Evidence map›Paper›PMID 28698371›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Deletion of Gas2l3 in mice leads to specific defects in cardiomyocyte cytokinesis during development.

Sabine Stopp, Marco Gründl, Marc Fackler, Jonas Malkmus, Marina Leone, Ronald Naumann, Stefan Frantz, Elmar Wolf, Björn von Eyss, Felix B Engel and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

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  16. GAS2L3: Coordinator of cardiomyocyte cytokinesis?Cell cycle (Georgetown, Tex.) · 2017
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 1 country.

Sabine StoppTheodor Boveri Institute, Biocenter, University of Wuerzburg, 97074 Wuerzburg, Germany.
Marco GründlTheodor Boveri Institute, Biocenter, University of Wuerzburg, 97074 Wuerzburg, Germany.
Marc FacklerTheodor Boveri Institute, Biocenter, University of Wuerzburg, 97074 Wuerzburg, Germany.
Jonas MalkmusTheodor Boveri Institute, Biocenter, University of Wuerzburg, 97074 Wuerzburg, Germany.
Marina LeoneExperimental Renal and Cardiovascular Research, Institute of Pathology, Department of Nephropathology, Friedrich-Alexander-Universität Erlangen-Nürnberg, 91054 Erlangen, Germany.
Ronald NaumannTransgenic Core Facility, Max-Planck-Institute of Molecular Cell Biology and Genetics, 01307 Dresden, Germany.
Stefan FrantzDepartment of Internal Medicine I, University Hospital Würzburg, 97080 Wuerzburg, Germany.
Elmar WolfTheodor Boveri Institute, Biocenter, University of Wuerzburg, 97074 Wuerzburg, Germany.
Björn von EyssTheodor Boveri Institute, Biocenter, University of Wuerzburg, 97074 Wuerzburg, Germany.
Felix B EngelExperimental Renal and Cardiovascular Research, Institute of Pathology, Department of Nephropathology, Friedrich-Alexander-Universität Erlangen-Nürnberg, 91054 Erlangen, Germany.
Stefan GaubatzTheodor Boveri Institute, Biocenter, University of Wuerzburg, 97074 Wuerzburg, Germany; stefan.gaubatz@biozentrum.uni-wuerzburg.de.
University of Würzburg · DEFriedrich-Alexander-Universität Erlangen-Nürnberg · DEMax Planck Institute of Molecular Cell Biology and Genetics · DEUniversitätsklinikum Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

GAS2L3 is a recently identified cytoskeleton-associated protein that interacts with actin filaments and tubulin. The in vivo function of GAS2L3 in mammals remains unknown. Here, we show that mice deficient in GAS2L3 die shortly after birth because of heart failure. Mammalian cardiomyocytes lose the ability to proliferate shortly after birth, and further increase in cardiac mass is achieved by hypertrophy. The proliferation arrest of cardiomyocytes is accompanied by binucleation through incomplete cytokinesis. We observed that GAS2L3 deficiency leads to inhibition of cardiomyocyte proliferation and to cardiomyocyte hypertrophy during embryonic development. Cardiomyocyte-specific deletion of GAS2L3 confirmed that the phenotype results from the loss of GAS2L3 in cardiomyocytes. Cardiomyocytes from

Indexed as

CytokinesisAnimalsCardiomyopathy, DilatedCyclin-Dependent Kinase Inhibitor p21Cytoskeletal ProteinsFibrosisGene DeletionGene Expression RegulationMiceMice, KnockoutMyocardiumMyocytes, CardiacTumor Suppressor Protein p53Cyclin-Dependent Kinase Inhibitor p21Cytoskeletal ProteinsGAS2L3 protein, mouseTumor Suppressor Protein p53binucleationcardiomyocytescytokinesisGAS2L3

Identifiers

PMID28698371
PMCPMC5544300
OpenAlexW2736292045

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.