ArticleThe Journal of comparative neurology2014
Allelic specificity of Ube3a expression in the mouse brain during postnatal development.
Article in The Journal of comparative neurology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
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Who cites it
96 citing papers in PubMed, 143 citations in OpenAlex.
- Mechanisms underlying the EEG biomarker in Dup15q syndrome.Molecular autism · 2019Trial
- Review
- Phenotyping iPSC-derived neurons from Angelman patients and partial rescue via JNK pathway inactivation.Journal of neurodevelopmental disorders · 2026Article
- Region-dependent differences in tonic inhibition underlie epileptic features in Angelman syndrome model mice.Epilepsia · 2026Article
- UBE3A isoform-selective and non-selective contributions to Angelman syndrome phenotypes.Molecular psychiatry · 2026Article
- Targeting UBE3A and downstream estrogen receptor-β signaling to restore oligodendroglial homeostasis in Angelman syndrome.bioRxiv : the preprint server for biology · 2026Article
- A dual-reporter mouse for therapeutic discovery in Angelman syndrome.JCI insight · 2026Article
- Multi-targeting zinc finger nuclease vector unsilences paternal UBE3A in a mouse model of Angelman syndrome.Gene therapy · 2026Article
- Review
- Article
- Brain-wide Genome Editing via STEP-RNPs for Treatment of Angelman Syndrome.bioRxiv : the preprint server for biology · 2025Article
- Courtship and distress ultrasonic vocalizations are altered in a mouse model of Angelman syndrome.Journal of neurodevelopmental disorders · 2025Article
- AAV-dCas9 vector unsilences paternal Ube3a in neurons by impeding Ube3a-ATS transcription.Communications biology · 2025Article
- Article
- Cell-cell communication-mediated cell-type-specific parent-of-origin effects in mammals.Nature communications · 2025Article
- Mom genes and dad genes: genomic imprinting in the regulation of social behaviors.Epigenomics · 2025Review
- Loss of UBE3A impacts both neuronal and non-neuronal cells in human cerebral organoids.Communications biology · 2025Article
- Acute administration of lovastatin had no pronounced effect on motor abilities, motor coordination, gait nor simple cognition in a mouse model of Angelman syndrome.Journal of neurodevelopmental disorders · 2025Article
- Small molecule ion channel agonist/antagonist screen reveals seizure suppression via glial Irk2 activation in a Drosophila model of Dup15q syndrome.Neurobiology of disease · 2025Article
- Unraveling the Roles of UBE3A in Neurodevelopment and Neurodegeneration.International journal of molecular sciences · 2025Review
36 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Genetic alterations of the maternal UBE3A allele result in Angelman syndrome (AS), a neurodevelopmental disorder characterized by severe developmental delay, lack of speech, and difficulty with movement and balance. The combined effects of maternal UBE3A mutation and cell type-specific epigenetic silencing of paternal UBE3A are hypothesized to result in a complete loss of functional UBE3A protein in neurons. However, the allelic specificity of UBE3A expression in neurons and other cell types in the brain has yet to be characterized throughout development, including the early postnatal period when AS phenotypes emerge. Here we define maternal and paternal allele-specific Ube3a protein expression throughout postnatal brain development in the mouse, a species that exhibits orthologous epigenetic silencing of paternal Ube3a in neurons and AS-like behavioral phenotypes subsequent to maternal Ube3a deletion. We find that neurons downregulate paternal Ube3a protein expression as they mature and, with the exception of neurons born from postnatal stem cell niches, do not express detectable paternal Ube3a beyond the first postnatal week. By contrast, neurons express maternal Ube3a throughout postnatal development, during which time localization of the protein becomes increasingly nuclear. Unlike neurons, astrocytes and oligodendrotyes biallelically express Ube3a. Notably, mature oligodendrocytes emerge as the predominant Ube3a-expressing glial cell type in the cortex and white matter tracts during postnatal development. These findings demonstrate the spatiotemporal characteristics of allele-specific Ube3a expression in key brain cell types, thereby improving our understanding of the developmental parameters of paternal Ube3a silencing and the cellular basis of AS.
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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.