ReviewPharmacology & therapeutics2015
Glycogen synthase kinase-3 (GSK3): regulation, actions, and diseases.
Review in Pharmacology & therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 932 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
932 citing papers in PubMed, 1 synthesis or guideline pooled it, 1,703 citations in OpenAlex.
- The effects of flavonoid baicalein on miRNA expressions in cancer: a systematic review.Naunyn-Schmiedeberg's archives of pharmacology · 2025Pooled it
- Host andGut microbes · 2026Article
- GSK3β inhibits the differentiation of follicular granulosa cells by promoting lipid accumulation through autophagy in chickens.Poultry science · 2026Article
- PI3K-Akt signaling network crosstalk in cerebral ischemia/reperfusion injury: Mechanisms and therapeutic implications.Chinese medical journal · 2026Review
- CREB1 and GSK3 Isoforms as Potential Adaptive Signaling Nodes in PI3K/Akt/mTOR Inhibitor Treated Philadelphia Chromosome-Positive B-ALL.International journal of molecular sciences · 2026Article
- Fgk3 interacts with FgMetR to regulate mycelial growth, conidia development, DON production, and pathogenicity in Fusarium graminearum.Stress biology · 2026Article
- LiCl induces GSK-3β mediated autophagy, DNA damage, and cell cycle arrest in HPV driven cervical cancer cells.Cancer chemotherapy and pharmacology · 2026Article
- Article
- Obeticholic Acid and Edaravone Protect Against Cisplatin-Induced Hepatotoxicity Through Modulation of Keap1/Nrf2/ARE, TNF-α/NF-κB, and AKT/GSK-3β Pathways.Journal of biochemical and molecular toxicology · 2026Article
- Disrupting fzd9b in Zebrafish Recapitulates Stress- and Anxiety-Like Behaviours Relevant to Williams Syndrome.Molecular neurobiology · 2026Article
- Healing from the Ocean: Targeting Shared Mechanisms in Autism and Epilepsy Using Algae-Derived Compounds.Marine drugs · 2026Review
- P2X7 Signaling in Neuroinflammation: Glial Crosstalk, Redox Integration, and Therapeutic Targeting.Journal of molecular neuroscience : MN · 2026Review
- Estrogen Withdrawal-Induced Cognitive Impairment in Menopausal Women: Mechanisms and Prospects for Integrated Interventions.International journal of molecular sciences · 2026Review
- The Molecular Pathology of Morules in Endometrial Carcinoma: Biological Significance and Clinical Implications.Pathology international · 2026Review
- Network Pharmacology Reveals the Potential Mechanism of Ketamine in Improving Cognitive Impairment in Patients With Depression.Alpha psychiatry · 2026Article
- Repurposing primaquine diphosphate for imatinib-resistant chronic myeloid leukemia via targeting BCR-ABL and Wnt/β-catenin pathway.iScience · 2026Article
- Evaluation of the Nrf2-Keap1 Pathway in Patients with Acute Cerebral Ischemic Disease.Medicina (Kaunas, Lithuania) · 2026Article
- PIAS1-mediated GSK3β SUMOylation exacerbates tauopathy and cognitive deficits in Alzheimer's disease models.Molecular psychiatry · 2026Article
- GSK3βGut · 2026Article
- Convergent mechanisms in Wnt and Hedgehog signaling.Science signaling · 2026Review
872 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Glycogen synthase kinase-3 (GSK3) may be the busiest kinase in most cells, with over 100 known substrates to deal with. How does GSK3 maintain control to selectively phosphorylate each substrate, and why was it evolutionarily favorable for GSK3 to assume such a large responsibility? GSK3 must be particularly adaptable for incorporating new substrates into its repertoire, and we discuss the distinct properties of GSK3 that may contribute to its capacity to fulfill its roles in multiple signaling pathways. The mechanisms regulating GSK3 (predominantly post-translational modifications, substrate priming, cellular trafficking, protein complexes) have been reviewed previously, so here we focus on newly identified complexities in these mechanisms, how each of these regulatory mechanism contributes to the ability of GSK3 to select which substrates to phosphorylate, and how these mechanisms may have contributed to its adaptability as new substrates evolved. The current understanding of the mechanisms regulating GSK3 is reviewed, as are emerging topics in the actions of GSK3, particularly its interactions with receptors and receptor-coupled signal transduction events, and differential actions and regulation of the two GSK3 isoforms, GSK3α and GSK3β. Another remarkable characteristic of GSK3 is its involvement in many prevalent disorders, including psychiatric and neurological diseases, inflammatory diseases, cancer, and others. We address the feasibility of targeting GSK3 therapeutically, and provide an update of its involvement in the etiology and treatment of several disorders.
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What OpenQuestion holds
Registered trials
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.