Evidence map›Paper›PMID 30700723›Full record

ArticleNature communications2019

ATM phosphorylation of the actin-binding protein drebrin controls oxidation stress-resistance in mammalian neurons and C. elegans.

Patricia Kreis, Christian Gallrein, Eugenia Rojas-Puente, Till G A Mack, Cristina Kroon, Viktor Dinkel, Claudia Willmes, Kai Murk, Susanne Tom-Dieck, Erin M Schuman and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. 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
1.6field-weighted citation impact, top 17% 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, 36 citations in OpenAlex.

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  11. PGEThe EMBO journal · 2022
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  17. ATM at the crossroads of reactive oxygen species and autophagy.International journal of biological sciences · 2021
    Review
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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

12 authors at 3 institutions in 1 country.

Patricia KreisInstitute of Biochemistry, Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany. patricia.kreis@charite.de.
Christian GallreinLeibniz-Research Institute for Molecular Pharmacology (FMP), Robert-Roessle-Straße 10, 13125, Berlin, Germany.
Eugenia Rojas-PuenteInstitute of Biochemistry, Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany.
Till G A MackInstitute of Biochemistry, Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany.
Cristina KroonInstitute of Biochemistry, Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany.
Viktor DinkelInstitute of Biochemistry, Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany.
Claudia WillmesInstitute of Biochemistry, Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany.
Kai MurkInstitute of Biochemistry, Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany.
Susanne Tom-DieckMax Planck Institute for Brain Research, Max-von-Laue Strasse 4, 60438, Frankfurt, Germany.
Erin M SchumanMax Planck Institute for Brain Research, Max-von-Laue Strasse 4, 60438, Frankfurt, Germany.ORCID http://orcid.org/0000-0001-7505-1855
Janine KirsteinLeibniz-Research Institute for Molecular Pharmacology (FMP), Robert-Roessle-Straße 10, 13125, Berlin, Germany. kirstein@fmp-berlin.de.ORCID http://orcid.org/0000-0003-4990-2497
Britta J EickholtInstitute of Biochemistry, Charité - Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany. britta.eickholt@charite.de.
Charité - Universitätsmedizin Berlin · DELeibniz Association · DEMax Planck Institute for Brain Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Drebrin (DBN) regulates cytoskeletal functions during neuronal development, and is thought to contribute to structural and functional synaptic changes associated with aging and Alzheimer's disease. Here we show that DBN coordinates stress signalling with cytoskeletal dynamics, via a mechanism involving kinase ataxia-telangiectasia mutated (ATM). An excess of reactive oxygen species (ROS) stimulates ATM-dependent phosphorylation of DBN at serine-647, which enhances protein stability and accounts for improved stress resilience in dendritic spines. We generated a humanized DBN Caenorhabditis elegans model and show that a phospho-DBN mutant disrupts the protective ATM effect on lifespan under sustained oxidative stress. Our data indicate a master regulatory function of ATM-DBN in integrating cytosolic stress-induced signalling with the dynamics of actin remodelling to provide protection from synapse dysfunction and ROS-triggered reduced lifespan. They further suggest that DBN protein abundance governs actin filament stability to contribute to the consequences of oxidative stress in physiological and pathological conditions.

Indexed as

Oxidative StressActinsAlzheimer DiseaseAmino Acid MotifsAnimalsAtaxia Telangiectasia Mutated ProteinsCaenorhabditis elegansCells, CulturedDendritic SpinesFemaleHumansMaleMiceMice, Inbred C57BLMice, KnockoutNeuronsActinsAtaxia Telangiectasia Mutated ProteinsAtm protein, mousedrebrinsNeuropeptidesReactive Oxygen Species

Identifiers

PMID30700723
PMCPMC6353951
OpenAlexW2912076408

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.