ArticleJournal of molecular neuroscience : MN2011
Proteasome inhibition drives HDAC6-dependent recruitment of tau to aggresomes.
Article in Journal of molecular neuroscience : MN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 50 citations in OpenAlex.
- Loss of SMARCAD1 Mitigates Tauopathy.Aging cell · 2026Article
- A novel insight into neurological disorders through HDAC6 protein-protein interactions.Scientific reports · 2024Article
- Inducing aggresome and stable tau aggregation in Neuro2a cells with an optogenetic tool.Biophysics and physicobiology · 2024Article
- Proteasomal Stimulation by MK886 and Its Derivatives Can Rescue Tau-Induced Neurite Pathology.Molecular neurobiology · 2023Article
- Autophagic sequestration of SQSTM1 disrupts the aggresome formation of ubiquitinated proteins during proteasome inhibition.Cell death & disease · 2022Article
- Mechanistic Insights into Selective Autophagy Subtypes in Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Tau Accumulation via Reduced Autophagy Mediates GGGGCC Repeat Expansion-Induced Neurodegeneration in Drosophila Model of ALS.Neuroscience bulletin · 2020Article
- Management of Hsp90-Dependent Protein Folding by Small Molecules Targeting the Aha1 Co-Chaperone.Cell chemical biology · 2020Article
- Review
- Histone Deacetylase 6 and the Disease Mechanisms of α-Synucleinopathies.Frontiers in synaptic neuroscience · 2020Review
- Activity of the poly(A) binding protein MSUT2 determines susceptibility to pathological tau in the mammalian brain.Science translational medicine · 2019Article
- USP10 is a critical factor for Tau-positive stress granule formation in neuronal cells.Scientific reports · 2019Article
- Tau Protein Squired by Molecular Chaperones During Alzheimer's Disease.Journal of molecular neuroscience : MN · 2018Review
- UCH-L1 Inhibition Suppresses tau Aggresome Formation during Proteasomal Impairment.Molecular neurobiology · 2018Article
- Complex neuroprotective and neurotoxic effects of histone deacetylases.Journal of neurochemistry · 2018Review
- Multimodal actions of the phytochemical sulforaphane suppress both AR and AR-V7 in 22Rv1 cells: Advocating a potent pharmaceutical combination against castration-resistant prostate cancer.Oncology reports · 2017Article
- Interaction of SQSTM1 with the motor protein dynein--SQSTM1 is required for normal dynein function and trafficking.Journal of cell science · 2014Article
- Article
- Fractalkine signaling and Tau hyper-phosphorylation are associated with autophagic alterations in lentiviral Tau and Aβ1-42 gene transfer models.Experimental neurology · 2014Article
- HDAC6 regulates mutant SOD1 aggregation through two SMIR motifs and tubulin acetylation.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Lesions containing aggregated and hyperphosphorylated tau protein are characteristic of neurodegenerative tauopathies. We have developed a cellular model of pathological tau deposition and clearance by overexpressing wild type human tau in HEK293 cells. When proteasome activity is inhibited, HEK293/tau cells accumulate tau protein in structures that bear many of the hallmarks of aggresomes. These include recruitment of tau into large spherical inclusions, accumulation of the retrograde motor protein dynein at the centrosome, formation of an intermediate filament cage around inclusions, and clustering of mitochondria at the aggresome. Tau aggresomes form rapidly and can be cleared upon relief of proteasome inhibition. We observe recruitment of pathological misfolded phospho-tau species to aggresomes. Immunoblotting reveals accumulation of detergent insoluble aggregated tau species. Knockdown of histone deacetylase 6, a protein known to interact with tau, reveals a requirement for HDAC6 activity in tau aggresome formation. Direct observation of the accumulation and clearance of abnormal tau species will allow us to dissect the cellular and molecular mechanisms at work in clearing aggresomal tau and its similarity to disease relevant pathological tau clearance mechanisms.
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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.