ArticleF1000Research2016
Does inactivation of USP14 enhance degradation of proteasomal substrates that are associated with neurodegenerative diseases?
Article in F1000Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Article
- Novel Small-Molecule Analogues of IU1 Ameliorate Amyloid-β Mediated Toxicity in Alzheimer's Disease Cell and Worm Models.International journal of molecular sciences · 2026Article
- AKT and DUBs: a bidirectional relationship.Cellular & molecular biology letters · 2025Review
- Alternative 3' UTR polyadenylation is disrupted in the rNLS8 mouse model of ALS/FTLD.Molecular brain · 2025Article
- USP14 inhibition enhances Parkin-independent mitophagy in iNeurons.Pharmacological research · 2024Article
- DUBs in Alzheimer's disease: mechanisms and therapeutic implications.Cell death discovery · 2024Review
- Understanding neurodevelopmental proteasomopathies as new rare disease entities: A review of current concepts, molecular biomarkers, and perspectives.Genes & diseases · 2024Review
- Review
- Protein clearance strategies for disease intervention.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- Deubiquitinating enzymes (DUBs): decipher underlying basis of neurodegenerative diseases.Molecular psychiatry · 2022Review
- Examination of genetic and pharmacological tools to study the proteasomal deubiquitinating enzyme ubiquitin-specific protease 14 in the nervous system.Journal of neurochemistry · 2021Article
- USP14: Structure, Function, and Target Inhibition.Frontiers in pharmacology · 2021Review
- The Effect of Dysfunctional Ubiquitin Enzymes in the Pathogenesis of Most Common Diseases.International journal of molecular sciences · 2020Review
- Unstructured Biology of Proteins from Ubiquitin-Proteasome System: Roles in Cancer and Neurodegenerative Diseases.Biomolecules · 2020Article
- Inactive USP14 and inactive UCHL5 cause accumulation of distinct ubiquitinated proteins in mammalian cells.PloS one · 2019Article
- Deubiquitylating enzymes and drug discovery: emerging opportunities.Nature reviews. Drug discovery · 2018Review
- Updating the guidelines for data transparency in the British Journal of Pharmacology - data sharing and the use of scatter plots instead of bar charts.British journal of pharmacology · 2017Article
- Neurotoxic mechanisms by which the USP14 inhibitor IU1 depletes ubiquitinated proteins and Tau in rat cerebral cortical neurons: Relevance to Alzheimer's disease.Biochimica et biophysica acta. Molecular basis of disease · 2017Article
- Does inactivation of USP14 enhance degradation of proteasomal substrates that are associated with neurodegenerative diseases?F1000Research · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A common pathological hallmark of age-related neurodegenerative diseases is the intracellular accumulation of protein aggregates such as α-synuclein in Parkinson's disease, TDP-43 in ALS, and tau in Alzheimer's disease. Enhancing intracellular clearance of aggregation-prone proteins is a plausible strategy for slowing progression of neurodegenerative diseases and there is great interest in identifying molecular targets that control protein turnover. One of the main routes for protein degradation is through the proteasome, a multisubunit protease that degrades proteins that have been tagged with a polyubiquitin chain by ubiquitin activating and conjugating enzymes. Published data from cellular models indicate that Ubiquitin-specific protease 14 (USP14), a deubiquitinating enzyme (DUB), slows the degradation of tau and TDP-43 by the proteasome and that an inhibitor of USP14 increases the degradation of these substrates. We conducted similar experiments designed to evaluate tau, TDP-43, or α-synuclein levels in cells after overexpressing USP14 or knocking down endogenous expression by siRNA.
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