Evidence map›Paper›PMID 20841359›Full record

ArticleThe Journal of biological chemistry2010

Inhibitory phosphorylation of GSK-3 by CaMKII couples depolarization to neuronal survival.

Bin Song, Bingquan Lai, Zhihao Zheng, Yuying Zhang, Jingyan Luo, Chong Wang, Yuan Chen, James R Woodgett, Mingtao Li

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

61 citing papers in PubMed, 97 citations in OpenAlex.

  1. Review
  2. Review
  3. 25International journal of molecular sciences · 2026
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. CaMKIIβ-mediated Phosphorylation Enhances Protein Stability of Spastin to Promote Neurite Outgrowth.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. CaMKII and CaCell biology and toxicology · 2023
    Article
  17. Article
  18. Article
  19. A Role for Second Messengers in Axodendritic Neuronal Polarity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Review
  20. Article

1 more citing papers are in PubMed but not listed here.

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 2 institutions in 2 countries.

Bin SongDepartment of Pharmacology, Zhongshan School of Medicine, Sun Yat-sen University, 74 Zhongshan Road II, Guangzhou 510080, China.
Bingquan Lai
Zhihao Zheng
Yuying Zhang
Jingyan Luo
Chong Wang
Yuan Chen
James R Woodgett
Mingtao Li
Sun Yat-sen University · CNUniversity of Toronto · CA

Funding

CIHR 74711CIHR FRN 12858
6 · The paper itself

Abstract

Glycogen synthase kinase-3 (GSK-3) plays a critical role in neuronal apoptosis. The two mammalian isoforms of the kinase, GSK-3α and GSK-3β, are inhibited by phosphorylation at Ser-21 and Ser-9, respectively. Depolarization, which is vital for neuronal survival, causes both an increase in Ser-21/9 phosphorylation and an inhibition of GSK-3α/β. However, the role of GSK-3 phosphorylation in depolarization-dependent neuron survival and the signaling pathway contributing to GSK-3 phosphorylation during depolarization remain largely unknown. Using several approaches, we showed that both isoforms of GSK-3 are important for mediating neuronal apoptosis. Nonphosphorylatable GSK-3α/β mutants (S21A/S9A) promoted apoptosis, whereas a peptide encompassing Ser-9 of GSK-3β protected neurons in a phosphorylation-dependent manner; these results indicate a critical role for Ser-21/9 phosphorylation on depolarization-dependent neuron survival. We found that Ser-21/9 phosphorylation of GSK-3 was mediated by Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) but not by Akt/PKB, PKA, or p90(RSK). CaMKII associated with and phosphorylated GSK-3α/β. Furthermore, the pro-survival effect of CaMKII was mediated by GSK-3 phosphorylation and inactivation. These findings identify a novel Ca(2+)/calmodulin/CaMKII/GSK-3 pathway that couples depolarization to neuronal survival.

Indexed as

Amino Acid SubstitutionAnimalsApoptosisCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2CalmodulinCell PolarityCell SurvivalGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHEK293 CellsHumansMutation, MissenseNeuronsPhosphorylationRatsCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2CalmodulinGlycogen Synthase Kinase 3glycogen synthase kinase 3 alphaGlycogen Synthase Kinase 3 betaGSK3B protein, humanGsk3b protein, rat

Identifiers

PMID20841359
PMCPMC3003410
OpenAlexW2090849482

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.