Evidence map›Paper›PMID 34573351›Full record

ReviewGenes2021

ATM's Role in the Repair of DNA Double-Strand Breaks.

Atsushi Shibata, Penny A Jeggo

Open access · goldAbstract readReview
In one paragraph

Review in Genes, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
5.0field-weighted citation impact, top 3% 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

75 citing papers in PubMed, 110 citations in OpenAlex.

  1. DNA Repair Mechanisms.Methods in molecular biology (Clifton, N.J.) · 2027
    Review
  2. How telomere attrition protects against cancer.Nature reviews. Genetics · 2026
    Review
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15 more citing papers are in PubMed but not listed here.

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 2 institutions in 2 countries.

Atsushi ShibataSignal Transduction Program, Gunma University Initiative for Advanced Research (GIAR), Gunma University, Gunma 371-8511, Japan.ORCID 0000-0001-8912-6977
Penny A JeggoGenome Damage and Stability Centre, School of Life Sciences, University of Sussex, Brighton BN1 9RQ, UK.
Gunma University · JPUniversity of Sussex · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ataxia telangiectasia mutated (ATM) is a central kinase that activates an extensive network of responses to cellular stress via a signaling role. ATM is activated by DNA double strand breaks (DSBs) and by oxidative stress, subsequently phosphorylating a plethora of target proteins. In the last several decades, newly developed molecular biological techniques have uncovered multiple roles of ATM in response to DNA damage-e.g., DSB repair, cell cycle checkpoint arrest, apoptosis, and transcription arrest. Combinational dysfunction of these stress responses impairs the accuracy of repair, consequently leading to dramatic sensitivity to ionizing radiation (IR) in ataxia telangiectasia (A-T) cells. In this review, we summarize the roles of ATM that focus on DSB repair.

Indexed as

DNA Breaks, Double-StrandedDNA RepairApoptosisAtaxia TelangiectasiaAtaxia Telangiectasia Mutated ProteinsCell Cycle CheckpointsChromatinHumansTranscription, GeneticAtaxia Telangiectasia Mutated ProteinsATM protein, humanChromatinATMDNA double-strand breakhomologous recombinationionizing radiationnon-homologous end joining

Identifiers

PMID34573351
PMCPMC8466060
OpenAlexW3196638751

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.