Evidence map›Paper›PMID 20219996›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

GSK-3 beta inhibits presynaptic vesicle exocytosis by phosphorylating P/Q-type calcium channel and interrupting SNARE complex formation.

Ling-Qiang Zhu, Dan Liu, Juan Hu, Jin Cheng, Shao-Hui Wang, Qun Wang, Fang Wang, Jian-Guo Chen, Jian-Zhi Wang

Open access · hybridAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

53 citing papers in PubMed, 101 citations in OpenAlex.

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  11. Mutations in DISC1 alter IPNeuronal signaling · 2021
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  18. GSK-3Neural plasticity · 2019
    Review
  19. Glycogen synthase kinase 3 beta regulates ethanol consumption and is a risk factor for alcohol dependence.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018
    Article
  20. 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 at 1 institution in 1 country.

Ling-Qiang ZhuDepartment of Pathophysiology, Institute of Neuroscience, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, People's Republic of China.
Dan Liu
Juan Hu
Jin Cheng
Shao-Hui Wang
Qun Wang
Fang Wang
Jian-Guo Chen
Jian-Zhi Wang
Huazhong University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glycogen synthase kinase-3 (GSK-3), a Ser/Thr protein kinase abundantly expressed in neurons, plays diverse functions in physiological and neurodegenerative conditions. Our recent study shows that upregulation of GSK-3 suppresses long-term potentiation and presynaptic release of glutamate; however, the underlying mechanism is elusive. Here, we show that activation of GSK-3beta retards the synaptic vesicle exocytosis in response to membrane depolarization. Using calcium imaging, whole-cell patch-clamp, as well as specific Ca(2+) channel inhibitors, we demonstrate that GSK-3beta phosphorylates the intracellular loop-connecting domains II and III (L(II-III)) of P/Q-type Ca(2+) channels, which leads to a decrease of intracellular Ca(2+) rise through the P/Q-type voltage-dependent calcium channel. To further illustrate the mechanisms of GSK-3beta's action, we show that activation of GSK-3beta interferes with the formation of the soluble N-ethylmaleimide-sensitive factor attachment protein (SNAP) receptor (SNARE) complex through: (1) weakening the association of synaptobrevin with SNAP25 and syntaxin; (2) reducing the interactions among the phosphorylated L(II-III) and synaptotagmin, SNAP25, and syntaxin; and (3) inhibiting dissociation of synaptobrevin from synaptophysin I. These results indicate that GSK-3beta negatively regulates synaptic vesicle fusion events via interfering with Ca(2+)-dependent SNARE complex formation.

Indexed as

Amino Acid SequenceAnimalsCalcium Channels, P-TypeCalcium Channels, Q-TypeCell LineCells, CulturedExocytosisGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaMolecular Sequence DataNeural InhibitionPhosphorylationPresynaptic TerminalsRatsSNARE ProteinsSynaptic VesiclesCalcium Channels, P-TypeCalcium Channels, Q-TypeGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGsk3b protein, ratSNARE Proteins

Identifiers

PMID20219996
PMCPMC6632254
OpenAlexW1978367401

What OpenQuestion holds

Textmetadata
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.