ArticleJournal of clinical biochemistry and nutrition2023
Oxidative stress induces tau hyperphosphorylation via MARK activation in neuroblastoma N1E-115 cells.
Article in Journal of clinical biochemistry and nutrition, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 3 citations in OpenAlex.
- Exploring and Targeting the Connection of Iron and Copper Homeostasis to Neurodegenerative Diseases.MedComm · 2026Review
- The Bright and Dark Sides of Nitric Oxide in Neurodegenerative Diseases.Journal of personalized medicine · 2026Review
- Oxidative Stress: Pathological Driver in Chronic Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- α-Tocotrienol Protects Neurons by Preventing Tau Hyperphosphorylation via Inhibiting Microtubule Affinity-Regulating Kinase Activation.International journal of molecular sciences · 2024Article
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Authors and funding
3 authors at 1 institution in 1 country.
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Abstract
Reactive oxygen species are considered a cause of neuronal cell death in Alzheimer's disease (AD). Abnormal tau phosphorylation is a proven pathological hallmark of AD. Microtubule affinity-regulating kinases (MARKs) regulate tau-microtubule binding and play a crucial role in neuronal survival. In this study, we hypothesized that oxidative stress increases the phosphorylation of Ser262 of tau protein through activation of MARKs, which is the main reason for the development of AD. We investigated the relationship between tau hyperphosphorylation on Ser262 and MARKs in N1E-115 cells subjected to oxidative stress by exposure to a low concentration of hydrogen peroxide. This work builds on the observation that hyperphosphorylation of tau is significantly increased by oxidative stress. MARKs activation correlated with tau hyperphosphorylation at Ser262, a site that is essential to maintain microtubule stability and is the initial phosphorylation site in AD. These results indicated that MARKs inhibitors might serve a role as therapeutic tools for the treatment of AD.
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