Evidence map›Paper›PMID 34219128›Full record

ArticleScientific reports2021

Exposure of the cytoplasm to low-dose X-rays modifies ataxia telangiectasia mutated-mediated DNA damage responses.

Munetoshi Maeda, Masanori Tomita, Mika Maeda, Hideki Matsumoto, Noriko Usami, Kyo Kume, Katsumi Kobayashi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.4field-weighted citation impact, top 41% 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

3 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Low-Dose Non-Targeted Effects and Mitochondrial Control.International journal of molecular sciences · 2023
    Review
  3. 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

7 authors at 4 institutions in 1 country.

Munetoshi MaedaProton Medical Research Division, Research and Development Department, The Wakasa Wan Energy Research Center, WERC, 64-52-1 Nagatani, Tsuruga, Fukui, 914-0192, Japan. mmaeda@werc.or.jp.
Masanori TomitaRadiation Safety Research Center, Nuclear Technology Research Laboratory, Central Research Institute of Electric Power Industry, CRIEPI, 2-11-1 Iwado Kita, Komae, Tokyo, 201-8511, Japan.
Mika MaedaProton Medical Research Division, Research and Development Department, The Wakasa Wan Energy Research Center, WERC, 64-52-1 Nagatani, Tsuruga, Fukui, 914-0192, Japan.
Hideki MatsumotoDepartment of Experimental Radiology and Health Physics, Faculty of Medical Sciences, University of Fukui, 23-3 Matsuoka-Shimoaitsuki, Eiheiji-cho, Fukui, 910-1193, Japan.
Noriko UsamiPhoton Factory, Institute of Materials Structure Science, High Energy Accelerator Research Organization, KEK, 1-1 Oho, Tsukuba, Ibaraki, 305-0801, Japan.
Kyo KumeProton Medical Research Division, Research and Development Department, The Wakasa Wan Energy Research Center, WERC, 64-52-1 Nagatani, Tsuruga, Fukui, 914-0192, Japan.
Katsumi KobayashiPhoton Factory, Institute of Materials Structure Science, High Energy Accelerator Research Organization, KEK, 1-1 Oho, Tsukuba, Ibaraki, 305-0801, Japan.
Foundation Wakasa Wan Energy Research Center · JPHigh Energy Accelerator Research Organization · JPCentral Research Institute of Electric Power Industry · JPUniversity of Fukui · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We recently showed that when a low X-ray dose is used, cell death is enhanced in nucleus-irradiated compared with whole-cell-irradiated cells; however, the role of the cytoplasm remains unclear. Here, we show changes in the DNA damage responses with or without X-ray microbeam irradiation of the cytoplasm. Phosphorylated histone H2AX foci, a surrogate marker for DNA double-strand breaks, in V79 and WI-38 cells are not observed in nucleus irradiations at ≤ 2 Gy, whereas they are observed in whole-cell irradiations. Addition of an ataxia telangiectasia mutated (ATM) kinase inhibitor to whole-cell irradiations suppresses foci formation at ≤ 2 Gy. ABL1 and p73 expression is upregulated following nucleus irradiation, suggesting the induction of p73-dependent cell death. Furthermore, CDKN1A (p21) is upregulated following whole-cell irradiation, indicating the induction of cell cycle arrest. These data reveal that cytoplasmic radioresponses modify ATM-mediated DNA damage responses and determine the fate of cells irradiated at low doses.

Indexed as

DNA Breaks, Double-StrandedDNA RepairSignal TransductionAnimalsAtaxia Telangiectasia Mutated ProteinsCell Cycle CheckpointsCell LineCricetulusCyclin-Dependent Kinase Inhibitor p21CytoplasmDNADNA DamageHumansAtaxia Telangiectasia Mutated ProteinsCyclin-Dependent Kinase Inhibitor p21DNA

Identifiers

PMID34219128
PMCPMC8255317
OpenAlexW3179383019

What OpenQuestion holds

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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.