Evidence map›Paper›PMID 29759113›Full record

ArticleeLife2018

Distinct roles of ATM and ATR in the regulation of ARP8 phosphorylation to prevent chromosome translocations.

Jiying Sun, Lin Shi, Aiko Kinomura, Atsuhiko Fukuto, Yasunori Horikoshi, Yukako Oma, Masahiko Harata, Masae Ikura, Tsuyoshi Ikura, Roland Kanaar and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in eLife, 2018. 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
–field-weighted citation impact
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.

  1. Article
  2. Strong Shift to ATR-Dependent Regulation of the GLife (Basel, Switzerland) · 2021
    Article
  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

11 authors.

Jiying SunDepartment of Cellular Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.ORCID 0000-0002-0563-1245
Lin ShiDepartment of Cellular Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Aiko KinomuraDepartment of Cellular Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Atsuhiko FukutoDepartment of Cellular Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Yasunori HorikoshiDepartment of Cellular Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.
Yukako OmaLaboratory of Molecular Biology, Graduate School of Agricultural Science, Tohoku University, Sendai, Japan.
Masahiko HarataLaboratory of Molecular Biology, Graduate School of Agricultural Science, Tohoku University, Sendai, Japan.
Masae IkuraLaboratory of Chromatin Regulatory Network, Department of Mutagenesis, Radiation Biology Center, Kyoto University, Kyoto, Japan.
Tsuyoshi IkuraLaboratory of Chromatin Regulatory Network, Department of Mutagenesis, Radiation Biology Center, Kyoto University, Kyoto, Japan.
Roland KanaarDepartment of Molecular Genetics, Oncode Institute, Rotterdam, Netherlands.ORCID 0000-0001-9364-8727
Satoshi TashiroDepartment of Cellular Biology, Research Institute for Radiation Biology and Medicine, Hiroshima University, Hiroshima, Japan.ORCID 0000-0001-7331-157X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chromosomal translocations are hallmarks of various types of cancers and leukemias. However, the molecular mechanisms of chromosome translocations remain largely unknown. The ataxia-telangiectasia mutated (ATM) protein, a DNA damage signaling regulator, facilitates DNA repair to prevent chromosome abnormalities. Previously, we showed that ATM deficiency led to the 11q23 chromosome translocation, the most frequent chromosome abnormalities in secondary leukemia. Here, we show that ARP8, a subunit of the INO80 chromatin remodeling complex, is phosphorylated after etoposide treatment. The etoposide-induced phosphorylation of ARP8 is regulated by ATM and ATR, and attenuates its interaction with INO80. The ATM-regulated phosphorylation of ARP8 reduces the excessive loading of INO80 and RAD51 onto the breakpoint cluster region. These findings suggest that the phosphorylation of ARP8, regulated by ATM, plays an important role in maintaining the fidelity of DNA repair to prevent the etoposide-induced 11q23 abnormalities.

Indexed as

Protein Processing, Post-TranslationalTranslocation, GeneticAtaxia Telangiectasia Mutated ProteinsATPases Associated with Diverse Cellular ActivitiesCell LineDNA-Binding ProteinsDNA HelicasesDNA RepairEtoposideHumansMicrofilament ProteinsPhosphorylationRad51 RecombinaseACTR8 protein, humanAtaxia Telangiectasia Mutated ProteinsATM protein, humanATPases Associated with Diverse Cellular ActivitiesATR protein, humanDNA-Binding ProteinsDNA HelicasesEtoposideINO80 protein, humanMicrofilament ProteinsRAD51 protein, humanRad51 RecombinaseARP8 phosphorylationATMATRchromosomeschromosome translocationsgene expressionhumanINO80RAD51

Identifiers

PMID29759113
PMCPMC5953535

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Registered trials

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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.