Evidence map›Paper›PMID 25151262›Full record

ArticleNature neuroscience2014

Mutual antagonism between Sox10 and NFIA regulates diversification of glial lineages and glioma subtypes.

Stacey M Glasgow, Wenyi Zhu, C Claus Stolt, Teng-Wei Huang, Fuyi Chen, Joseph J LoTurco, Jeffrey L Neul, Michael Wegner, Carrie Mohila, Benjamin Deneen

Open access · greenAbstract read
In one paragraph

Article in Nature neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
4.4field-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

94 citing papers in PubMed, 194 citations in OpenAlex.

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  12. A fetal oncogene NUAK2 is an emerging therapeutic target in glioblastoma.bioRxiv : the preprint server for biology · 2025
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34 more citing papers are in PubMed but not listed here.

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

10 authors at 4 institutions in 2 countries.

Stacey M GlasgowCenter for Cell and Gene Therapy, Baylor College of Medicine, Houston, Texas, USA.
Wenyi Zhu1] Center for Cell and Gene Therapy, Baylor College of Medicine, Houston, Texas, USA. [2] Integrative Molecular and Biomedical Sciences Graduate Program, Baylor College of Medicine, Houston, Texas, USA.
C Claus StoltInstitut für Biochemie, Emil-Fischer-Zentrum, Universität Erlangen-Nürnberg, Erlangen, Germany.
Teng-Wei Huang1] Program in Developmental Biology, Baylor College of Medicine, Houston, Texas, USA. [2] Duncan Neurological Research Institute at Texas Children's Hospital, Houston, Texas, USA.
Fuyi ChenDepartment of Physiology and Neurobiology, University of Connecticut, Storrs, Connecticut, USA.
Joseph J LoTurcoDepartment of Physiology and Neurobiology, University of Connecticut, Storrs, Connecticut, USA.
Jeffrey L Neul1] Program in Developmental Biology, Baylor College of Medicine, Houston, Texas, USA. [2] Duncan Neurological Research Institute at Texas Children's Hospital, Houston, Texas, USA. [3] Department of Pediatrics, Neurology, and Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA. [4] Department of Neuroscience, Baylor College of Medicine, Houston, Texas, USA.ORCID 0000000256285872
Michael WegnerInstitut für Biochemie, Emil-Fischer-Zentrum, Universität Erlangen-Nürnberg, Erlangen, Germany.
Carrie MohilaDepartment of Pathology, Texas Children's Hospital, Houston, Texas, USA.
Benjamin Deneen1] Center for Cell and Gene Therapy, Baylor College of Medicine, Houston, Texas, USA. [2] Integrative Molecular and Biomedical Sciences Graduate Program, Baylor College of Medicine, Houston, Texas, USA. [3] Program in Developmental Biology, Baylor College of Medicine, Houston, Texas, USA. [4] Duncan Neurological Research Institute at Texas Children's Hospital, Houston, Texas, USA. [5] Department of Pediatrics, Neurology, and Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA. [6] Department of Neuroscience, Baylor College of Medicine, Houston, Texas, USA.
Baylor College of Medicine · USFriedrich-Alexander-Universität Erlangen-Nürnberg · DEUniversity of Connecticut · USTexas Children's Hospital · US

Funding

Steps towards a paternal gene activation therapy for Angelman syndromeU54HD083092 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI NELSON, DAVID LOREN, NEUL, JEFFREY L · 2014 to 2019
$7.8M
Training In Cell and Gene TherapyT32HL092332 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI MALCOLM K. BRENNER, Bruno Di Stefano · 2008 to 2026
$6.9M
Transcriptional regulation of gliogenesis in the CNSR01NS071153 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI DENEEN, BENJAMIN · 2010 to 2022
$5.0M
MOLECULAR REGULATION OF NEOCORTICAL NEUROGENESISR01MH056524 · NIMH · UNIVERSITY OF CONNECTICUT STORRS · PI LOTURCO, JOSEPH J · 2003 to 2012
$3.3M
Characterizing autonomic dysfunction in Rett syndrome and other MECP2 disordersR01HD062553 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI NEUL, JEFFREY L · 2010 to 2014
$1.7M
DYSLEXIA SUSCEPTIBILITY GENES AND MECHANISMS OF NEURONAL DEVELOPMENTR01HD055655 · NICHD · UNIVERSITY OF CONNECTICUT STORRS · PI LOTURCO, JOSEPH J · 2008 to 2012
$1.6M
NHLBI NIH HHS 5-T32HL092332-08NHLBI NIH HHS T32 HL092332NICHD NIH HHS R01 HD055655NICHD NIH HHS R01HD055655NICHD NIH HHS R01 HD062553NICHD NIH HHS U54 HD083092NIMH NIH HHS R01 MH056524NIMH NIH HHS R01MH056524NINDS NIH HHS R01 NS071153
6 · The paper itself

Abstract

Lineage progression and diversification is regulated by the coordinated action of unique sets of transcription factors. Oligodendrocytes (OL) and astrocytes (AS) comprise the glial sub-lineages in the CNS, and the manner in which their associated regulatory factors orchestrate lineage diversification during development and disease remains an open question. Sox10 and NFIA are key transcriptional regulators of gliogenesis associated with OL and AS. We found that NFIA inhibited Sox10 induction of OL differentiation through direct association and antagonism of its function. Conversely, we found that Sox10 antagonized NFIA function and suppressed AS differentiation in mouse and chick systems. Using this developmental paradigm as a model for glioma, we found that this relationship similarly regulated the generation of glioma subtypes. Our results describe the antagonistic relationship between Sox10 and NFIA that regulates the balance of OL and AS fate during development and demonstrate for the first time, to the best of our knowledge, that the transcriptional processes governing glial sub-lineage diversification oversee the generation of glioma subtypes.

Indexed as

AnimalsAnimals, NewbornBasic Helix-Loop-Helix ProteinsCell DifferentiationCells, CulturedCerebral CortexChick EmbryoChromatin ImmunoprecipitationElectroporationEmbryo, MammalianGliomaGreen Fluorescent ProteinsHomeodomain ProteinsMiceMyelin Basic ProteinNerve Tissue ProteinsBasic Helix-Loop-Helix ProteinsGreen Fluorescent ProteinsHomeodomain ProteinsMyelin Basic ProteinNerve Tissue ProteinsNfia protein, mouseNFI Transcription FactorsNkx6-1 protein, mouseOlig2 protein, mouseOligodendrocyte Transcription Factor 2SOX10 protein, humanSOXE Transcription Factors

Identifiers

PMID25151262
PMCPMC4313923
OpenAlexW2048708798

What OpenQuestion holds

Textmetadata
LicenceTDM
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.