ArticleThe Journal of biological chemistry2008
Differential regulation of STAT family members by glycogen synthase kinase-3.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.
What it found
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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.
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Who cites it
104 citing papers in PubMed, 182 citations in OpenAlex.
- Serum β-catenin, GSK-3β, and IL-6 levels in medication-naive children with ADHD: a preliminary case-control study.Journal of neural transmission (Vienna, Austria : 1996) · 2026Article
- Reimagining GSK-3β Therapeutics in Alzheimer's Disease: From Inhibition to Activity Normalization and Targeted Degradation.Journal of molecular neuroscience : MN · 2026Review
- Dual Inhibition of GSK3 and JAK by BIO Suppresses Osteoblast Differentiation and Mineralization of Human Mesenchymal Cells.Current issues in molecular biology · 2026Article
- Article
- Glycogen synthase kinase-3: the master switch driving neurodegeneration in Alzheimer's disease and Parkinson's disease.Archives of toxicology · 2025Review
- Fabrication of Lithium/Strontium-Releasing Smart Bioactive Glasses with Anti-Inflammatory and Osteogenic Effects Tailored to Pathological Stages.Macromolecular bioscience · 2025Article
- Balancing Immunity: GSK-3's Divergent Roles in Dendritic Cell-Mediated T-Cell Priming and Memory Responses.International journal of molecular sciences · 2025Review
- Applications of Osteoimmunomodulation Models in Evaluating Osteogenic Biomaterials.Journal of functional biomaterials · 2025Review
- Targeting PI3K Signaling to Overcome Tumor Immunosuppression: Synergistic Strategies to Enhance Cancer Vaccine Efficacy.Vaccines · 2025Review
- GSK3α/β Restrain IFN-γ-Inducible Costimulatory Molecule Expression in Alveolar Macrophages, Limiting CD4+ T Cell Activation.ImmunoHorizons · 2024Article
- Glycogen synthase kinase 3β: the nexus of chemoresistance, invasive capacity, and cancer stemness in pancreatic cancer.Cancer drug resistance (Alhambra, Calif.) · 2024Review
- Article
- Molecular mechanisms and therapeutic potential of lithium in Alzheimer's disease: repurposing an old class of drugs.Frontiers in pharmacology · 2024Review
- JAK-STAT signaling in inflammation and stress-related diseases: implications for therapeutic interventions.Molecular biomedicine · 2023Review
- Role of GSK-3β Inhibitors: New Promises and Opportunities for Alzheimer's Disease.Advanced pharmaceutical bulletin · 2023Review
- γ-aminobutyric acid B2 receptor: A potential therapeutic target for cholangiocarcinoma in patients with diabetes mellitus.World journal of gastroenterology · 2023Article
- P2X7 receptor inhibition ameliorates ubiquitin-proteasome system dysfunction associated with Alzheimer's disease.Alzheimer's research & therapy · 2023Article
- Inhibiting the glycerophosphodiesterase EDI3 in ER-HER2+ breast cancer cells resistant to HER2-targeted therapy reduces viability and tumour growth.Journal of experimental & clinical cancer research : CR · 2023Article
- Beta 2 adrenergic receptor and mu opioid receptor interact to potentiate the aggressiveness of human breast cancer cell by activating the glycogen synthase kinase 3 signaling.Breast cancer research : BCR · 2022Article
- Sepsis-associated brain injury: underlying mechanisms and potential therapeutic strategies for acute and long-term cognitive impairments.Journal of neuroinflammation · 2022Review
44 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Excessive neuroinflammation contributes to many neurological disorders and is poorly controlled therapeutically. The signal transducer and activator of transcription (STAT) family of transcription factors has a central role in inflammatory reactions, being stimulated by multiple cytokines and interferons and regulating the expression of many proteins involved in inflammation. We found that STAT3 activation is highly dependent on glycogen synthase kinase-3 (GSK3). Inhibitors of GSK3 greatly reduced (>75%) the activating STAT3 tyrosine phosphorylation in mouse primary astrocytes, microglia, and macrophage-derived RAW264.7 cells induced by interferon-gamma (IFNgamma), IFNalpha, interleukin-6, or insulin. GSK3 inhibitors blocked STAT3 DNA binding activity and the expression of STAT3-induced GFAP and Bcl-3. GSK3 dependence was selective for activation of STAT3 and STAT5, whereas STAT1 and STAT6 activation were GSK3-independent. Knockdown of the two GSK3 isoforms showed STAT3 and STAT5 activation were dependent on GSK3beta, but not GSK3alpha. The regulatory mechanism involved GSK3beta binding STAT3 and promoting its association with the IFNgamma receptor-associated intracellular signaling complex responsible for activating STAT3. Furthermore, GSK3beta associated with the IFNgamma receptor and was activated by stimulation with IFNgamma. Thus, inhibitors of GSK3 reduce the activation of STAT3 and STAT5, providing a mechanism to differentially regulate STATs to modulate the inflammatory response.
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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.