Tau protein isoforms, phosphorylation and role in neurodegenerative disorders.

By L. Buée, T. Bussiere, V. Buée-Scherrer, A. Delacourte, Patrick R. Hof. Brain research. Brain research reviews, 2000

2,043 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/c399bb2d39008442517a76b72fe3000272830904

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Citations in the corpus

Tau mislocalization to dendritic spines mediates synaptic dysfunction independently of neurodegeneration (2010, methodology): “Kolmogorov-Smirnov (B), ANOVA followed by Fisher’s PLSD post hoc analysis (C, E, and F), *p < 0.05, ***p < 0.001. flanked by proline-rich regions (Buée et al., 2000; Avila et al., 2004).”
Pathology of Neurodegenerative Diseases. (2017, background): “Tau is a microtubule-associated phosphoprotein abundant in axons involved in promoting polymerization and stabilization of microtubules (Binder et al. 1985; Buee et al. 2000; Mandelkow and Mandelkow 2012).”
APP processing in Alzheimer's disease (2011, background): “sist largely of hyperphosphorylated twisted filaments of the microtubule-associated protein tau [4,5].”
Neuropathology and Cognitive Impairment in Alzheimer Disease: A Complex but Coherent Relationship (2009, background): “These cases are now presumed to reflect tauopathies, which are a diverse group of diseases that may be associated with genetic (tau mutations) or environmental (Guamian or postencephalitic parkinsonism) factors (3, 5).”
Therapeutics of Alzheimer's disease: Past, present and future. (2014, background): “By regulatingmicrotubule assembly, tau modulates the functional organization of the neurons, particularly axonal morphology, growth, and polarity (Buee et al., 2000).”
Role of tau protein in both physiological and pathological conditions. (2004, background): “(32) and in that of Ingram and Spillantini (147).”
Pre-mRNA splicing and human disease. (2003, background): “…protein tau into neuronal cytoplasmic inclusions is associated with several neuropathological conditions characterized by progressive dementia including Alzheimer’s disease, Pick’s disease, and frontotemporal dementia and Parkinsonism linked to Chromosome 17 (FTDP-17; Buee et al. 2000).”
Post-translational modifications of tau protein: implications for Alzheimer's disease. (2011, positive): “Among the 16 exons of tau gene, exons 2, 3 and 10 undergo alternative splicing, whereas exon 4A is only transcribed in the peripheral nervous system (Andreadis et al., 1992; Buee et al., 2000; Panda et al., 2003) (Fig.”
Mitophagy and Alzheimer’s disease: cellular and molecular mechanisms (2017, background): “Microtubules are a component of the cellular cytoskeleton on which mitochondria, lysosomes, and other organelles are transported [48].”
Age-Dependent Neurofibrillary Tangle Formation, Neuron Loss, and Memory Impairment in a Mouse Model of Human Tauopathy (P301L) (2005, background): “Surprisingly, rTg(tauP301L)4510 uble 64 kDa tau species observed in this mouse model comigrates with a major hyperphosphorylated tau species observed in human NFTs in AD and other tauopathies (Buee et al., 2000).”