Evidence map›Paper›PMID 38338943›Full record

ArticleInternational journal of molecular sciences2024

The ATM Ser49Cys Variant Effects ATM Function as a Regulator of Oncogene-Induced Senescence.

Caroline Atkinson, Aideen M McInerney-Leo, Martina Proctor, Catherine Lanagan, Alexander J Stevenson, Farhad Dehkhoda, Mary Caole, Ellie Maas, Stephen Ainger, Antonia L Pritchard and 6 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.2field-weighted citation impact, top 47% 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

0 citing papers in PubMed, 1 citations in OpenAlex.

No citing paper in PubMed yet.

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

16 authors at 4 institutions in 2 countries.

Caroline AtkinsonMater Research Institute, The University of Queensland, Brisbane, QLD 4102, Australia.
Aideen M McInerney-LeoDermatology Research Centre, Frazer Institute, The University of Queensland, Brisbane, QLD 4102, Australia.
Martina ProctorMater Research Institute, The University of Queensland, Brisbane, QLD 4102, Australia.
Catherine LanaganMater Research Institute, The University of Queensland, Brisbane, QLD 4102, Australia.
Alexander J StevensonMater Research Institute, The University of Queensland, Brisbane, QLD 4102, Australia.
Farhad DehkhodaDermatology Research Centre, Frazer Institute, The University of Queensland, Brisbane, QLD 4102, Australia.ORCID 0000-0002-6485-9952
Mary CaoleMater Research Institute, The University of Queensland, Brisbane, QLD 4102, Australia.
Ellie MaasDermatology Research Centre, Frazer Institute, The University of Queensland, Brisbane, QLD 4102, Australia.ORCID 0000-0002-1035-7279
Stephen AingerDermatology Research Centre, Frazer Institute, The University of Queensland, Brisbane, QLD 4102, Australia.
Antonia L PritchardQueensland Institute for Medical Research Berghofer, Brisbane, QLD 4006, Australia.
Peter A JohanssonQueensland Institute for Medical Research Berghofer, Brisbane, QLD 4006, Australia.
Paul LeoCentre of Genomics and Personalised Health, Queensland University of Technology, Brisbane, QLD 4059, Australia.
Nicholas K HaywardQueensland Institute for Medical Research Berghofer, Brisbane, QLD 4006, Australia.
Richard A SturmDermatology Research Centre, Frazer Institute, The University of Queensland, Brisbane, QLD 4102, Australia.
Emma L DuncanDepartment of Twin Research and Genetic Epidemiology, School of Life Course & Population Sciences, Faculty of Life Sciences and Medicine, King's College London, London SE1 1UL, UK.
Brian GabrielliMater Research Institute, The University of Queensland, Brisbane, QLD 4102, Australia.ORCID 0000-0003-3933-1651
The University of Queensland · AUQIMR Berghofer Medical Research Institute · AUKing's College London · GBQueensland University of Technology · AU

Funding

Mater Foundation-Smiling for Smiddy n/aNational Health and Medical Research Council 1104186
6 · The paper itself

Abstract

An apical component of the cell cycle checkpoint and DNA damage repair response is the ataxia-telangiectasia mutated (ATM) Ser/Thr protein kinase. A variant of ATM, Ser49Cys (rs1800054; minor allele frequency = 0.011), has been associated with an elevated risk of melanoma development; however, the functional consequence of this variant is not defined. ATM-dependent signalling in response to DNA damage has been assessed in a panel of patient-derived lymphoblastoid lines and primary human melanocytic cell strains heterozygous for the ATM Ser49Cys variant allele. The ATM Ser49Cys allele appears functional for acute p53-dependent signalling in response to DNA damage. Expression of the variant allele did reduce the efficacy of oncogene expression in inducing senescence. These findings demonstrate that the

Indexed as

Ataxia Telangiectasia Mutated ProteinsMelanomaAtaxia TelangiectasiaCell Cycle ProteinsDNA-Binding ProteinsDNA DamageHumansOncogenesPhosphorylationProtein Serine-Threonine KinasesTumor Suppressor Protein p53Tumor Suppressor ProteinsAtaxia Telangiectasia Mutated ProteinsATM protein, humanCell Cycle ProteinsDNA-Binding ProteinsProtein Serine-Threonine KinasesTumor Suppressor Protein p53Tumor Suppressor ProteinsATMDNA damageionising radiationp53senescence

Identifiers

PMID38338943
PMCPMC10855307
OpenAlexW4391310297

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.