Enhanced degradation of mutant huntingtin by rho kinase inhibition is mediated through activation of proteasome and macroautophagy
Open accessAbstract
Enhancing the degradation of mutant protein is one of the most investigated approaches in experimental therapy of the polyglutamine-related disorders such as Huntington disease (HD). Inhibition of rho-associated kinases (ROCKs) reduced the aggregation and levels of mutant huntingtin in cellular models of HD via activation of the ubiquitin proteasome system (UPS) and macroautophagy. This unique effect makes the Rho/ROCK pathway and its downstream effectors attractive therapeutic targets for polyglutamine-related diseases.
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The mechanism of Y27632-mediated reduction of Htt toxicity involves an increase in both proteasomal degradation of Htt and macroautophagy.
“The mechanism was later found to involve Y27632-mediated increase in both proteasomal degradation of Htt and macroautophagy [200].”
From RhoA Signaling in Neurodegenerative Diseases (2022) · cites this paper as [200]
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- Authors
- Bauer, P. O., & Nukina, N.
- Affiliations
- RIKEN Center for Brain Science (JP)
- Corresponding author
- Nukina, Nobuyuki
- Venue
- Autophagy
- Publisher
- Informa UK Limited
- Published
- 2009-07
- Volume
- 5
- Issue
- 5
- Pages
- 747-748
- ISSN
- 1554-8627 (ISSN-L)
- 1554-8635
- OpenAlex
- W1983733701
- Cited by
- 32
- References
- 0
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2022: 1 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 2 · 2016: 3 · 2015: 4 · 2014: 3 · 2013: 4 · 2012: 3
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Autophagy (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Japan Society for the Promotion of Science (17025044)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Health Sciences › Medicine › Physiology › Lysosomal Storage Disorders Research
- Keywords
- mutant huntingtin, Rho kinase inhibition, Rho/ROCK signaling, polyglutamine diseases, Huntington's disease, ubiquitin-proteasome system, macroautophagy, protein degradation, protein aggregation, therapeutic target
- MeSH terms
- Huntingtin Protein, Amides, Animals, Autophagy, HeLa Cells, Humans, Nerve Tissue Proteins, Nuclear Proteins, Protein Processing, Post-Translational, Pyridines, Proteasome Endopeptidase Complex, Protein Kinase Inhibitors, Mutant Proteins, Mice, rho-Associated Kinases
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