Evidence map›Paper›PMID 26179612›Full record

ArticleMolecular neurobiology2016

Loss of GSK-3 Causes Abnormal Astrogenesis and Behavior in Mice.

Eui-Man Jung, Minhan Ka, Woo-Yang Kim

Abstract read
In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

29 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Article
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  4. Review
  5. Augmentation of functional recovery viaJournal of orthopaedic translation · 2024
    Article
  6. Astrocyte regulation of synaptic signaling in psychiatric disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Review
  7. Review
  8. Article
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  15. Review
  16. Astrocytes in Bipolar Disorder.Advances in neurobiology · 2021
    Article
  17. Article
  18. Article
  19. Article
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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

3 authors at 1 institution in 1 country.

Eui-Man JungDepartment of Developmental Neuroscience, Munroe-Meyer Institute, University of Nebraska Medical Center, Omaha, NE, 68198, USA.
Minhan KaDepartment of Developmental Neuroscience, Munroe-Meyer Institute, University of Nebraska Medical Center, Omaha, NE, 68198, USA.
Woo-Yang KimDepartment of Developmental Neuroscience, Munroe-Meyer Institute, University of Nebraska Medical Center, Omaha, NE, 68198, USA. wooyang.kim@unmc.edu.
University of Nebraska Medical Center · US

Funding

The Molecular Biology of Neurosurgery SystemsP20GM103471 · NIGMS · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI SMITH, SHELLEY D · 2012 to 2013
$4.1M
NIGMS NIH HHS P20 GM103471
6 · The paper itself

Abstract

Altered activity of glycogen synthase kinase-3 (GSK-3) is associated with psychiatric diseases and neurodegenerative diseases. GSK-3 is a key regulator in multiple aspects of neuronal differentiation in the brain. However, little is known about the role of GSK-3 in astrocyte development. To examine the role of GSK-3 in astrocytes, we generated a conditional knockout mouse using a glial fibrillary acidic protein (GFAP)-cre driver, in which the GSK-3 alpha and beta genes are deleted in astrocytes. We found that GFAP-cre-mediated GSK-3 deletion led to a larger brain. The number and size of astrocytes were increased in GSK-3 mutant brains. The levels of GFAP and phospho-STAT3, indicators of astrogenesis, were elevated in GSK-3 mutants. Furthermore, we found upregulation of astrocyte regulatory molecules such as phospho-AKT, phospho-S6, and cyclin D in GSK-3 mutant brains. Finally, GSK-3 mutant mice exhibited aberrant anxiety and social behavior. Our results suggest that GSK-3 plays a significant role in astrocyte development and behavioral control in mice.

Indexed as

Behavior, AnimalNeurogenesisAnimalsAnxietyAstrocytesBrainCaspase 3Cell CountCell ProliferationGene DeletionGlial Fibrillary Acidic ProteinGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHypertrophyMiceMice, Mutant StrainsCaspase 3Glial Fibrillary Acidic ProteinGlycogen Synthase Kinase 3glycogen synthase kinase 3 alphaGlycogen Synthase Kinase 3 betaRNA, MessengerAstrocyteAstrogenesisBrain sizeGFAPGSK-3Hypertrophy

Identifiers

PMID26179612
PMCPMC4716001
OpenAlexW893812942

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.