ArticleCell death & disease2023
The deubiquitinase Leon/USP5 interacts with Atg1/ULK1 and antagonizes autophagy.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- The role of ubiquitin system in ageing-related diseases and potential therapeutic opportunities.Molecular biomedicine · 2026Review
- CircADAM9 activates autophagy via miR-302b-3p/ULK1 axis to improve depressive-like behaviors.Biology direct · 2026Article
- Ubiquitin-specific protease 5 promotes EV-A71 replication by de-ubiquitinating MAVS and IRF3.Virologica Sinica · 2025Article
- The deubiquitinase USP45 inhibits autophagy through actin regulation by Coronin 1B.The Journal of cell biology · 2025Article
- The deubiquitinase USP5 prevents accumulation of protein aggregates in cardiomyocytes.Science advances · 2025Article
- Editorial: The role of autophagy in cardiovascular disease.Frontiers in cell and developmental biology · 2025Article
- Molecular mechanism on autophagy associated cardiovascular dysfunction inFrontiers in cell and developmental biology · 2025Review
- Role of protein degradation systems in colorectal cancer.Cell death discovery · 2024Review
- Dual function of the Leon/USP5 deubiquitinase in the ubiquitin-proteasome and autophagic pathways.Autophagy reports · 2023Article
Corrections and comments
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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
Accumulating evidence has shown that the quality of proteins must be tightly monitored and controlled to maintain cellular proteostasis. Misfolded proteins and protein aggregates are targeted for degradation through the ubiquitin proteasome (UPS) and autophagy-lysosome systems. The ubiquitination and deubiquitinating enzymes (DUBs) have been reported to play pivotal roles in the regulation of the UPS system. However, the function of DUBs in the regulation of autophagy remain to be elucidated. In this study, we found that knockdown of Leon/USP5 caused a marked increase in the formation of autophagosomes and autophagic flux under well-fed conditions. Genetic analysis revealed that overexpression of Leon suppressed Atg1-induced cell death in Drosophila. Immunoblotting assays further showed a strong interaction between Leon/USP5 and the autophagy initiating kinase Atg1/ULK1. Depletion of Leon/USP5 led to increased levels of Atg1/ULK1. Our findings indicate that Leon/USP5 is an autophagic DUB that interacts with Atg1/ULK1, negatively regulating the autophagic process.
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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.