ArticleScientific reports2017
In vivo regulation of glycogen synthase kinase 3β activity in neurons and brains.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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Who cites it
72 citing papers in PubMed.
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- Propofol-Induced Metabolic, Apoptotic, and Wnt-Frizzled-Related Transcript Changes in MIA PaCa-2 Cells: In Vitro and Bioinformatic Analyses.Current issues in molecular biology · 2026Article
- Current Landscape of Glycogen Synthase Kinase-3β PET Tracers: Progress, Limitations, and Perspectives-A Narrative Review.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Aberrant histone acetylation and dysregulated synaptic plasticity in cognitive impairment induced by a high-methionine diet.Neural regeneration research · 2026Article
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- Sex-dependent neurobiological and metabolic dysfunction in an aged rat model of post-traumatic stress disorder.Communications biology · 2026Article
- Panx1 deficiency exacerbates GAN diet-induced obesity by destabilizing β-catenin via GSK3β.iScience · 2026Article
- Senescent Factors Suppress Innate Antiviral Immunity in Aged Mice via Two Distinct Mechanisms.Aging cell · 2026Article
- Altering PTPRD via genetics or pharmacology modulates 3xTg-AD mouse neurofibrillary pathology.Frontiers in neuroscience · 2026Article
- Decoding ATXN2 Phosphocode: Structural Insights and Therapeutic Opportunities in Disease.The protein journal · 2025Review
- Integrative machine learning and molecular simulation approaches identify GSK3β inhibitors for neurodegenerative disease therapy.Scientific reports · 2025Article
- Xenon gas as a potential treatment for opioid use disorder, alcohol use disorder, and related disorders.Medical gas research · 2025Review
- Limettin and PD98059 Mitigated Alzheimer's Disease Like Pathology Induced by Streptozotocin in Mouse Model: Role of p-ERK1/2/p-GSK-3β/p-CREB/BDNF Pathway.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Venetoclax confers synthetic lethality to chidamide in preclinical models with transformed follicular lymphoma.Clinical epigenetics · 2025Article
- Lithium fine tunes lipid membranes through phospholipid binding.Scientific reports · 2025Article
- Progressive Alcohol-Related Brain Atrophy and White Matter Pathology Are Linked to Long-Term Inhibitory Effects on mTOR Signaling.Biomolecules · 2025Article
- QSP Modeling Shows Pathological Synergism Between Insulin Resistance and Amyloid-Beta Exposure in Upregulating VCAM1 Expression at the BBB Endothelium.CPT: pharmacometrics & systems pharmacology · 2025Article
- Exploring novel and potent glycogen synthase kinase-3β inhibitors through systematic drug designing approach.Scientific reports · 2025Article
- The dual role of glycogen synthase kinase-3 beta (GSK3β) in neurodegenerative pathologies: interplay between autophagy and disease progression.Frontiers in pharmacology · 2025Review
12 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glycogen synthase kinase 3β (GSK3β) is a multifunctional protein kinase involved in many cellular activities including development, differentiation and diseases. GSK3β is thought to be constitutively activated by autophosphorylation at Tyr216 and inactivated by phosphorylation at Ser9. The GSK3β activity has previously been evaluated by inhibitory Ser9 phosphorylation, but it does not necessarily indicate the kinase activity itself. Here, we applied the Phos-tag SDS-PAGE technique to the analysis of GSK3β phosphoisotypes in cells and brains. There were three phosphoisotypes of GSK3β; double phosphorylation at Ser9 and Tyr216, single phosphorylation at Tyr216 and the nonphosphorylated isotype. Active GSK3β with phosphorylation at Tyr216 represented half or more of the total GSK3β in cultured cells. Although levels of phospho-Ser9 were increased by insulin treatment, Ser9 phosphorylation occurred only in a minor fraction of GSK3β. In mouse brains, GSK3β was principally in the active form with little Ser9 phosphorylation, and the phosphoisotypes of GSK3β changed depending on the regions of the brain, age, sex and disease conditions. These results indicate that the Phos-tag SDS-PAGE method provides a simple and appropriate measurement of active GSK3β in vivo, and the activity is regulated by the mechanism other than phosphorylation on Ser9.
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