Evidence map›Paper›PMID 30610294›Full record

ReviewCurrent genetics2019

Versatility of the Mec1

Isaac Corcoles-Saez, Kangzhen Dong, Rita S Cha

Open access · hybridAbstract readReview
In one paragraph

Review in Current genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing 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

19 citing papers in PubMed, 30 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

3 authors at 1 institution in 1 country.

Isaac Corcoles-SaezSchool of Medical Sciences and North West Cancer Research Institute, Bangor University, Bangor, LL57 2UW, UK. i.corcoles-saez@bangor.ac.uk.
Kangzhen DongSchool of Medical Sciences and North West Cancer Research Institute, Bangor University, Bangor, LL57 2UW, UK.
Rita S ChaSchool of Medical Sciences and North West Cancer Research Institute, Bangor University, Bangor, LL57 2UW, UK. r.cha@bangor.ac.uk.ORCID http://orcid.org/0000-0001-8223-1520
Bangor University · GB

Funding

North West Cancer Research Fund CR1024North West Cancer Research Fund CR961
6 · The paper itself

Abstract

The ataxia-telangiectasia mutated/ATM and Rad3-related (ATM/ATR) family proteins are evolutionarily conserved serine/threonine kinases best known for their roles in mediating the DNA damage response. Upon activation, ATM/ATR phosphorylate numerous targets to stabilize stalled replication forks, repair damaged DNA, and inhibit cell cycle progression to ensure survival of the cell and safeguard integrity of the genome. Intriguingly, separation of function alleles of the human ATM and MEC1, the budding yeast ATM/ATR, were shown to confer widespread protein aggregation and acute sensitivity to different types of proteotoxic agents including heavy metal, amino acid analogue, and an aggregation-prone peptide derived from the Huntington's disease protein. Further analyses unveiled that ATM and Mec1 promote resistance to perturbation in protein homeostasis via a mechanism distinct from the DNA damage response. In this minireview, we summarize the key findings and discuss ATM/ATR as a multifaceted signalling protein capable of mediating cellular response to both DNA and protein damage.

Indexed as

DNA DamageDNA RepairDNA ReplicationOxidative StressProteostasisAtaxia Telangiectasia Mutated ProteinsHumansSignal TransductionAtaxia Telangiectasia Mutated ProteinsATM protein, humanATR protein, humanAmino acid analoguesATM/ATRCheckpoint kinasesDun1Heavy metalsHuntingtinMec1ProteostasisProteotoxic stressRad53Sml1

Identifiers

PMID30610294
PMCPMC6510830
OpenAlexW2907341146

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.