Evidence map›Paper›PMID 24003211›Full record

ReviewCold Spring Harbor perspectives in biology2013

DNA damage sensing by the ATM and ATR kinases.

Alexandre Maréchal, Lee Zou

Open access · bronzeAbstract readReview
In one paragraph

Review in Cold Spring Harbor perspectives in biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 869 papers.

0numbers the graph read from it
0cells of the map it votes in
869citing 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

869 citing papers in PubMed, 1,460 citations in OpenAlex.

  1. Merkel Cell Polyomavirus and DNA Damage Response.International journal of molecular sciences · 2026
    Review
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809 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 1 institution in 1 country.

Alexandre MaréchalMassachusetts General Hospital Cancer Center, Harvard Medical School, Charlestown, Massachusetts 02129, USA.
Lee Zou
Harvard University · US

Funding

Regulation of the ATR Checkpoint Kinase by DNA DamageR01GM076388 · NIGMS · MASSACHUSETTS GENERAL HOSPITAL · PI ZOU, LEE · 2006 to 2018
$4.3M
NIGMS NIH HHS GM076388NIGMS NIH HHS R01 GM076388
6 · The paper itself

Abstract

In eukaryotic cells, maintenance of genomic stability relies on the coordinated action of a network of cellular processes, including DNA replication, DNA repair, cell-cycle progression, and others. The DNA damage response (DDR) signaling pathway orchestrated by the ATM and ATR kinases is the central regulator of this network in response to DNA damage. Both ATM and ATR are activated by DNA damage and DNA replication stress, but their DNA-damage specificities are distinct and their functions are not redundant. Furthermore, ATM and ATR often work together to signal DNA damage and regulate downstream processes. Here, we will discuss the recent findings and current models of how ATM and ATR sense DNA damage, how they are activated by DNA damage, and how they function in concert to regulate the DDR.

Indexed as

Models, MolecularAtaxia Telangiectasia Mutated ProteinsChromatinDNA DamageReceptor Cross-TalkSignal TransductionAtaxia Telangiectasia Mutated ProteinsATR protein, humanChromatin

Identifiers

PMID24003211
PMCPMC3753707
OpenAlexW2153466677

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.