Evidence map›Paper›PMID 31816862›Full record

ReviewInternational journal of molecular sciences2019

DNA Oxidation and Excision Repair Pathways.

Tae-Hee Lee, Tae-Hong Kang

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 100 citations in OpenAlex.

  1. Relationship betweenMedicina (Kaunas, Lithuania) · 2024
    Pooled it
  2. Review
  3. Article
  4. Ribonucleotide errors, RNase HII, and ribonucleotide excision repair.Critical reviews in biochemistry and molecular biology · 2026
    Review
  5. DNA Damage and Repair in Pancreatic Cancer-The Latest Findings.International journal of molecular sciences · 2025
    Review
  6. Transcription-Coupled Repair and R-Loop Crosstalk in Genome Stability.International journal of molecular sciences · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Mutation and apoptosis are well-coordinated for protecting against DNA damage-inducing toxicity in Drosophila.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2023
    Article
  17. Article
  18. Review
  19. Neuroprotective Effect ofBioengineering (Basel, Switzerland) · 2022
    Article
  20. 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

2 authors at 1 institution in 1 country.

Tae-Hee LeeDepartment of Biological Science, Dong-A University, Busan 49315, Korea.
Tae-Hong KangDepartment of Biological Science, Dong-A University, Busan 49315, Korea.
Dong-A University · KR

Funding

National Research Foundation of Korea (NRF) funded by the Ministry of Education NRF-2018R1D1A3B07043817 and NRF-2015R1D1A1A01056994
6 · The paper itself

Abstract

The physiological impact of the aberrant oxidation products on genomic DNA were demonstrated by embryonic lethality or the cancer susceptibility and/or neurological symptoms of animal impaired in the base excision repair (BER); the major pathway to maintain genomic integrity against non-bulky DNA oxidation. However, growing evidence suggests that other DNA repair pathways or factors that are not primarily associated with the classical BER pathway are also actively involved in the mitigation of oxidative assaults on the genomic DNA, according to the corresponding types of DNA oxidation. Among others, factors dedicated to lesion recognition in the nucleotide excision repair (NER) pathway have been shown to play eminent roles in the process of lesion recognition and stimulation of the enzyme activity of some sets of BER factors. Besides, substantial bulky DNA oxidation can be preferentially removed by a canonical NER mechanism; therefore, loss of function in the NER pathway shares common features arising from BER defects, including cancer predisposition and neurological disorders, although NER defects generally are nonlethal. Here we discuss recent achievements for delineating newly arising roles of NER lesion recognition factors to facilitate the BER process, and cooperative works of BER and NER pathways in response to the genotoxic oxidative stress.

Indexed as

DNA RepairAnimalsDNAHealthHumansKineticsModels, BiologicalOxidation-ReductionDNAbase excision repair (BER)nucleotide excision repair (NER)oxidative DNA damagereactive oxygen species (ROS)

Identifiers

PMID31816862
PMCPMC6929053
OpenAlexW2993258893

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.