Evidence map›Paper›PMID 25247188›Full record

ReviewBioMed research international2014

Multifunctional role of ATM/Tel1 kinase in genome stability: from the DNA damage response to telomere maintenance.

Enea Gino Di Domenico, Elena Romano, Paola Del Porto, Fiorentina Ascenzioni

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

22 citing papers in PubMed, 41 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

4 authors at 2 institutions in 1 country.

Enea Gino Di DomenicoPasteur Institute-Cenci Bolognetti Foundation, Department of Biology and Biotechnology "Charles Darwin", Sapienza University of Rome, 00185 Rome, Italy.ORCID 0000-0001-6295-6006
Elena RomanoDepartment of Biology and Biotechnology "Charles Darwin", Sapienza University of Rome, 00185 Rome, Italy.ORCID 0000-0003-0343-5125
Paola Del PortoDepartment of Biology and Biotechnology "Charles Darwin", Sapienza University of Rome, 00185 Rome, Italy.ORCID 0000-0003-4802-8910
Fiorentina AscenzioniPasteur Institute-Cenci Bolognetti Foundation, Department of Biology and Biotechnology "Charles Darwin", Sapienza University of Rome, 00185 Rome, Italy.ORCID 0000-0001-8725-9207
Istituto Pasteur · ITSapienza University of Rome · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mammalian protein kinase ataxia telangiectasia mutated (ATM) is a key regulator of the DNA double-strand-break response and belongs to the evolutionary conserved phosphatidylinositol-3-kinase-related protein kinases. ATM deficiency causes ataxia telangiectasia (AT), a genetic disorder that is characterized by premature aging, cerebellar neuropathy, immunodeficiency, and predisposition to cancer. AT cells show defects in the DNA damage-response pathway, cell-cycle control, and telomere maintenance and length regulation. Likewise, in Saccharomyces cerevisiae, haploid strains defective in the TEL1 gene, the ATM ortholog, show chromosomal aberrations and short telomeres. In this review, we outline the complex role of ATM/Tel1 in maintaining genomic stability through its control of numerous aspects of cellular survival. In particular, we describe how ATM/Tel1 participates in the signal transduction pathways elicited by DNA damage and in telomere homeostasis and its importance as a barrier to cancer development.

Indexed as

AnimalsAtaxia Telangiectasia Mutated ProteinsCell SurvivalDNADNA DamageGenomic InstabilityHumansTelomereTelomere HomeostasisAtaxia Telangiectasia Mutated ProteinsDNA

Identifiers

PMID25247188
PMCPMC4163350
OpenAlexW2025699269

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.