ReviewBiological psychiatry2022
The DUB Club: Deubiquitinating Enzymes and Neurodevelopmental Disorders.
Review in Biological psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
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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.
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Who cites it
22 citing papers in PubMed, 28 citations in OpenAlex.
- USP15 mutation associated with autism spectrum disorder alters progenitor fate and neuronal maturation in human brain organoids.Molecules and cells · 2026Article
- Protein Posttranslational Modifications in Immunity: Molecular Mechanisms and Therapeutic Targets.MedComm · 2026Review
- Discovery of a Potent Fluorescence Polarization Probe for Identifying USP1 Allosteric Inhibitors.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Deubiquitinating Enzymes as Therapeutic Candidates in Hepatocellular Carcinoma and Other Liver Disease.International journal of molecular sciences · 2026Review
- A De NovoInternational journal of molecular sciences · 2026Article
- A novel OTUD5 variant disrupts neural progenitor cell homeostasis: mechanistic insights from HEK293T cell-based analyses.Stem cell research & therapy · 2026Article
- IAPs in cancers: molecular mechanisms, clinical prognostic value, and translational therapeutic potential.Journal of translational medicine · 2026Review
- Complexes Formed by the K63-Specific Deubiquitinating Enzyme BRCC36: New Promising Therapeutic Targets in Human Disease.Biomolecules · 2025Review
- The Role of Ubiquitination and Deubiquitination in the Pathogenesis of Acute Kidney Injury: Progress in Research.Biomedicines · 2025Review
- A novel USP27X missense variant identified in an individual with intellectual disability.Journal of human genetics · 2025Article
- CXCL13 Damages Blood Spinal Cord Barrier by Promoting RNF6/Sqstm1-Ubiquitination Induced Autophagy in Experimental Allergic Encephalomyelitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Sequence variants in HECTD1 result in a variable neurodevelopmental disorder.American journal of human genetics · 2025Article
- The Hao-Fountain syndrome protein USP7 regulates neuronal connectivity in the brain via a novel p53-independent ubiquitin signaling pathway.Cell reports · 2025Article
- Drug Repurposing for COVID-19 by Constructing a Comorbidity Network with Central Nervous System Disorders.International journal of molecular sciences · 2024Article
- Deubiquitinases in muscle physiology and disorders.Biochemical Society transactions · 2024Review
- The Emerging Role of Ubiquitin-Specific Protease 36 (USP36) in Cancer and Beyond.Biomolecules · 2024Review
- Article
- Molecular signatures in Mendelian neurodevelopment: a focus on ubiquitination driven DNA methylation aberrations.Frontiers in molecular neuroscience · 2024Review
- Article
- Regulation of apoptosis by ubiquitination in liver cancer.American journal of cancer research · 2023Review
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Protein ubiquitination is a widespread, multifunctional, posttranslational protein modification, best known for its ability to direct protein degradation via the ubiquitin proteasome system (UPS). Ubiquitination is also reversible, and the human genome encodes over 90 deubiquitinating enzymes (DUBs), many of which appear to target specific subsets of ubiquitinated proteins. This review focuses on the roles of DUBs in neurodevelopmental disorders (NDDs). We present the current genetic evidence connecting 12 DUBs to a range of NDDs and the functional studies implicating at least 19 additional DUBs as candidate NDD genes. We highlight how the study of DUBs in NDDs offers critical insights into the role of protein degradation during brain development. Because one of the major known functions of a DUB is to antagonize the UPS, loss of function of DUB genes has been shown to culminate in loss of abundance of its protein substrates. The identification and study of NDD DUB substrates in the developing brain is revealing that they regulate networks of proteins that themselves are encoded by NDD genes. We describe the new technologies that are enabling the full resolution of DUB protein networks in the developing brain, with the view that this knowledge can direct the development of new therapeutic paradigms. The fact that the abundance of many NDD proteins is regulated by the UPS presents an exciting opportunity to combat NDDs caused by haploinsufficiency, because the loss of abundance of NDD proteins can be potentially rectified by antagonizing their UPS-based degradation.
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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 Socratic graph.