ArticleBiology open2014
Modification of the Drosophila model of in vivo Tau toxicity reveals protective phosphorylation by GSK3β.
Article in Biology open, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 30 citations in OpenAlex.
- Disodium cromoglycate restricts human tau hyperphosphorylation and manifestation of associated phenotypes by inhibiting GSK3β activity in Drosophila disease models.Molecular biology reports · 2026Article
- GSK-3β coordinates axonal microtubule organization through Shot and Tau.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Article
- Alzheimer's disease: insights into pathology, molecular mechanisms, and therapy.Protein & cell · 2025Review
- Reinstated Activity of Human Tau-induced Enhanced Insulin Signaling Restricts Disease Pathogenesis by Regulating the Functioning of Kinases/Phosphatases and Tau Hyperphosphorylation in Drosophila.Molecular neurobiology · 2024Article
- Simple model systems reveal conserved mechanisms of Alzheimer's disease and related tauopathies.Molecular neurodegeneration · 2023Review
- Specific post-translational modifications of soluble tau protein distinguishes Alzheimer's disease and primary tauopathies.Nature communications · 2023Article
- The Effect of theInternational journal of molecular sciences · 2023Article
- FTD-associated mutations in Tau result in a combination of dominant and recessive phenotypes.Neurobiology of disease · 2022Article
- Tau seeds are subject to aberrant modifications resulting in distinct signatures.Cell reports · 2021Article
- Early Mitochondrial Fragmentation and Dysfunction in a Drosophila Model for Alzheimer's Disease.Molecular neurobiology · 2021Article
- Cleavage of human tau at Asp421 inhibits hyperphosphorylated tau induced pathology in a Drosophila model.Scientific reports · 2020Article
- Low-dose ionizing radiation alleviates Aβ42-induced cell death via regulating AKT and p38 pathways inBiology open · 2019Article
- Article
- Peptides derived from the knuckle epitope of BMP-9 induce the cholinergic differentiation and inactivate GSk3beta in human SH-SY5Y neuroblastoma cells.Scientific reports · 2017Article
- Tau excess impairs mitosis and kinesin-5 function, leading to aneuploidy and cell death.Disease models & mechanisms · 2016Article
- Rescue from tau-induced neuronal dysfunction produces insoluble tau oligomers.Scientific reports · 2015Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Hyperphosphorylation of the microtubule associated protein, Tau, is the hallmark of a group of neurodegenerative disorders known as the tauopathies which includes Alzheimer's disease. Precisely how and why Tau phosphorylation is increased in disease is not fully understood, nor how individual sites modify Tau function. Several groups have used the Drosophila visual system as an in vivo model to examine how the toxicity of Tau varies with phosphorylation status. This system relies on overexpression of Tau from transgenes but is susceptible to position effects altering expression and activity of the transgenes. We have refined the system by eliminating position effects through the use of site-specific integration. By standardising Tau expression levels we have been able to compare directly the toxicity of different isoforms of Tau and Tau point mutants that abolish important phosphorylation events. We have also examined the importance of human kinases in modulating Tau toxicity in vivo. We were able to confirm that human GSK3β phosphorylates Tau and increases toxicity but, unexpectedly, we identified that preventing phosphorylation of Ser404 is a protective event. When phosphorylation at this site is prevented, Tau toxicity in the Drosophila visual system is increased in the presence of GSK3β. Our data suggest that not all phosphorylation events on Tau are associated with toxicity.
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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.