ArticleMolecular biology of the cell2000
Distinct FTDP-17 missense mutations in tau produce tau aggregates and other pathological phenotypes in transfected CHO cells.
Article in Molecular biology of the cell, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 128 citations in OpenAlex.
- MAPT-derived circTau6 induces tau pathogenesis and neurodegeneration by encoding Tau variants.Molecular psychiatry · 2026Article
- A metabolite extracted from Escherichia coli suppresses tau aggregation.The Biochemical journal · 2026Article
- Deubiquitinating Enzymes Ubiquitin-Specific Proteases 7 and 10 Regulate TAU Aggregation.International journal of molecular sciences · 2025Article
- Macrocyclic β-arch peptides that mimic the structure and function of disease-associated tau folds.Nature chemistry · 2025Article
- Tau Lysine Pseudomethylation Regulates Microtubule Binding and Enhances Prion-like Tau Aggregation.International journal of molecular sciences · 2023Article
- Tau mutation S356T in the three repeat isoform leads to microtubule dysfunction and promotes prion-like seeded aggregation.Frontiers in neuroscience · 2023Article
- Towards a Mechanistic Model of Tau-Mediated Pathology in Tauopathies: What Can We Learn from Cell-Based In Vitro Assays?International journal of molecular sciences · 2022Review
- Heparan Sulfate Proteoglycans (HSPGs) Serve as the Mediator Between Monomeric Tau and Its Subsequent Intracellular ERK1/2 Pathway Activation.Journal of molecular neuroscience : MN · 2022Article
- Asparagine residue 368 is involved in Alzheimer's disease tau strain-specific aggregation.The Journal of biological chemistry · 2020Article
- Tau Ser208 phosphorylation promotes aggregation and reveals neuropathologic diversity in Alzheimer's disease and other tauopathies.Acta neuropathologica communications · 2020Article
- Impaired tau-microtubule interactions are prevalent among pathogenic tau variants arising from missense mutations.The Journal of biological chemistry · 2019Article
- T-complex protein 1-ring complex enhances retrograde axonal transport by modulating tau phosphorylation.Traffic (Copenhagen, Denmark) · 2018Article
- Tau Fibril Formation in Cultured Cells Compatible with a Mouse Model of Tauopathy.International journal of molecular sciences · 2018Article
- Formulated Chinese Medicine Shaoyao Gancao Tang Reduces Tau Aggregation and Exerts Neuroprotection through Anti-Oxidation and Anti-Inflammation.Oxidative medicine and cellular longevity · 2018Article
- Bidirectional interplay of HSF1 degradation and UPR activation promotes tau hyperphosphorylation.PLoS genetics · 2017Article
- The Distance between N and C Termini of Tau and of FTDP-17 Mutants Is Modulated by Microtubule Interactions in Living Cells.Frontiers in molecular neuroscience · 2017Article
- Stabilizing the Hsp70-Tau Complex Promotes Turnover in Models of Tauopathy.Cell chemical biology · 2016Article
- Conserved Lysine Acetylation within the Microtubule-Binding Domain Regulates MAP2/Tau Family Members.PloS one · 2016Article
- Appoptosin-Mediated Caspase Cleavage of Tau Contributes to Progressive Supranuclear Palsy Pathogenesis.Neuron · 2015Article
- Cellular factors modulating the mechanism of tau protein aggregation.Cellular and molecular life sciences : CMLS · 2015Review
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple tau gene mutations are pathogenic for hereditary frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), with filamentous tau aggregates as the major lesions in the CNS of these patients. Recent studies have shown that bacterially expressed recombinant tau proteins with FTDP-17 missense mutations cause functional impairments, i.e., a reduced ability of mutant tau to bind to or promote the assembly of microtubules. To investigate the biological consequences of FTDP-17 tau mutants and assess their ability to form filamentous aggregates, we engineered Chinese hamster ovary cell lines to stably express tau harboring one or several different FTDP-17 mutations and showed that different tau mutants produced distinct pathological phenotypes. For example, delta K, but not several other single tau mutants (e.g., V337 M, P301L, R406W), developed insoluble amorphous and fibrillar aggregates, whereas a triple tau mutant (VPR) containing V337M, P301L, and R406W substitutions also formed similar aggregates. Furthermore, the aggregates increased in size over time in culture. Significantly, the formation of aggregated delta K and VPR tau protein correlated with reduced affinity of these mutants to bind microtubules. Reduced phosphorylation and altered proteolysis was also observed in R406W and delta K tau mutants. Thus, distinct pathological phenotypes, including the formation of insoluble filamentous tau aggregates, result from the expression of different FTDP-17 tau mutants in transfected Chinese hamster ovary cells and implies that these missense mutations cause diverse neurodegenerative FTDP-17 syndromes by multiple mechanisms.
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