ArticleThe Journal of cell biology1998
Overexpression of tau protein inhibits kinesin-dependent trafficking of vesicles, mitochondria, and endoplasmic reticulum: implications for Alzheimer's disease.
Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 335 papers, 1 of them a synthesis that pooled it.
What it found
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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
335 citing papers in PubMed, 1 synthesis or guideline pooled it, 807 citations in OpenAlex.
- The Role of Protein Misfolding and Tau Oligomers (TauOs) in Alzheimer's Disease (AD).International journal of molecular sciences · 2019Pooled it
- When Pathologies Collide: The Intersection of Tau and Alpha-Synuclein in Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- Stoichiometric 14-3-3ζ binding promotes phospho-Tau microtubule dissociation and reduces aggregation and condensation.Communications biology · 2025Article
- Is the Voltage-Dependent Anion Channel a Major Player in Neurodegenerative Diseases?International journal of molecular sciences · 2025Review
- Cytoskeletal Proteins and Alzheimer's Disease Pathogenesis: Focusing on the Interplay with Tau Pathology.Biomolecules · 2025Review
- Cellular and molecular mechanisms of pathological tau phosphorylation in traumatic brain injury: implications for chronic traumatic encephalopathy.Molecular neurodegeneration · 2025Review
- Examining the vulnerability of adult neuron subtypes to tau-mediated toxicity in Drosophila.Translational psychiatry · 2025Article
- Tau-targeting nanoparticles for treatment of Alzheimer's disease.Exploration (Beijing, China) · 2025Review
- Extracellular PHF-tau modulates astrocyte mitochondrial dynamics and mediates neuronal connectivity.Translational neurodegeneration · 2025Article
- Mechanism and regulation of kinesin motors.Nature reviews. Molecular cell biology · 2025Review
- Deciphering T Cell Dynamics in Alzheimer's Disease Pathogenesis: Insights and Implications.Current neuropharmacology · 2025Review
- Engine breakdown of lysosomes and related organelles and the resulting physiology.Frontiers in cell and developmental biology · 2025Review
- Mesenchymal Stem Cell-Derived Exosomes as a Neuroregeneration Treatment for Alzheimer's Disease.Biomedicines · 2024Review
- Mitochondrial plasticity and synaptic plasticity crosstalk; in health and Alzheimer's disease.CNS neuroscience & therapeutics · 2024Review
- Abnormal expression of Tau in damaged oligodendrocytes of HLD1 mice.Neural regeneration research · 2024Article
- Real-Time Tracking of Vesicles in Living Cells Reveals That Tau-Hyperphosphorylation Suppresses Unidirectional Transport by Motor Proteins.Chemical & biomedical imaging · 2024Article
- Lung endothelium, tau, and amyloids in health and disease.Physiological reviews · 2024Review
- STAT3 ameliorates truncated tau-induced cognitive deficits.Neural regeneration research · 2024Article
- Initial Molecular Mechanisms of the Pathogenesis of Parkinson's Disease in a Mouse Neurotoxic Model of the Earliest Preclinical Stage of This Disease.International journal of molecular sciences · 2024Article
- Tau oligomerization on microtubules in health and disease.Cytoskeleton (Hoboken, N.J.) · 2024Article
275 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The neuronal microtubule-associated protein tau plays an important role in establishing cell polarity by stabilizing axonal microtubules that serve as tracks for motor-protein-driven transport processes. To investigate the role of tau in intracellular transport, we studied the effects of tau expression in stably transfected CHO cells and differentiated neuroblastoma N2a cells. Tau causes a change in cell shape, retards cell growth, and dramatically alters the distribution of various organelles, known to be transported via microtubule-dependent motor proteins. Mitochondria fail to be transported to peripheral cell compartments and cluster in the vicinity of the microtubule-organizing center. The endoplasmic reticulum becomes less dense and no longer extends to the cell periphery. In differentiated N2a cells, the overexpression of tau leads to the disappearance of mitochondria from the neurites. These effects are caused by tau's binding to microtubules and slowing down intracellular transport by preferential impairment of plus-end-directed transport mediated by kinesin-like motor proteins. Since in Alzheimer's disease tau protein is elevated and mislocalized, these observations point to a possible cause for the gradual degeneration of neurons.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.