Evidence map›Paper›PMID 29461205›Full record

ArticleeLife2018

PTEN negatively regulates the cell lineage progression from NG2

Estibaliz González-Fernández, Hey-Kyeong Jeong, Masahiro Fukaya, Hyukmin Kim, Rabia R Khawaja, Isha N Srivastava, Ari Waisman, Young-Jin Son, Shin H Kang

Abstract read
In one paragraph

Article in eLife, 2018. 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
–field-weighted citation impact
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.

  1. Review
  2. Article
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  10. Review
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  13. Review
  14. White Matter Stroke Induces a Unique Oligo-Astrocyte Niche That Inhibits Recovery.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  15. PTEN in Autism and Neurodevelopmental Disorders.Cold Spring Harbor perspectives in medicine · 2019
    Review
  16. Article
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

9 authors.

Estibaliz González-FernándezShriners Hospitals Pediatric Research Center, Temple University Lewis Katz School of Medicine, Philadelphia, Unites States.
Hey-Kyeong JeongShriners Hospitals Pediatric Research Center, Temple University Lewis Katz School of Medicine, Philadelphia, Unites States.
Masahiro FukayaDepartment of Anatomy, Kitasato University School of Medicine, Sagamihara, Japan.
Hyukmin KimShriners Hospitals Pediatric Research Center, Temple University Lewis Katz School of Medicine, Philadelphia, Unites States.
Rabia R KhawajaShriners Hospitals Pediatric Research Center, Temple University Lewis Katz School of Medicine, Philadelphia, Unites States.
Isha N SrivastavaShriners Hospitals Pediatric Research Center, Temple University Lewis Katz School of Medicine, Philadelphia, Unites States.
Ari WaismanInstitute for Molecular Medicine, University Medical Center of the Johannes Gutenberg University of Mainz, Mainz, Germany.
Young-Jin SonShriners Hospitals Pediatric Research Center, Temple University Lewis Katz School of Medicine, Philadelphia, Unites States.ORCID http://orcid.org/0000-0001-5725-9775
Shin H KangShriners Hospitals Pediatric Research Center, Temple University Lewis Katz School of Medicine, Philadelphia, Unites States.ORCID http://orcid.org/0000-0002-3692-9802

Funding

UCD Mutant Mouse Regional Resource CenterU42OD012210 · OD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI KC KENT LLOYD · 2012 to 2026
$29.2M
Role of Oligodendroglia in the Pathogenesis of ALSR01NS089586 · NINDS · TEMPLE UNIV OF THE COMMONWEALTH · PI KANG, SHIN H · 2016 to 2020
$2.1M
NIH HHS U42 OD012210NINDS NIH HHS R01NS07693NINDS NIH HHS R01 NS089586NINDS NIH HHS R01NS089586
6 · The paper itself

Abstract

Oligodendrocytes (OLs), the myelin-forming CNS glia, are highly vulnerable to cellular stresses, and a severe myelin loss underlies numerous CNS disorders. Expedited OL regeneration may prevent further axonal damage and facilitate functional CNS repair. Although adult OL progenitors (OPCs) are the primary players for OL regeneration, targetable OPC-specific intracellular signaling mechanisms for facilitated OL regeneration remain elusive. Here, we report that OPC-targeted PTEN inactivation in the mouse, in contrast to OL-specific manipulations, markedly promotes OL differentiation and regeneration in the mature CNS. Unexpectedly, an additional deletion of mTOR did not reverse the enhanced OL development from PTEN-deficient OPCs. Instead, ablation of GSK3β, another downstream signaling molecule that is negatively regulated by PTEN-Akt, enhanced OL development. Our results suggest that PTEN persistently suppresses OL development in an mTOR-independent manner, and at least in part, via controlling GSK3β activity. OPC-targeted PTEN-GSK3β inactivation may benefit facilitated OL regeneration and myelin repair.

Indexed as

Cell DifferentiationSignal TransductionAnimalsGlycogen Synthase Kinase 3 betaMiceOligodendrogliaPTEN PhosphohydrolaseStem CellsTOR Serine-Threonine KinasesGlycogen Synthase Kinase 3 betamTOR protein, mousePTEN PhosphohydrolasePten protein, mouseTOR Serine-Threonine KinasesGSK3bmousemTORmyelinationneuroscienceoligodendrocytesprogenitorsPTEN

Identifiers

PMID29461205
PMCPMC5839742

What OpenQuestion holds

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LicenceCC BY
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.