ReviewCells2018
Deubiquitinating Enzymes Related to Autophagy: New Therapeutic Opportunities?
Review in Cells, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 38 citations in OpenAlex.
- CYLD-mediated lysine63 deubiquitination regulates synaptic transmission and autophagy to mitigate age-related sequelae.Nature communications · 2026Article
- Targeting the OTU family: a core therapeutic strategy for reshaping the immunosuppressive microenvironment and reversing drug resistance in HCC by coordinating the autophagy-ferroptosis balance.Cell death discovery · 2026Review
- The host ubiquitination system dynamically regulates the inflammatory response of macrophages to bacteria.Frontiers in immunology · 2026Review
- Research progress of deubiquitinating enzymes in cerebral ischemia-reperfusion injury.Frontiers in aging neuroscience · 2025Review
- Roles of ubiquitin‑specific protease 13 in normal physiology and tumors (Review).Oncology letters · 2024Review
- Ectopic USP15 expression inhibits HIV-1 transcription involving changes in YY1 deubiquitination and stability.Frontiers in cellular and infection microbiology · 2024Article
- The deubiquitinase Leon/USP5 interacts with Atg1/ULK1 and antagonizes autophagy.Cell death & disease · 2023Article
- The exploitation of host autophagy and ubiquitin machinery byAutophagy · 2023Review
- Silencing USP19 alleviates cigarette smoke extract-induced mitochondrial dysfunction in BEAS-2B cells by targeting FUNDC1.Open medicine (Warsaw, Poland) · 2023Article
- Genome-wide analysis of genes encoding core components of the ubiquitin system during cerebral cortex development.Molecular brain · 2022Article
- Inhibition of Ubiquitin-Specific Protease-13 Improves Behavioral Performance in Alpha-Synuclein Expressing Mice.International journal of molecular sciences · 2022Article
- Deubiquitinases in Neurodegeneration.Cells · 2022Review
- The deubiquitinase USP11 is a versatile and conserved regulator of autophagy.The Journal of biological chemistry · 2021Article
- Connection Lost, MAM: Errors in ER-Mitochondria Connections in Neurodegenerative Diseases.Brain sciences · 2021Review
- Novel Ubiquitin Specific Protease-13 Inhibitors Alleviate Neurodegenerative Pathology.Metabolites · 2021Article
- The Roles of the Ubiquitin-Proteasome System in the Endoplasmic Reticulum Stress Pathway.International journal of molecular sciences · 2021Review
- Molecular Mechanisms of DUBs Regulation in Signaling and Disease.International journal of molecular sciences · 2021Review
- Advances in deubiquitinating enzymes in lung adenocarcinoma.Journal of Cancer · 2021Review
- Inhibition of deubiquitination by PR-619 induces apoptosis and autophagy via ubi-protein aggregation-activated ER stress in oesophageal squamous cell carcinoma.Cell proliferation · 2021Article
- The function and regulation of OTU deubiquitinases.Frontiers of medicine · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is an evolutionary conserved catabolic process that allows for the degradation of intracellular components by lysosomes. This process can be triggered by nutrient deprivation, microbial infections or other challenges to promote cell survival under these stressed conditions. However, basal levels of autophagy are also crucial for the maintenance of proper cellular homeostasis by ensuring the selective removal of protein aggregates and dysfunctional organelles. A tight regulation of this process is essential for cellular survival and organismal health. Indeed, deregulation of autophagy is associated with a broad range of pathologies such as neuronal degeneration, inflammatory diseases, and cancer progression. Ubiquitination and deubiquitination of autophagy substrates, as well as components of the autophagic machinery, are critical regulatory mechanisms of autophagy. Here, we review the main evidence implicating deubiquitinating enzymes (DUBs) in the regulation of autophagy. We also discuss how they may constitute new therapeutic opportunities in the treatment of pathologies such as cancers, neurodegenerative diseases or infections.
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What OpenQuestion holds
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.