Evidence map›Paper›PMID 31845986›Full record

ArticleJournal of radiation research2020

Oxidation resistance 1 prevents genome instability through maintenance of G2/M arrest in gamma-ray-irradiated cells.

Ako Matsui, Junya Kobayashi, Shin-Ichiro Kanno, Kazunari Hashiguchi, Masahiro Miyaji, Yukihiro Yoshikawa, Akira Yasui, Qiu-Mei Zhang-Akiyama

Open access · goldAbstract read
In one paragraph

Article in Journal of radiation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed, 11 citations in OpenAlex.

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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

8 authors at 3 institutions in 1 country.

Ako MatsuiLaboratory of Stress Response Biology, Department of Zoology, Division of Biological Sciences, Graduate School of Science, Kyoto University, Kitashirakawa-Oiwakecho, Sakyo-ku, Kyoto 606-8502, Japan.
Junya KobayashiDepartment of Genome Dynamics, Radiation Biology Center, Graduate School of Biostudies, Kyoto University, Yoshidakonoe-cho, Sakyo-ku, Kyoto 606-8501, Japan.
Shin-Ichiro KannoDivision of Dynamic Proteome in Cancer and Aging, Institute of Development, Aging and Cancer, Tohoku University, 4-1 Seiryocho, Aobaku, Sendai 980-8575, Japan.
Kazunari HashiguchiLaboratory of Stress Response Biology, Department of Zoology, Division of Biological Sciences, Graduate School of Science, Kyoto University, Kitashirakawa-Oiwakecho, Sakyo-ku, Kyoto 606-8502, Japan.
Masahiro MiyajiLaboratory of Stress Response Biology, Department of Zoology, Division of Biological Sciences, Graduate School of Science, Kyoto University, Kitashirakawa-Oiwakecho, Sakyo-ku, Kyoto 606-8502, Japan.
Yukihiro YoshikawaLaboratory of Stress Response Biology, Department of Zoology, Division of Biological Sciences, Graduate School of Science, Kyoto University, Kitashirakawa-Oiwakecho, Sakyo-ku, Kyoto 606-8502, Japan.
Akira YasuiDivision of Dynamic Proteome in Cancer and Aging, Institute of Development, Aging and Cancer, Tohoku University, 4-1 Seiryocho, Aobaku, Sendai 980-8575, Japan.
Qiu-Mei Zhang-AkiyamaLaboratory of Stress Response Biology, Department of Zoology, Division of Biological Sciences, Graduate School of Science, Kyoto University, Kitashirakawa-Oiwakecho, Sakyo-ku, Kyoto 606-8502, Japan.
Kyoto University · JPTohoku University · JPFukuoka Dental College · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human oxidation resistance 1 (OXR1) was identified as a protein that decreases genomic mutations in Escherichia coli caused by oxidative DNA damage. However, the mechanism by which OXR1 defends against genome instability has not been elucidated. To clarify how OXR1 maintains genome stability, the effects of OXR1-depletion on genome stability were investigated in OXR1-depleted HeLa cells using gamma-rays (γ-rays). The OXR1-depleted cells had higher levels of superoxide and micronucleus (MN) formation than control cells after irradiation. OXR1-overexpression alleviated the increases in reactive oxygen species (ROS) level and MN formation after irradiation. The increased MN formation in irradiated OXR1-depleted cells was partially attenuated by the ROS inhibitor N-acetyl-L-cysteine, suggesting that OXR1-depeletion increases ROS-dependent genome instability. We also found that OXR1-depletion shortened the duration of γ-ray-induced G2/M arrest. In the presence of the cell cycle checkpoint inhibitor caffeine, the level of MN formed after irradiation was similar between control and OXR1-depleted cells, demonstrating that OXR1-depletion accelerates MN formation through abrogation of G2/M arrest. In OXR1-depleted cells, the level of cyclin D1 protein expression was increased. Here we report that OXR1 prevents genome instability by cell cycle regulation as well as oxidative stress defense.

Indexed as

Gamma RaysG2 Phase Cell Cycle CheckpointsGenomic InstabilityHeLa CellsHumansHydrogen PeroxideMicronucleus, GermlineMitochondrial ProteinsMitosisModels, BiologicalOxidative StressSuperoxidesHydrogen PeroxideMitochondrial ProteinsOXR1 protein, humanSuperoxidescell cycle arrestgenome stabilityoxidative stressOXR1radiation

Identifiers

PMID31845986
PMCPMC6976731
OpenAlexW2995245944

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.