ArticleScientific reports2015
Stimulation of EphB2 attenuates tau phosphorylation through PI3K/Akt-mediated inactivation of glycogen synthase kinase-3β.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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38 citing papers in PubMed, 53 citations in OpenAlex.
- Neurexins, Ephrin receptors, and N-cadherin signaling as emerging mechanisms in synaptic dysfunction and neurodegenerative diseases.Communications biology · 2026Review
- Trace amine-associated receptor 1 (TAAR1): an emerging therapeutic target for neurodegenerative, neurodevelopmental, and neurotraumatic disorders.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Traditional Chinese Medicine-derived formulations and extracts modulating the PI3K/AKT pathway in Alzheimer's disease.Frontiers in pharmacology · 2025Review
- Article
- Fusobacterium nucleatum-induced exosomal HOTTIP promotes gastric cancer progression through the microRNA-885-3p/EphB2 axis.Cancer science · 2023Article
- Exon-intron split analysis reveals posttranscriptional regulatory signals induced by high and low n-6/n-3 polyunsaturated fatty acid ratio diets in piglets.Journal of animal science · 2023Article
- Naringin Protects against Tau Hyperphosphorylation in ABehavioural neurology · 2023Article
- APPsα rescues CDK5 and GSK3β dysregulation and restores normal spine density in Tau transgenic mice.Frontiers in cellular neuroscience · 2023Article
- Interactions between genes involved in physiological dysregulation and axon guidance: role in Alzheimer's disease.Frontiers in genetics · 2023Article
- Upregulation of endocytic protein expression in the Alzheimer's disease male human brain.Aging brain · 2023Article
- Signaling metabolite β-aminoisobutyric acid as a metabolic regulator, biomarker, and potential exercise pill.Frontiers in endocrinology · 2023Review
- Obesity as a Risk Factor for Dementia and Alzheimer's Disease: The Role of Leptin.International journal of molecular sciences · 2022Review
- Neurogenetic disorders across the lifespan: from aberrant development to degeneration.Nature reviews. Neurology · 2022Review
- Roles of Eph-Ephrin Signaling in the Eye Lens Cataractogenesis, Biomechanics, and Homeostasis.Frontiers in cell and developmental biology · 2022Review
- Roles and Mechanisms of Axon-Guidance Molecules in Alzheimer's Disease.Molecular neurobiology · 2021Review
- Protective Effect of Hydroxysafflor Yellow A against Chronic Mild Stress-induced Memory Impairments by Suppressing Tau Phosphorylation in Mice.Current medical science · 2021Article
- Latent trait modeling of tau neuropathology in progressive supranuclear palsy.Acta neuropathologica · 2021Article
- With the Permission of Microtubules: An Updated Overview on Microtubule Function During Axon Pathfinding.Frontiers in molecular neuroscience · 2021Review
- Research Progress on Alzheimer's Disease and Resveratrol.Neurochemical research · 2020Review
- Review
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal tau hyperphosphorylation is an early pathological marker of Alzheimer's disease (AD), however, the upstream factors that regulate tau phosphorylation are not illustrated and there is no efficient strategy to arrest tau hyperphosphorylation. Here, we find that activation of endogenous EphB2 receptor by ligand stimulation (ephrinB1/Fc) or by ectopic expression of EphB2 plus the ligand stimulation induces a remarkable tau dephosphorylation at multiple AD-associated sites in SK-N-SH cells and human embryonic kidney cells that stably express human tau (HEK293-tau). In cultured hippocampal neurons and the hippocampus of human tau transgenic mice, dephosphorylation of tau proteins was also detected by stimulation of EphB2 receptor. EphB2 activation inhibits glycogen synthase kinase-3β (GSK-3β), a crucial tau kinase, and activates phosphatidylinositol-3-kinase (PI3K)/Akt both in vitro and in vivo, whereas simultaneous inhibition of PI3K or upregulation of GSK-3β abolishes the EphB2 stimulation-induced tau dephosphorylation. Finally, we confirm that ephrinB1/Fc treatment induces tyrosine phosphorylation (activation) of EphB2, while deletion of the tyrosine kinase domain (VM) of EphB2 eliminates the receptor stimulation-induced GSK-3β inhibition and tau dephosphorylation. We conclude that activation of EphB2 receptor kinase arrests tau hyperphosphorylation through PI3K-/Akt-mediated GSK-3β inhibition. Our data provide a novel membranous target to antagonize AD-like tau pathology.
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