ArticleThe Journal of biological chemistry2010
A caspase cleaved form of tau is preferentially degraded through the autophagy pathway.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 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.
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.
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Who cites it
89 citing papers in PubMed, 1 synthesis or guideline pooled it, 150 citations in OpenAlex.
- Targeting Ubiquitin-Proteasome Pathway by Natural Products: Novel Therapeutic Strategy for Treatment of Neurodegenerative Diseases.Frontiers in physiology · 2020Pooled it
- Trial
- A HaloTag-4R-Tau Pulse-Chase Sensor Reveals Neddylation Inhibition Promotes Degradation of Tau in iNeurons.bioRxiv : the preprint server for biology · 2026Article
- Probing tau citrullination in Alzheimer's disease brains and mouse models of tauopathy.Acta neuropathologica · 2025Article
- Autophagy and Cellular Senescence in Alzheimer's Disease: Key Drivers of Neurodegeneration.CNS neuroscience & therapeutics · 2025Review
- Sleep-wake variation in body temperature regulates tau secretion and correlates with CSF and plasma tau.The Journal of clinical investigation · 2025Article
- The interplay between physical exercise and autophagy signaling in brain health, neurodegenerative diseases and aging.Frontiers in aging neuroscience · 2025Review
- Autophagy-lysosomal-associated neuronal death in neurodegenerative disease.Acta neuropathologica · 2024Review
- Article
- Transgenic Dendra2::tau expression allows in vivo monitoring of tau proteostasis in Caenorhabditis elegans.Disease models & mechanisms · 2024Article
- Visualization Analysis of Tau Protein in the Brain of Alzheimer's Disease: A Scoping Literature Review.Current Alzheimer research · 2024Article
- Post-Translational Modifications in Tau and Their Roles in Alzheimer's Pathology.Current Alzheimer research · 2024Review
- "Dirty Dancing" of Calcium and Autophagy in Alzheimer's Disease.Life (Basel, Switzerland) · 2023Review
- Neurobiochemical, Peptidomic, and Bioinformatic Approaches to Characterize Tauopathy Peptidome Biomarker Candidates in Experimental Mouse Model of Traumatic Brain Injury.Molecular neurobiology · 2023Article
- Brain insulin resistance linked Alzheimer's and Parkinson's disease pathology: An undying implication of epigenetic and autophagy modulation.Inflammopharmacology · 2023Review
- 24-Hydroxycholesterol Induces Tau Proteasome-Dependent Degradation via the SIRT1/PGC1α/Nrf2 Pathway: A Potential Mechanism to Counteract Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2023Article
- Concomitant Neuronal Tau Deposition and FKBP52 Decrease Is an Early Feature of Different Human and Experimental Tauopathies.Journal of Alzheimer's disease : JAD · 2023Article
- Age-related changes in tau and autophagy in human brain in the absence of neurodegeneration.PloS one · 2023Article
- Review
- The emerging role of autophagy and mitophagy in tauopathies: From pathogenesis to translational implications in Alzheimer's disease.Frontiers in aging neuroscience · 2022Review
29 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
2 authors at 1 institution in 1 country.
Funding
Abstract
The microtubule-associated protein tau plays a central role in the pathogenesis of Alzheimer disease (AD) and abnormally accumulates as neurofibrillary tangles; therefore, the pathways by which tau is degraded have been examined extensively. In AD brain tau is abnormally truncated at Asp(421) (tauDeltaC), which increases its fibrillogenic properties and results in compromised neuronal function. Given the fact that the accumulation of tauDeltaC is a pathogenic process in AD, in this study we examined whether full-length tau and tauDeltaC are degraded through similar or different mechanisms. To this end a tetracycline-inducible model was used to show that tauDeltaC was degraded significantly faster than full-length tau (FL-tau). Pharmacological inhibition of the proteasome or autophagy pathways demonstrated that although FL-tau is degraded by the proteasome, tauDeltaC is cleared predominantly by macroautophagy. We also found that tauDeltaC binds C terminus of Hsp70-interacting protein more efficiently than tau. This interaction leads to an increased ubiquitylation of tauDeltaC in a reconstituted in vitro assay, but surprisingly, tau (full-length or truncated) was not ubiquitylated in situ. The finding that tauDeltaC and FL-tau are differentially processed by these degradation systems provides important insights for the development of therapeutic strategies, which are focused on modulating degradation systems to preferentially clear pathological forms of the proteins.
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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.