ArticleThe Journal of physiology2014
A catalytic independent function of the deubiquitinating enzyme USP14 regulates hippocampal synaptic short-term plasticity and vesicle number.
Article in The Journal of physiology, 2014. 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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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- Modulation of temporoammonic-CA1 synapses by neuropeptide Y is through Y1 receptors in mice.Neuropeptides · 2025Article
- HERC1 E3 Ubiquitin Ligase Is Necessary for Autophagy Processes and for the Maintenance and Homeostasis of Vesicles in Motor Nerve Terminals, but Not for Proteasomal Activity.International journal of molecular sciences · 2025Article
- Proteotoxic stress and the ubiquitin proteasome system.Seminars in cell & developmental biology · 2024Review
- In the moonlight: non-catalytic functions of ubiquitin and ubiquitin-like proteases.Frontiers in molecular biosciences · 2024Review
- Bicuculline restores frequency-dependent hippocampal I/E ratio and circuit function in PGC-1ɑ null mice.Neuroscience research · 2022Article
- Small-Molecule Inhibitors Targeting Proteasome-Associated Deubiquitinases.International journal of molecular sciences · 2021Review
- 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
- Deubiquitination Reactions on the Proteasome for Proteasome Versatility.International journal of molecular sciences · 2020Review
- Sustained ER stress promotes hyperglycemia by increasing glucagon action through the deubiquitinating enzyme USP14.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Proteome-wide analysis of USP14 substrates revealed its role in hepatosteatosis via stabilization of FASN.Nature communications · 2018Article
- Stretchable organic optoelectronic sensorimotor synapse.Science advances · 2018Article
- Target-cell-specific Short-term Plasticity Reduces the Excitatory Drive onto CA1 Interneurons Relative to Pyramidal Cells During Physiologically-derived Spike Trains.Neuroscience · 2018Article
- An inhibitor of the proteasomal deubiquitinating enzyme USP14 induces tau elimination in cultured neurons.The Journal of biological chemistry · 2017Article
- Meddling with Fate: The Proteasomal Deubiquitinating Enzymes.Journal of molecular biology · 2017Review
- USP14 de-ubiquitinates vimentin and miR-320a modulates USP14 and vimentin to contribute to malignancy in gastric cancer cells.Oncotarget · 2017Article
- Klotho regulates CA1 hippocampal synaptic plasticity.Neuroscience · 2017Article
- Sphingosine 1-phosphate lyase ablation disrupts presynaptic architecture and function via an ubiquitin- proteasome mediated mechanism.Scientific reports · 2016Article
- Bassoon and piccolo regulate ubiquitination and link presynaptic molecular dynamics with activity-regulated gene expression.The Journal of physiology · 2016Review
- Post-endocytotic Deubiquitination and Degradation of the Metabotropic γ-Aminobutyric Acid Receptor by the Ubiquitin-specific Protease 14.The Journal of biological chemistry · 2016Article
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6 authors at 5 institutions in 1 country.
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Abstract
The ubiquitin proteasome system is required for the rapid and precise control of protein abundance that is essential for synaptic function. USP14 is a proteasome-bound deubiquitinating enzyme that recycles ubiquitin and regulates synaptic short-term synaptic plasticity. We previously reported that loss of USP14 in ax(J) mice causes a deficit in paired pulse facilitation (PPF) at hippocampal synapses. Here we report that USP14 regulates synaptic function through a novel, deubiquitination-independent mechanism. Although PPF is usually inversely related to release probability, USP14 deficiency impairs PPF without altering basal release probability. Instead, the loss of USP14 causes a large reduction in the number of synaptic vesicles. Over-expression of a catalytically inactive form of USP14 rescues the PPF deficit and restores synaptic vesicle number, indicating that USP14 regulates presynaptic structure and function independently of its role in deubiquitination. Finally, the PPF deficit caused by loss of USP14 can be rescued by pharmacological inhibition of proteasome activity, suggesting that inappropriate protein degradation underlies the PPF impairment. Overall, we demonstrate a novel, deubiquitination-independent function for USP14 in influencing synaptic architecture and plasticity.
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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.