ArticleNeurotoxicity research2020
Autophagy and Ubiquitin-Proteasome System Coordinate to Regulate the Protein Quality Control of Neurodegenerative Disease-Associated DCTN1.
Article in Neurotoxicity research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Autophagy and mitophagy at the synapse and beyond: implications for learning, memory and neurological disorders.Autophagy · 2026Review
- Functional validation to explore the protective role of miR-223 in Staphylococcus aureus-induced bovine mastitis.Journal of animal science and biotechnology · 2025Article
- Amino Acid-Starved Cancer Cells Utilize Macropinocytosis and Ubiquitin-Proteasome System for Nutrient Acquisition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Hypoxic Preconditioned Neural Stem Cell-Derived Extracellular Vesicles Contain Distinct Protein Cargo from Their Normal Counterparts.Current issues in molecular biology · 2023Article
- Bioinformatics and Next-Generation Data Analysis for Identification of Genes and Molecular Pathways Involved in Subjects with Diabetes and Obesity.Medicina (Kaunas, Lithuania) · 2023Article
- Cogs in the autophagic machine-equipped to combat dementia-prone neurodegenerative diseases.Frontiers in molecular neuroscience · 2023Review
- CHIP Decline Is Associated With Isoflurane-Induced Neurodegeneration in Aged Mice.Frontiers in neuroscience · 2022Article
- Dysregulated Dynein-Mediated Trafficking of Nephrin Causes INF2-related Podocytopathy.Journal of the American Society of Nephrology : JASN · 2021Article
- Releasing the Lockdown: An Emerging Role for the Ubiquitin-Proteasome System in the Breakdown of Transient Protein Inclusions.Biomolecules · 2020Review
- Cell-Clearing Systems Bridging Repeat Expansion Proteotoxicity and Neuromuscular Junction Alterations in ALS and SBMA.International journal of molecular sciences · 2020Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Motor neuron diseases are neurodegenerative diseases that are characterized by degeneration of the upper and lower motor neurons in the central nervous system. Mutations in Dynactin 1 (DCTN1), a component in the Dynein/Dynactin motor complex, have been previously identified to cause motor neuron diseases and other neurodegenerative disorders. Recent studies showed that motor neuron disease-linked mutation, such as G59S mutation, could lead to dysfunction and protein aggregation of DCTN1. However, the cellular pathway involved in the clearance of DCTN1 aggregates is still not fully elucidated. In this study, we employed a culture cell model of DCTN1-linked neurodegeneration and explored the role of cellular protein control systems in the regulation of wild type and mutant DCTN1. We find that the ubiquitin-proteasome system, but not autophagy, is the primary protein degradation system for the turnover of both wild type and G59S DCTN1 under normal conditions. However, it turns out that autophagy can play a role in the clearance of protein aggregates of G59S DCTN1 when the proteasome activity is inhibited. Importantly, overexpression of TFEB, a master regulator of autophagy, promotes the autophagic clearance of G59S DCTN1 aggregates and ameliorates G59S DCTN1-induced cytotoxicity when the proteasomes are impaired. In conclusion, autophagy may play as a backup system to protect cells against the cytotoxicity induced by aggregate-prone DCTN1 when proteasomal function is damaged.
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