Evidence map›Paper›PMID 36543123›Full record

ArticleCell reports2022

SOX2 is essential for astrocyte maturation and its deletion leads to hyperactive behavior in mice.

Yan Wang, Sheng Zhang, Zhaohui Lan, Vui Doan, Bokyung Kim, Sihan Liu, Meina Zhu, Vanessa L Hull, Sami Rihani, Chun-Li Zhang and 2 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.6field-weighted citation impact, top 9% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

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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.

Yan WangInstitute for Pediatric Regenerative Medicine, Shriners Hospitals for Children Northern California, Sacramento, CA 95817, USA; Department of Neurology, School of Medicine, University of California, Davis, Davis, CA 95817, USA.
Sheng ZhangInstitute for Pediatric Regenerative Medicine, Shriners Hospitals for Children Northern California, Sacramento, CA 95817, USA; Department of Neurology, School of Medicine, University of California, Davis, Davis, CA 95817, USA.
Zhaohui LanInstitute for Pediatric Regenerative Medicine, Shriners Hospitals for Children Northern California, Sacramento, CA 95817, USA; Department of Neurology, School of Medicine, University of California, Davis, Davis, CA 95817, USA.
Vui DoanInstitute for Pediatric Regenerative Medicine, Shriners Hospitals for Children Northern California, Sacramento, CA 95817, USA.
Bokyung KimInstitute for Pediatric Regenerative Medicine, Shriners Hospitals for Children Northern California, Sacramento, CA 95817, USA; Department of Neurology, School of Medicine, University of California, Davis, Davis, CA 95817, USA.
Sihan LiuInstitute for Pediatric Regenerative Medicine, Shriners Hospitals for Children Northern California, Sacramento, CA 95817, USA; Department of Neurology, School of Medicine, University of California, Davis, Davis, CA 95817, USA.
Meina ZhuInstitute for Pediatric Regenerative Medicine, Shriners Hospitals for Children Northern California, Sacramento, CA 95817, USA; Department of Neurology, School of Medicine, University of California, Davis, Davis, CA 95817, USA.
Vanessa L HullInstitute for Pediatric Regenerative Medicine, Shriners Hospitals for Children Northern California, Sacramento, CA 95817, USA; Department of Neurology, School of Medicine, University of California, Davis, Davis, CA 95817, USA.
Sami RihaniInstitute for Pediatric Regenerative Medicine, Shriners Hospitals for Children Northern California, Sacramento, CA 95817, USA; Department of Neurology, School of Medicine, University of California, Davis, Davis, CA 95817, USA.
Chun-Li ZhangDepartment of Molecular Biology and Hamon Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
John A GrayDepartment of Neurology, School of Medicine, University of California, Davis, Davis, CA 95817, USA; Center for Neuroscience, University of California, Davis, Davis, CA 95618, USA.
Fuzheng GuoInstitute for Pediatric Regenerative Medicine, Shriners Hospitals for Children Northern California, Sacramento, CA 95817, USA; Department of Neurology, School of Medicine, University of California, Davis, Davis, CA 95817, USA. Electronic address: fzguo@ucdavis.edu.
University of California, Davis · USShriners Hospitals for Children - Northern California · USThe University of Texas Southwestern Medical Center · US

Funding

The curious case of PARP1 in CNS myelin formation and repairR01NS123165 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Fuzheng Guo · 2022 to 2026
$2.5M
Glial HIFa: mechanisms and implications in hypoxia/ischemia-induced oligodendroglial pathologyR01NS123080 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI GUO, FUZHENG · 2021 to 2025
$2.3M
Chemical Reprogramming of Traumatic Brain InjuryR01NS099073 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI ZHANG, CHUN-LI · 2017 to 2021
$1.8M
The Wnt-independent role of TCF7l2 in CNS myelin formation and repairR01NS094559 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI GUO, FUZHENG · 2016 to 2020
$1.4M
Using genetic approaches to explore the role of group I PAKs in developmental myelination of the mammalian CNSR21NS125464 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI GUO, FUZHENG · 2022 to 2022
$439k
A paradigm shift in our understanding of oligodendroglial HIFa-regulated CNS angiogenesisR21NS109790 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI GUO, FUZHENG · 2018 to 2019
$432k
NINDS NIH HHS R01 NS094559NINDS NIH HHS R01 NS099073NINDS NIH HHS R01 NS123080NINDS NIH HHS R01 NS123165NINDS NIH HHS R21 NS109790NINDS NIH HHS R21 NS125464
6 · The paper itself

Abstract

Children with SOX2 deficiency develop ocular disorders and extra-ocular CNS anomalies. Animal data show that SOX2 is essential for retinal and neural stem cell development. In the CNS parenchyma, SOX2 is primarily expressed in astroglial and oligodendroglial cells. Here, we report a crucial role of astroglial SOX2 in postnatal brain development. Astroglial Sox2-deficient mice develop hyperactivity in locomotion and increased neuronal excitability in the corticostriatal circuit. Sox2 deficiency inhibits postnatal astrocyte maturation molecularly, morphologically, and electrophysiologically without affecting astroglia proliferation. Mechanistically, SOX2 directly binds to a cohort of astrocytic signature and functional genes, the expression of which is significantly reduced in Sox2-deficient CNS and astrocytes. Consistently, Sox2 deficiency remarkably reduces glutamate transporter expression and compromised astrocyte function of glutamate uptake. Our study provides insights into the cellular mechanisms underlying brain defects in children with SOX2 mutations and suggests a link of astrocyte SOX2 with extra-ocular abnormalities in SOX2-mutant subjects.

Indexed as

AstrocytesNeural Stem CellsAnimalsBrainCell DifferentiationMiceNeuronsastrocyte maturationastrocyte proliferationastrocytesbrain developmentCP: Neuroscienceglutamate uptakehyperactive locomotorhyperactivitySOX2SOX2 disorderSOX2-regulated genes

Identifiers

PMID36543123
PMCPMC9875714
OpenAlexW4312085035

What OpenQuestion holds

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LicenceCC BY
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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.