in Escherichia coli cells.

Pengcheng Wang, Nicholas J Amato, Qianqian Zhai, Yinsheng Wang

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Metabolic Activation and DNA Interactions of CarcinogenicInternational journal of molecular sciences · 2022
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. DNA replication studies ofThe Journal of biological chemistry · 2019
    Article
  12. Cytotoxic and mutagenic properties ofThe Journal of biological chemistry · 2018
    Article
  13. Article
  14. Article
  15. Chemical Analysis of DNA Damage.Analytical chemistry · 2018
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Pengcheng WangEnvironmental Toxicology Graduate Program,University of California, Riverside, CA 92521-0403, USA.
Nicholas J AmatoDepartment of Chemistry, University of California, Riverside, CA 92521-0403, USA.
Qianqian ZhaiDepartment of Chemistry, University of California, Riverside, CA 92521-0403, USA.
Yinsheng WangEnvironmental Toxicology Graduate Program,University of California, Riverside, CA 92521-0403, USA Department of Chemistry, University of California, Riverside, CA 92521-0403, USA Yinsheng.Wang@ucr.edu.
University of California, Riverside · US

Funding

Research Training in Environmental ToxicologyT32ES018827 · NIEHS · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI Yinsheng Wang · 2010 to 2026
$5.3M
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 ES025121NIEHS NIH HHS T32 ES018827
6 · The paper itself

Abstract

Due to the abundant presence of alkylating agents in living cells and the environment, DNA alkylation is generally unavoidable. Among the alkylated DNA lesions, O(4)-alkylthymidine (O(4)-alkyldT) are known to be highly mutagenic and persistent in mammalian tissues. Not much is known about how the structures of the alkyl group affect the repair and replicative bypass of the O(4)-alkyldT lesions, or how the latter process is modulated by translesion synthesis polymerases. Herein, we synthesized oligodeoxyribonucleotides harboring eight site-specifically inserted O(4)-alkyldT lesions and examined their impact on DNA replication in Escherichia coli cells. We showed that the replication past all the O(4)-alkyldT lesions except (S)- and (R)-sBudT was highly efficient, and these lesions directed very high frequencies of dGMP misincorporation in E. coli cells. While SOS-induced DNA polymerases play redundant roles in bypassing most of the O(4)-alkyldT lesions, the bypass of (S)- and (R)-sBudT necessitated Pol V. Moreover, Ada was not involved in the repair of any O(4)-alkyldT lesions, Ogt was able to repair O(4)-MedT and, to a lesser extent, O(4)-EtdT and O(4)-nPrdT, but not other O(4)-alkyldT lesions. Together, our study provided important new knowledge about the repair of the O(4)-alkyldT lesions and their recognition by the E. coli replication machinery.

Indexed as

DNA RepairDNA ReplicationMutagenesisDNA AdductsDNA DamageDNA-Directed DNA PolymeraseEscherichia coliMutationSOS Response, GeneticsThymidineDNA AdductsDNA-Directed DNA PolymeraseThymidine

Identifiers

PMID26400162
PMCPMC4678858
OpenAlexW1452050606

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.