Evidence map›Paper›PMID 29779899›Full record

ArticleStem cell reports2018

Signaling-Dependent Control of Apical Membrane Size and Self-Renewal in Rosette-Stage Human Neuroepithelial Stem Cells.

Jan-Philip Medelnik, Kathleen Roensch, Satoshi Okawa, Antonio Del Sol, Osvaldo Chara, Levan Mchedlishvili, Elly M Tanaka

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed, 35 citations in OpenAlex.

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  9. The role of lipids in genome integrity and pluripotency.Biochemical Society transactions · 2024
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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

7 authors at 4 institutions in 4 countries.

Jan-Philip MedelnikResearch Institute for Molecular Pathology (IMP), Vienna Biocenter (VBC), Campus-Vienna-Biocenter 1, 1030 Vienna, Austria; DFG Research Center for Regenerative Therapies, Technische Universität Dresden, Fetscherstraße 105, 01307 Dresden, Germany; Max Planck Institute of Molecular Cell Biology and Genetics, Pfotenhauerstraße 108, 01307 Dresden, Germany. Electronic address: jan.medelnik@imp.ac.at.
Kathleen RoenschDFG Research Center for Regenerative Therapies, Technische Universität Dresden, Fetscherstraße 105, 01307 Dresden, Germany; Max Planck Institute of Molecular Cell Biology and Genetics, Pfotenhauerstraße 108, 01307 Dresden, Germany.
Satoshi OkawaComputational Biology Group, Luxembourg Centre for Systems Biomedicine, University of Luxembourg, 6, Avenue du Swing, Belvaux 4367, Luxembourg.
Antonio Del SolComputational Biology Group, Luxembourg Centre for Systems Biomedicine, University of Luxembourg, 6, Avenue du Swing, Belvaux 4367, Luxembourg.
Osvaldo CharaCenter for Information Services and High Performance Computing (ZIH), Technische Universität Dresden, 01062 Dresden, Germany; Systems Biology Group (SysBio), Instituto de Física de Líquidos y Sistemas Biológicos (IFLySIB), CONICET, Universidad Nacional de La Plata (UNLP), B1900BTE, La Plata, Argentina.
Levan MchedlishviliDFG Research Center for Regenerative Therapies, Technische Universität Dresden, Fetscherstraße 105, 01307 Dresden, Germany; Max Planck Institute of Molecular Cell Biology and Genetics, Pfotenhauerstraße 108, 01307 Dresden, Germany.
Elly M TanakaResearch Institute for Molecular Pathology (IMP), Vienna Biocenter (VBC), Campus-Vienna-Biocenter 1, 1030 Vienna, Austria; DFG Research Center for Regenerative Therapies, Technische Universität Dresden, Fetscherstraße 105, 01307 Dresden, Germany; Max Planck Institute of Molecular Cell Biology and Genetics, Pfotenhauerstraße 108, 01307 Dresden, Germany.
Max Planck Institute of Molecular Cell Biology and Genetics · DEUniversity of Luxembourg · LUTU Dresden · DEVienna Biocenter · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the developing nervous system, neural stem cells are polarized and maintain an apical domain facing a central lumen. The presence of apical membrane is thought to have a profound influence on maintaining the stem cell state. With the onset of neurogenesis, cells lose their polarization, and the concomitant loss of the apical domain coincides with a loss of the stem cell identity. Little is known about the molecular signals controlling apical membrane size. Here, we use two neuroepithelial cell systems, one derived from regenerating axolotl spinal cord and the other from human embryonic stem cells, to identify a molecular signaling pathway initiated by lysophosphatidic acid that controls apical membrane size and consequently controls and maintains epithelial organization and lumen size in neuroepithelial rosettes. This apical domain size increase occurs independently of effects on proliferation and involves a serum response factor-dependent transcriptional induction of junctional and apical membrane components.

Indexed as

Cell Self RenewalNeurogenesisSignal TransductionBiomarkersCell Culture TechniquesCell DifferentiationCell MembraneCell PolarityCell ProliferationEmbryonic Stem CellsFluorescent Antibody TechniqueGene ExpressionHumansLysophospholipidsNeural Stem CellsNeuroepithelial CellsBiomarkerslysophosphatidic acidLysophospholipidsapical domaincell polarizationhuman embryonic stem cellslumen formation/organizationlysophosphatidic acidneural progenitor cellsneural rosettesneural stem cellsneuroepithelial cells

Identifiers

PMID29779899
PMCPMC5993681
OpenAlexW2783440722

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.