ArticleThe American journal of pathology2002
Tau assembly in inducible transfectants expressing wild-type or FTDP-17 tau.
Article in The American journal of pathology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 66 citations in OpenAlex.
- Article
- Rho-kinase ROCK inhibitors reduce oligomeric tau protein.Neurobiology of aging · 2020Article
- Pharmacological induction of heat shock proteins ameliorates toxicity of mutant PKCγ in spinocerebellar ataxia type 14.The Journal of biological chemistry · 2018Article
- Tau Fibril Formation in Cultured Cells Compatible with a Mouse Model of Tauopathy.International journal of molecular sciences · 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
- RNA stores tau reversibly in complex coacervates.PLoS biology · 2017Article
- Quantitative and combinatory determination of in situ phosphorylation of tau and its FTDP-17 mutants.Scientific reports · 2016Article
- Long- and short-term CDK5 knockdown prevents spatial memory dysfunction and tau pathology of triple transgenic Alzheimer's mice.Frontiers in aging neuroscience · 2014Article
- Physiological and pathological phosphorylation of tau by Cdk5.Frontiers in molecular neuroscience · 2014Review
- Protein phosphorylation in neurodegeneration: friend or foe?Frontiers in molecular neuroscience · 2014Review
- Lentiviral delivery of the human wild-type tau protein mediates a slow and progressive neurodegenerative tau pathology in the rat brain.Molecular therapy : the journal of the American Society of Gene Therapy · 2013Article
- Isomerase Pin1 stimulates dephosphorylation of tau protein at cyclin-dependent kinase (Cdk5)-dependent Alzheimer phosphorylation sites.The Journal of biological chemistry · 2013Article
- Genotype-specific differences between mouse CNS stem cell lines expressing frontotemporal dementia mutant or wild type human tau.PloS one · 2012Article
- Tau and tauopathies.Progress in molecular biology and translational science · 2012Review
- The role of tau in neurodegenerative diseases and its potential as a therapeutic target.Scientifica · 2012Review
- The frontotemporal dementia mutation R406W blocks tau's interaction with the membrane in an annexin A2-dependent manner.The Journal of cell biology · 2011Article
- A caspase cleaved form of tau is preferentially degraded through the autophagy pathway.The Journal of biological chemistry · 2010Article
- Overexpression of wild-type murine tau results in progressive tauopathy and neurodegeneration.The American journal of pathology · 2009Article
- Concentration-dependent effects of proteasomal inhibition on tau processing in a cellular model of tauopathy.International journal of clinical and experimental pathology · 2009Article
- The cochaperone BAG2 sweeps paired helical filament- insoluble tau from the microtubule.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Conditional expression systems for 4-repeat wild-type (WT) tau or the corresponding mutants V337M and R406W were established in human neuroglioma H4 cells to study the effect of tau mutations on the physicochemical properties of tau, and to develop a cellular model for the formation of filamentous tau characteristic of frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17) and Alzheimer's disease. Upon induction tau expression increased, reaching maximal levels at 5 to 7 days. WT tau was phosphorylated at amino acids T181, S202/T205, T231, and S396/S404. The R406W mutation decreased tau phosphorylation at each of these sites as did the V337M mutation except for S396/S404 sites that increased. Most tau in postnuclear cell lysates was recovered in the supernatant fraction after centrifugation at 200,000 x g. The amount of tau in the pellet fraction increased more in mutant transfectants compared to WT when the induction was extended beyond 5 days. This particulate tau could be partially extracted with salt, Triton X-100, or sarkosyl. Of the transfectants, R406W had the highest proportion of sarkosyl-insoluble tau by day 7. This insoluble fraction was thioflavin S-positive and contained 15- to 5-nm-wide filaments with tau immunoreactivities. The R406W filaments were more abundant than those detected in similar preparations from WT or V337M transfectants. At the light microscopy level, most tau was found with microtubules, or diffusely distributed in the cytoplasm, but none of this appeared thioflavin S-positive. The results suggest that conditional tau transfectants are in a pretangle stage making them an attractive model system for studying intracellular tangle accumulation and for testing potential therapeutic agents as inhibitors for tau aggregation.
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