ArticleThe Journal of comparative neurology2017
Subcellular organization of UBE3A in neurons.
Article in The Journal of comparative neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- UBE3A isoform-selective and non-selective contributions to Angelman syndrome phenotypes.Molecular psychiatry · 2026Article
- Ubiquitin ligase signalling networks shape presynaptic development, function and disease.The Journal of physiology · 2025Review
- UBE3A promotes foam cell formation and counters remyelination by targeting ABCA1 for proteasomal degradation.Nature communications · 2025Article
- Localization of human UBE3A isoform 3 is highly sensitive to amino acid substitutions at p.Met21 position.Human molecular genetics · 2025Article
- A human Angelman Syndrome class II pluripotent stem cell line with fluorescent paternalFrontiers in cell and developmental biology · 2025Article
- Neuronal UBE3A substrates hold therapeutic potential for Angelman syndrome.Current opinion in neurobiology · 2024Review
- The role of glia in the dysregulation of neuronal spinogenesis in Ube3a-dependent ASD.Experimental neurology · 2024Article
- Epigenetics in rare neurological diseases.Frontiers in cell and developmental biology · 2024Review
- Regional and cellular organization of the autism-associated protein UBE3A/E6AP and its antisense transcript in the brain of the developing rhesus monkey.Frontiers in neuroanatomy · 2024Article
- Cerebral organoids as an in vitro model to study autism spectrum disorders.Gene therapy · 2023Review
- Molecular and behavioral consequences of Ube3a gene overdosage in mice.JCI insight · 2022Article
- Dual-isoform hUBE3A gene transfer improves behavioral and seizure outcomes in Angelman syndrome model mice.JCI insight · 2021Article
- Deleting a UBE3A substrate rescues impaired hippocampal physiology and learning in Angelman syndrome mice.Scientific reports · 2021Article
- Secreted retrovirus-like GAG-domain-containing protein PEG10 is regulated by UBE3A and is involved in Angelman syndrome pathophysiology.Cell reports. Medicine · 2021Article
- UBE3A reinstatement as a disease-modifying therapy for Angelman syndrome.Developmental medicine and child neurology · 2021Review
- Loss of nuclear UBE3A activity is the predominant cause of Angelman syndrome in individuals carrying UBE3A missense mutations.Human molecular genetics · 2021Article
- Evaluation of UBE3A antibodies in mice and human cerebral organoids.Scientific reports · 2021Article
- Mono-ubiquitination of Rabphilin 3A by UBE3A serves a non-degradative function.Scientific reports · 2021Article
- Abnormalities of synaptic mitochondria in autism spectrum disorder and related neurodevelopmental disorders.Journal of molecular medicine (Berlin, Germany) · 2021Review
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Authors and funding
6 authors.
Funding
Abstract
Ubiquitination regulates a broad array of cellular processes, and defective ubiquitination is implicated in several neurological disorders. Loss of the E3 ubiquitin-protein ligase UBE3A causes Angelman syndrome. Despite its clinical importance, the normal role of UBE3A in neurons is still unclear. As a step toward deciphering its possible functions, we performed high-resolution light and electron microscopic immunocytochemistry. We report a broad distribution of UBE3A in neurons, highlighted by concentrations in axon terminals and euchromatin-rich nuclear domains. Our findings suggest that UBE3A may act locally to regulate individual synapses while also mediating global, neuronwide influences through the regulation of gene transcription. J. Comp. Neurol. 525:233-251, 2017. © 2016 Wiley Periodicals, Inc.
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