Evidence map›Paper›PMID 24333443›Full record

ArticleBiochemical and biophysical research communications2014

Akt-independent GSK3 inactivation downstream of PI3K signaling regulates mammalian axon regeneration.

Bo-Yin Zhang, Saijilafu, Chang-Mei Liu, Rui-Ying Wang, Qingsan Zhu, Zhongxian Jiao, Feng-Quan Zhou

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

31 citing papers in PubMed, 40 citations in OpenAlex.

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  3. The roles of circular RNAs in nerve injury and repair.Frontiers in molecular neuroscience · 2024
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  6. Regulation of GSK3β by SerMolecular neurobiology · 2021
    Article
  7. Review
  8. Article
  9. Time course analysis of sensory axon regenerationNeural regeneration research · 2020
    Article
  10. [Research progress on intrinsic signaling pathways in axon regeneration].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2020
    Review
  11. Article
  12. 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

7 authors at 3 institutions in 2 countries.

Bo-Yin ZhangDepartment of Orthopaedic Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, United States; Department of Orthopaedic Surgery, China-Japan Union Hospital of Jilin University, Changchun, Jilin 130033, China.
SaijilafuDepartment of Orthopaedic Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, United States.
Chang-Mei LiuDepartment of Orthopaedic Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, United States.
Rui-Ying WangDepartment of Orthopaedic Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, United States.
Qingsan ZhuDepartment of Orthopaedic Surgery, China-Japan Union Hospital of Jilin University, Changchun, Jilin 130033, China.
Zhongxian JiaoDepartment of Orthopaedic Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, United States.
Feng-Quan ZhouDepartment of Orthopaedic Surgery, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, United States; The Solomon H. Snyder Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, MD 21287, United States. Electronic address: fzhou4@jhmi.edu.
Johns Hopkins University · USJilin University · CNUnion Hospital · CN

Funding

Role of CLASP in neuronal morphogenesis during developmentR01NS064288 · NINDS · JOHNS HOPKINS UNIVERSITY · PI ZHOU, FENGQUAN · 2009 to 2013
$1.8M
NINDS NIH HHS R01 NS064288NINDS NIH HHS R01NS064288
6 · The paper itself

Abstract

Inactivation of glycogen synthase kinase 3 (GSK3) has been shown to mediate axon growth during development and regeneration. Phosphorylation of GSK3 by the kinase Akt is well known to be the major mechanism by which GSK3 is inactivated. However, whether such regulatory mechanism of GSK3 inactivation is used in neurons to control axon growth has not been directly studied. Here by using GSK3 mutant mice, in which GSK3 is insensitive to Akt-mediated inactivation, we show that sensory axons regenerate normally in vitro and in vivo after peripheral axotomy. We also find that GSK3 in sensory neurons of the mutant mice is still inactivated in response to peripheral axotomy and such inactivation is required for sensory axon regeneration. Lastly, we provide evidence that GSK3 activity is negatively regulated by PI3K signaling in the mutant mice upon peripheral axotomy, and the PI3K-GSK3 pathway is functionally required for sensory axon regeneration. Together, these results indicate that in response to peripheral nerve injury GSK3 inactivation, regulated by an alternative mechanism independent of Akt-mediated phosphorylation, controls sensory axon regeneration.

Indexed as

Nerve RegenerationAnimalsAxonsEnzyme ActivationGene Expression RegulationGlycogen Synthase Kinase 3MiceMice, KnockoutPeripheral Nerve InjuriesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionGlycogen Synthase Kinase 3Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktAxon regenerationGSK3 signalingIn vivo electroporationPI3K signaling

Identifiers

PMID24333443
PMCPMC3916952
OpenAlexW2021240982

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.