Evidence map›Paper›PMID 30174298›Full record

ReviewDNA repair2018

Structural basis of DNA lesion recognition for eukaryotic transcription-coupled nucleotide excision repair.

Wei Wang, Jun Xu, Jenny Chong, Dong Wang

Open access · greenAbstract readReview
In one paragraph

Review in DNA repair, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

39 citing papers in PubMed, 64 citations in OpenAlex.

  1. Topology Resetting During Transcription-Coupled Nucleotide Excision Repair.International journal of molecular sciences · 2026
    Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Transcription-Coupled Repair and R-Loop Crosstalk in Genome Stability.International journal of molecular sciences · 2025
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Elf1 promotes Rad26's interaction with lesion-arrested Pol II for transcription-coupled repair.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  15. Article
  16. New roles for elongation factors in RNA polymerase II ubiquitylation and degradation.Biochimica et biophysica acta. Gene regulatory mechanisms · 2023
    Review
  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.

Wei WangDivision of Pharmaceutical Sciences, Skaggs School of Pharmacy & Pharmaceutical Sciences, University of California San Diego, La Jolla, CA, 92093, United States.
Jun XuDivision of Pharmaceutical Sciences, Skaggs School of Pharmacy & Pharmaceutical Sciences, University of California San Diego, La Jolla, CA, 92093, United States.
Jenny ChongDivision of Pharmaceutical Sciences, Skaggs School of Pharmacy & Pharmaceutical Sciences, University of California San Diego, La Jolla, CA, 92093, United States; Department of Cellular & Molecular Medicine, University of California San Diego, La Jolla, CA, 92093, United States.
Dong WangDivision of Pharmaceutical Sciences, Skaggs School of Pharmacy & Pharmaceutical Sciences, University of California San Diego, La Jolla, CA, 92093, United States; Department of Cellular & Molecular Medicine, University of California San Diego, La Jolla, CA, 92093, United States. Electronic address: dongwang@ucsd.edu.
University of California, San Diego · US

Funding

Molecular Mechanisms for DNA Damage Processing by Transcription MachineryR01GM102362 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI WANG, DONG · 2013 to 2025
$5.6M
NIGMS NIH HHS R01 GM102362
6 · The paper itself

Abstract

Eukaryotic transcription-coupled nucleotide excision repair (TC-NER) is a pathway that removes DNA lesions capable of blocking RNA polymerase II (Pol II) transcription from the template strand. This process is initiated by lesion-arrested Pol II and the recruitment of Cockayne Syndrome B protein (CSB). In this review, we will focus on the lesion recognition steps of eukaryotic TC-NER and summarize the recent research progress toward understanding the structural basis of Pol II-mediated lesion recognition and Pol II-CSB interactions. We will discuss the roles of CSB in both TC-NER initiation and transcription elongation. Finally, we propose an updated model of tripartite lesion recognition and verification for TC-NER in which CSB ensures Pol II-mediated recognition of DNA lesions for TC-NER.

Indexed as

DNA DamageDNA RepairTranscription, GeneticCockayne SyndromeDNAEukaryotaHumansMolecular StructureDNACockayne syndromeDNA damageLesion recognitionNucleotide excision repairRNA polymerase IITranscriptional arrestTranscription-coupled nucleotide excision repair

Identifiers

PMID30174298
PMCPMC6340766
OpenAlexW2888600868

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.