ArticleThe Journal of biological chemistry2009
Phosphorylated Tau interacts with c-Jun N-terminal kinase-interacting protein 1 (JIP1) in Alzheimer disease.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
91 citing papers in PubMed, 149 citations in OpenAlex.
- Metal Binding to Tau Protein: Physiological and Pathological Relevance.Biochemistry · 2026Review
- Tau T205 phosphorylation modulates engram cell recruitment and remote memory in mice.Nature communications · 2026Article
- Article
- RhoA/ROCK/GSK3β Signaling: A Keystone in Understanding Alzheimer's Disease.Current issues in molecular biology · 2025Review
- Role of Tau Protein Hyperphosphorylation in Diabetic Retinal Neurodegeneration.Journal of ophthalmology · 2025Review
- Correlation of β2-microglobulin with postoperative delirium and 3-year mortality undergoing knee or hip replacement surgery: a prospective cohort study.Frontiers in medicine · 2025Article
- Unraveling the role and mechanism of mitochondria in postoperative cognitive dysfunction: a narrative review.Journal of neuroinflammation · 2024Review
- Understanding Glycogen Synthase Kinase-3: A Novel Avenue for Alzheimer's Disease.Molecular neurobiology · 2024Review
- MSUT2 regulates tau spreading via adenosinergic signaling mediated ASAP1 pathway in neurons.Acta neuropathologica · 2024Article
- TDP-43 pathology and functional deficits in wild-type and ALS/FTD mutant cyclin F mouse models.Neuropathology and applied neurobiology · 2023Article
- Tau; One Protein, So Many Diseases.Biology · 2023Review
- Molecular Mechanisms of Neuroinflammation in Aging and Alzheimer's Disease Progression.International journal of molecular sciences · 2023Review
- Common mechanisms underlying axonal transport deficits in neurodegenerative diseases: a mini review.Frontiers in molecular neuroscience · 2023Review
- Bassoon contributes to tau-seed propagation and neurotoxicity.Nature neuroscience · 2022Article
- The Link between Oxidative Stress, Mitochondrial Dysfunction and Neuroinflammation in the Pathophysiology of Alzheimer's Disease: Therapeutic Implications and Future Perspectives.Antioxidants (Basel, Switzerland) · 2022Review
- Tau interactome maps synaptic and mitochondrial processes associated with neurodegeneration.Cell · 2022Article
- Decreased anterograde transport coupled with sustained retrograde transport contributes to reduced axonal mitochondrial density in tauopathy neurons.Frontiers in molecular neuroscience · 2022Article
- The Many Faces of Post-Ischemic Tau Protein in Brain Neurodegeneration of the Alzheimer's Disease Type.Cells · 2021Review
- Tau Protein Interaction Partners and Their Roles in Alzheimer's Disease and Other Tauopathies.International journal of molecular sciences · 2021Review
- Therapeutic Ultrasound as a Treatment Modality for Physiological and Pathological Ageing Including Alzheimer's Disease.Pharmaceutics · 2021Review
31 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
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In Alzheimer disease (AD) and frontotemporal dementia the microtubule-associated protein Tau becomes progressively hyperphosphorylated, eventually forming aggregates. However, how Tau dysfunction is associated with functional impairment is only partly understood, especially at early stages when Tau is mislocalized but has not yet formed aggregates. Impaired axonal transport has been proposed as a potential pathomechanism, based on cellular Tau models and Tau transgenic mice. We recently reported K369I mutant Tau transgenic K3 mice with axonal transport defects that suggested a cargo-selective impairment of kinesin-driven anterograde transport by Tau. Here, we show that kinesin motor complex formation is disturbed in the K3 mice. We show that under pathological conditions hyperphosphorylated Tau interacts with c-Jun N-terminal kinase- interacting protein 1 (JIP1), which is associated with the kinesin motor protein complex. As a result, transport of JIP1 into the axon is impaired, causing JIP1 to accumulate in the cell body. Because we found trapping of JIP1 and a pathological Tau/JIP1 interaction also in AD brain, this may have pathomechanistic implications in diseases with a Tau pathology. This is supported by JIP1 sequestration in the cell body of Tau-transfected primary neuronal cultures. The pathological Tau/JIP1 interaction requires phosphorylation of Tau, and Tau competes with the physiological binding of JIP1 to kinesin light chain. Because JIP1 is involved in regulating cargo binding to kinesin motors, our findings may, at least in part, explain how hyperphosphorylated Tau mediates impaired axonal transport in AD and frontotemporal dementia.
Indexed as
Identifiers
What OpenQuestion holds
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.