Evidence map›Paper›PMID 29500351›Full record

ArticleNature communications2018

Nfat/calcineurin signaling promotes oligodendrocyte differentiation and myelination by transcription factor network tuning.

Matthias Weider, Laura Julia Starost, Katharina Groll, Melanie Küspert, Elisabeth Sock, Miriam Wedel, Franziska Fröb, Christian Schmitt, Tina Baroti, Anna C Hartwig and 12 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 81 citations in OpenAlex.

  1. Review
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  7. Regulators of Oligodendrocyte Differentiation.Cold Spring Harbor perspectives in biology · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors at 3 institutions in 1 country.

Matthias WeiderInstitut für Biochemie, Emil-Fischer-Zentrum, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91054, Erlangen, Germany.
Laura Julia StarostInstitute of Neuropathology, University Hospital Münster, D-48149, Münster, Germany.
Katharina GrollInstitute of Neuropathology, University Hospital Münster, D-48149, Münster, Germany.
Melanie KüspertInstitut für Biochemie, Emil-Fischer-Zentrum, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91054, Erlangen, Germany.
Elisabeth SockInstitut für Biochemie, Emil-Fischer-Zentrum, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91054, Erlangen, Germany.
Miriam WedelInstitut für Biochemie, Emil-Fischer-Zentrum, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91054, Erlangen, Germany.
Franziska FröbInstitut für Biochemie, Emil-Fischer-Zentrum, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91054, Erlangen, Germany.
Christian SchmittInstitut für Biochemie, Emil-Fischer-Zentrum, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91054, Erlangen, Germany.
Tina BarotiInstitut für Biochemie, Emil-Fischer-Zentrum, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91054, Erlangen, Germany.
Anna C HartwigInstitut für Biochemie, Emil-Fischer-Zentrum, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91054, Erlangen, Germany.
Simone HillgärtnerInstitut für Biochemie, Emil-Fischer-Zentrum, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91054, Erlangen, Germany.
Sandra PiefkeInstitut für Biochemie, Emil-Fischer-Zentrum, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91054, Erlangen, Germany.
Tanja FadlerInstitut für Biochemie, Emil-Fischer-Zentrum, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91054, Erlangen, Germany.
Marc EhrlichInstitute of Neuropathology, University Hospital Münster, D-48149, Münster, Germany.
Corinna EhlertInstitute of Neuropathology, University Hospital Münster, D-48149, Münster, Germany.
Martin StehlingDepartment of Cell and Developmental Biology, Max Planck Institute for Molecular Biomedicine, D-48149, Münster, Germany.
Stefanie AlbrechtInstitute of Neuropathology, University Hospital Münster, D-48149, Münster, Germany.
Ammar JabaliInstitute of Neuropathology, University Hospital Münster, D-48149, Münster, Germany.
Hans R SchölerDepartment of Cell and Developmental Biology, Max Planck Institute for Molecular Biomedicine, D-48149, Münster, Germany.
Jürgen WinklerDepartment of Molecular Neurology, University Hospital Erlangen, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91054, Erlangen, Germany.
Tanja KuhlmannInstitute of Neuropathology, University Hospital Münster, D-48149, Münster, Germany. Tanja.Kuhlmann@ukmuenster.de.
Michael WegnerInstitut für Biochemie, Emil-Fischer-Zentrum, Friedrich-Alexander-Universität Erlangen-Nürnberg, D-91054, Erlangen, Germany. michael.wegner@fau.de.ORCID http://orcid.org/0000-0002-4586-3294
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEUniversity Hospital Münster · DEMax Planck Institute for Molecular Biomedicine · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oligodendrocytes produce myelin for rapid transmission and saltatory conduction of action potentials in the vertebrate central nervous system. Activation of the myelination program requires several transcription factors including Sox10, Olig2, and Nkx2.2. Functional interactions among them are poorly understood and important components of the regulatory network are still unknown. Here, we identify Nfat proteins as Sox10 targets and regulators of oligodendroglial differentiation in rodents and humans. Overall levels and nuclear fraction increase during differentiation. Inhibition of Nfat activity impedes oligodendrocyte differentiation in vitro and in vivo. On a molecular level, Nfat proteins cooperate with Sox10 to relieve reciprocal repression of Olig2 and Nkx2.2 as precondition for oligodendroglial differentiation and myelination. As Nfat activity depends on calcium-dependent activation of calcineurin signaling, regulatory network and oligodendroglial differentiation become sensitive to calcium signals. NFAT proteins are also detected in human oligodendrocytes, downregulated in active multiple sclerosis lesions and thus likely relevant in demyelinating disease.

Indexed as

Cell DifferentiationSignal TransductionAnimalsCalcineurinConserved SequenceEvolution, MolecularGene Expression RegulationHomeobox Protein Nkx-2.2Homeodomain ProteinsHumansMiceMyelin SheathNFATC Transcription FactorsNuclear ProteinsOligodendrocyte Transcription Factor 2OligodendrogliaCalcineurinHomeobox Protein Nkx-2.2Homeodomain ProteinsNFATC Transcription Factorsnkx2.2b protein, zebrafishNKX2-2 protein, humanNkx2-2 protein, mouseNkx2-2 protein, ratNuclear ProteinsOlig2 protein, mouseOligodendrocyte Transcription Factor 2SOXE Transcription FactorsTranscription FactorsZebrafish Proteins

Identifiers

PMID29500351
PMCPMC5834605
OpenAlexW2807226597

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.