ReviewCurrent opinion in neurobiology2024
Neuronal UBE3A substrates hold therapeutic potential for Angelman syndrome.
Review in Current opinion in neurobiology, 2024. 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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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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Who cites it
9 citing papers in PubMed.
- Article
- Phenotyping iPSC-derived neurons from Angelman patients and partial rescue via JNK pathway inactivation.Journal of neurodevelopmental disorders · 2026Article
- UBE3A isoform-selective and non-selective contributions to Angelman syndrome phenotypes.Molecular psychiatry · 2026Article
- Crossing the finish line towards a disease-modifying treatment for Angelman syndrome.Journal of neurodevelopmental disorders · 2026Review
- Extracellular vesicle dysfunction contributes to synaptic and cognitive deficits in a mouse model of Angelman syndrome.Progress in neurobiology · 2026Article
- Progress and opportunity in developmental neurobiology and youth mental health.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Review
- Extracellular Vesicles in Angelman Syndrome: Expanding UBE3A Role beyond a Cell Autonomous Mechanism.Journal of experimental neurology · 2026Article
- UBE3A stabilization of β-catenin preserves synaptic proteins essential for motor and cognitive functions in Angelman Syndrome.Molecular autism · 2025Article
- Emerging roles for E3 ubiquitin ligases in neural development and disease.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Emerging therapies for Angelman syndrome, a severe neurodevelopmental disorder, are focused on restoring UBE3A gene expression in the brain. Further therapeutic opportunities may arise from a better understanding of how UBE3A gene products-both long and short isoforms of the ubiquitin ligase E3A (UBE3A)-function in neurons. Great strides have been made recently toward identifying ubiquitin substrates of UBE3A in vitro and in heterologous expression systems. From this work, a particularly close relationship between UBE3A and subunits of the 19S regulatory particle of the proteasome has become evident. We propose that further research cognizant of isoform-specific UBE3A functional roles will be instrumental in elucidating key UBE3A/substrate relationships within distinct neuronal compartments, lending to the discovery of novel therapeutic targets and valuable clinical biomarkers for the treatment of Angelman syndrome.
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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.