Evidence map›Paper›PMID 35457230›Full record

ReviewInternational journal of molecular sciences2022

Glycogen Synthase Kinase 3: Ion Channels, Plasticity, and Diseases.

Mate Marosi, Parsa Arman, Giuseppe Aceto, Marcello D'Ascenzo, Fernanda Laezza

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Article
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  4. Review
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  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Chronic, combinatorial targeting of NMDARs and 5-HTNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
    Article
  13. Article
  14. Article
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  16. Article
  17. Article
  18. Review
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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

5 authors at 2 institutions in 2 countries.

Mate MarosiDepartment of Pharmacology & Toxicology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Parsa ArmanDepartment of Pharmacology & Toxicology, University of Texas Medical Branch, Galveston, TX 77555, USA.
Giuseppe AcetoDepartment of Neuroscience, Università Cattolica del Sacro Cuore, 00168 Roma, Italy.
Marcello D'AscenzoDepartment of Neuroscience, Università Cattolica del Sacro Cuore, 00168 Roma, Italy.ORCID 0000-0003-0073-412X
Fernanda LaezzaDepartment of Pharmacology & Toxicology, University of Texas Medical Branch, Galveston, TX 77555, USA.ORCID 0000-0003-1141-1852
The University of Texas Medical Branch at Galveston · USUniversità Cattolica del Sacro Cuore · IT

Funding

Neurotrophin-dependent regulation of voltage-gated sodium channelsR01MH124351 · NIMH · UNIVERSITY OF TEXAS MED BR GALVESTON · PI LAEZZA, FERNANDA · 2020 to 2024
$3.0M
Neurotoxicology of deltamethrin in the developing brainR01ES031823 · NIEHS · UNIVERSITY OF TEXAS MED BR GALVESTON · PI GREEN, THOMAS ARTHUR, LAEZZA, FERNANDA · 2020 to 2024
$2.8M
NIEHS NIH HHS R01 ES031823NIH HHS NIH/NIMH R01MH124351/NH/NIH HHS/United StatesNIH HHS R01ES031823/NH/NIH HHS/United StatesNIMH NIH HHS R01 MH124351
6 · The paper itself

Abstract

Glycogen synthase kinase 3β (GSK3) is a multifaceted serine/threonine (S/T) kinase expressed in all eukaryotic cells. GSK3β is highly enriched in neurons in the central nervous system where it acts as a central hub for intracellular signaling downstream of receptors critical for neuronal function. Unlike other kinases, GSK3β is constitutively active, and its modulation mainly involves inhibition via upstream regulatory pathways rather than increased activation. Through an intricate converging signaling system, a fine-tuned balance of active and inactive GSK3β acts as a central point for the phosphorylation of numerous primed and unprimed substrates. Although the full range of molecular targets is still unknown, recent results show that voltage-gated ion channels are among the downstream targets of GSK3β. Here, we discuss the direct and indirect mechanisms by which GSK3β phosphorylates voltage-gated Na

Indexed as

Glycogen Synthase Kinase 3NeuronsGlycogen Synthase Kinase 3 betaIon ChannelsPhosphorylationProtein Serine-Threonine KinasesGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaIon ChannelsProtein Serine-Threonine KinasesGSK3β-mediated phosphorylationintracellular fibroblast growth factors (iFGF)neuronal excitabilityneuronal plasticityneuropsychiatric disordersprotein–protein interactionsodium- and potassium-currentvoltage-gated ion channels

Identifiers

PMID35457230
PMCPMC9028019
OpenAlexW4224123012

What OpenQuestion holds

Textmetadata
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.