ArticleThe American journal of pathology2001
Molecular analysis of mutant and wild-type tau deposited in the brain affected by the FTDP-17 R406W mutation.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- Slowly progressive dementia caused by MAPT R406W mutations: longitudinal report on a new kindred and systematic review.Alzheimer's research & therapy · 2018Pooled it
- Tau filaments with the Alzheimer fold in human MAPT mutants V337M and R406W.Nature structural & molecular biology · 2025Article
- MAPT mutations associated with familial tauopathies lead to formation of conformationally distinct oligomers that have cross-seeding ability.Protein science : a publication of the Protein Society · 2024Article
- Tau filaments with the Alzheimer fold in cases withbioRxiv : the preprint server for biology · 2024Article
- New SNCA mutation and structures of α-synuclein filaments from juvenile-onset synucleinopathy.Acta neuropathologica · 2023Article
- Patients carrying the mutation p.R406W in MAPT present with non-conforming phenotypic spectrum.Brain : a journal of neurology · 2023Article
- Human Induced Pluripotent Stem Cell Models of Frontotemporal Dementia With Tau Pathology.Frontiers in cell and developmental biology · 2021Review
- A Comprehensive Resource for Induced Pluripotent Stem Cells from Patients with Primary Tauopathies.Stem cell reports · 2019Article
- Pathological Progression Induced by the Frontotemporal Dementia-Associated R406W Tau Mutation in Patient-Derived iPSCs.Stem cell reports · 2019Article
- Integrative system biology analyses of CRISPR-edited iPSC-derived neurons and human brains reveal deficiencies of presynaptic signaling in FTLD and PSP.Translational psychiatry · 2018Article
- A Conserved Cytoskeletal Signaling Cascade Mediates Neurotoxicity of FTDP-17 Tau MutationsThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Reactive oxygen species induce neurite degeneration before induction of cell death.Journal of clinical biochemistry and nutrition · 2016Article
- Quantitative and combinatory determination of in situ phosphorylation of tau and its FTDP-17 mutants.Scientific reports · 2016Article
- Cellular factors modulating the mechanism of tau protein aggregation.Cellular and molecular life sciences : CMLS · 2015Review
- Invited review: Frontotemporal dementia caused by microtubule-associated protein tau gene (MAPT) mutations: a chameleon for neuropathology and neuroimaging.Neuropathology and applied neurobiology · 2015Review
- Protein phosphorylation in neurodegeneration: friend or foe?Frontiers in molecular neuroscience · 2014Review
- The frontotemporal dementia mutation R406W blocks tau's interaction with the membrane in an annexin A2-dependent manner.The Journal of cell biology · 2011Article
- P301S mutant human tau transgenic mice manifest early symptoms of human tauopathies with dementia and altered sensorimotor gating.PloS one · 2011Article
- Aggregation of detergent-insoluble tau is involved in neuronal loss but not in synaptic loss.The Journal of biological chemistry · 2010Article
- Effect of Pin1 or microtubule binding on dephosphorylation of FTDP-17 mutant Tau.The Journal of biological chemistry · 2009Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) is a familial neurological disorder, characterized genetically by autosomal dominant inheritance, clinically by behavioral abnormalities and parkinsonism, and neuropathologically by tauopathy. Linkage analyses of affected families have led to identification of several exonic and intronic mutations in the tau gene. In this study, we analyzed molecular species of tau in the soluble and insoluble fractions of brain affected by the FTDP-17 R406W mutation. Protein chemical analysis and Western blotting using site-specific antibodies indicated that almost equal amounts of wild-type and mutant tau were present in the Sarkosyl-insoluble fraction of the R406W brain. Consistent with this, wild-type and mutant tau colocalized in neurofibrillary tangles in the frontal cortex and hippocampus of the R406W brain. In contrast to soluble R406W tau, which was less phosphorylated than soluble wild-type tau, the Sarkosyl-insoluble mutant tau was highly phosphorylated as well as the insoluble wild-type tau.
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Registered trials
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