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Nuclear Tau, a Key Player in Neuronal DNA Protection
Open accessAbstract
Tau, a neuronal protein involved in neurodegenerative disorders such as Alzheimer disease, which is primarily described as a microtubule-associated protein, has also been observed in the nuclei of neuronal and non-neuronal cells. However, the function of the nuclear form of Tau in neurons has not yet been elucidated. In this work, we demonstrate that acute oxidative stress and mild heat stress (HS) induce the accumulation of dephosphorylated Tau in neuronal nuclei. Using chromatin immunoprecipitation assays, we demonstrate that the capacity of endogenous Tau to interact with neuronal DNA increased following HS. Comet assays performed on both wild-type and Tau-deficient neuronal cultures showed that Tau fully protected neuronal genomic DNA against HS-induced damage. Interestingly, HS-induced DNA damage observed in Tau-deficient cells was completely rescued after the overexpression of human Tau targeted to the nucleus. These results highlight a novel role for nuclear Tau as a key player in early stress response.
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“In particular, intranuclear tau is thought to bind to chromatin and stabilize it in response to cellular stressors such heat [149].”
From DNA repair deficiency and senescence in concussed professional athletes involved in contact sports (2019) · cites this paper as [149]
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“prevents DNA damage by oxidative stress 94, 106”
From Altered Machinery of Protein Synthesis in Alzheimer's: From the Nucleolus to the Ribosome (2016) · cites this paper as [94]
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“When the heat stress occurs, tau protein binds to DNA and enhances DNA repair [80].”
BackgroundSelf-citation
Metadata
- Authors
- Sultan, A., Nesslany, F., Violet, M., Bégard, S., Loyens, A., Talahari, S., Mansuroglu, Z., Marzin, D., Sergeant, N., Humez, S., Colin, M., Bonnefoy, E., Buée, L., & Galas, M.-C.
- Affiliations
- Inserm (FR)
- Institut Pasteur de Lille (FR)
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Galas, Marie-Christine
- ORCID
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2011-02
- Volume
- 286
- Issue
- 6
- Pages
- 4566-4575
- ISSN
- 0021-9258 (ISSN-L)
- PMC
- PMC3039398
- OpenAlex
- W2155048015
- Cited by
- 421
- References
- 54
- Citations by year
- 2026: 24 · 2025: 16 · 2024: 21 · 2023: 31 · 2022: 29 · 2021: 44 · 2020: 39 · 2019: 24 · 2018: 48 · 2017: 27 · 2016: 23 · 2015: 25 · 2014: 26 · 2013: 18 · 2012: 16
- FWCI
- 9.41
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Biological Chemistry (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- European Commission (200611)
- Agence Nationale de la Recherche
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Heat shock proteins research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- heat stress, oxidative stress, DNA damage, neurodegeneration, Alzheimer's disease, microtubule-associated proteins, stress response
- MeSH terms
- Alzheimer Disease, Animals, Cell Nucleus, Cells, Cultured, DNA, Humans, Neurons, Phosphorylation, tau Proteins, Mice, Knockout, Heat-Shock Response, Mice
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