Evidence map›Paper›PMID 38571319›Full record

ArticleCell cycle (Georgetown, Tex.)2024

Homologous recombination contributes to the repair of acetaldehyde-induced DNA damage.

Kosuke Yamazaki, Tomohiro Iguchi, Yutaka Kanoh, Kazuto Takayasu, Trinh Thi To Ngo, Ayaka Onuki, Hideya Kawaji, Shunji Oshima, Tomomasa Kanda, Hisao Masai and 1 more

Open access · greenAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.6field-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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
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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

11 authors at 3 institutions in 1 country.

Kosuke YamazakiDepartment of Basic Medical Sciences, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Tomohiro IguchiDepartment of Basic Medical Sciences, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Yutaka KanohDepartment of Basic Medical Sciences, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Kazuto TakayasuDepartment of Basic Medical Sciences, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Trinh Thi To NgoDepartment of Basic Medical Sciences, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Ayaka OnukiDepartment of Basic Medical Sciences, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Hideya KawajiResearch Center for Genome and Medical Sciences, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Shunji OshimaSustainable Technology Laboratories, Asahi Quality & Innovations Ltd, Ibaraki, Japan.
Tomomasa KandaAsahi Quality & Innovations, Ltd, Ibaraki, Japan.
Hisao MasaiDepartment of Basic Medical Sciences, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Hiroyuki SasanumaDepartment of Basic Medical Sciences, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Tokyo Metropolitan Institute of Medical Science · JPAsahi Breweries (Japan) · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acetaldehyde, a chemical that can cause DNA damage and contribute to cancer, is prevalently present in our environment, e.g. in alcohol, tobacco, and food. Although aldehyde potentially promotes crosslinking reactions among biological substances including DNA, RNA, and protein, it remains unclear what types of DNA damage are caused by acetaldehyde and how they are repaired. In this study, we explored mechanisms involved in the repair of acetaldehyde-induced DNA damage by examining the cellular sensitivity to acetaldehyde in the collection of human TK6 mutant deficient in each genome maintenance system. Among the mutants, mismatch repair mutants did not show hypersensitivity to acetaldehyde, while mutants deficient in base and nucleotide excision repair pathways or homologous recombination (HR) exhibited higher sensitivity to acetaldehyde than did

Indexed as

AcetaldehydeDNA DamageDNA RepairHomologous RecombinationCell LineDNA-Binding ProteinsHumansMutationRad51 RecombinaseAcetaldehydeDNA-Binding ProteinsRad51 RecombinaseacetaldehydeDNA-protein adductsHomologous recombination

Identifiers

PMID38571319
PMCPMC11174073
OpenAlexW4393947042

What OpenQuestion holds

Textmetadata
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.