ArticleScientific reports2016
Persistent neuronal Ube3a expression in the suprachiasmatic nucleus of Angelman syndrome model mice.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- A Meta-Analysis Characterizing Stem-Like Gene Expression in the Suprachiasmatic Nucleus and Its Circadian Clock.BioMed research international · 2018Pooled it
- Article
- Activation of the imprinted Prader-Willi syndrome locus by CRISPR-based epigenome editing.Cell genomics · 2025Article
- A human Angelman Syndrome class II pluripotent stem cell line with fluorescent paternalFrontiers in cell and developmental biology · 2025Article
- Activation of the imprinted Prader-Willi Syndrome locus by CRISPR-based epigenome editing.bioRxiv : the preprint server for biology · 2024Article
- UBE3A: The Role in Autism Spectrum Disorders (ASDs) and a Potential Candidate for Biomarker Studies and Designing Therapeutic Strategies.Diseases (Basel, Switzerland) · 2023Review
- Death of a Protein: The Role of E3 Ubiquitin Ligases in Circadian Rhythms of Mice and Flies.International journal of molecular sciences · 2022Review
- Circadian Rhythms and Sleep Are Dependent Upon Expression Levels of Key Ubiquitin LigaseFrontiers in behavioral neuroscience · 2022Article
- Emerging Gene and Small Molecule Therapies for the Neurodevelopmental Disorder Angelman Syndrome.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- An Unbiased Drug Screen for Seizure Suppressors in Duplication 15q Syndrome Reveals 5-HTBiological psychiatry · 2020Article
- Angelman syndrome and melatonin: What can they teach us about sleep regulation.Journal of pineal research · 2020Review
- Deficits in higher visual area representations in a mouse model of Angelman syndrome.Journal of neurodevelopmental disorders · 2020Article
- Circadian biology and sleep in monogenic neurological disorders and its potential application in drug discovery.Current opinion in behavioral sciences · 2019Article
- Baby food and bedtime: Evidence for opposite phenotypes from different genetic and epigenetic alterations in Prader-Willi and Angelman syndromes.SAGE open medicine · 2019Review
- Prader-Willi locus Snord116 RNA processing requires an active endogenous allele and neuron-specific splicing by Rbfox3/NeuN.Human molecular genetics · 2018Article
- Epigenetic and Cellular Diversity in the Brain through Allele-Specific Effects.Trends in neurosciences · 2018Review
- AdultThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Enhanced Nociception in Angelman Syndrome Model Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Imprinting analysis by droplet digital PCR coupled with locked nucleic acid TaqMan probes.EpigeneticsArticle
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations or deletions of the maternal allele of the UBE3A gene cause Angelman syndrome (AS), a severe neurodevelopmental disorder. The paternal UBE3A/Ube3a allele becomes epigenetically silenced in most neurons during postnatal development in humans and mice; hence, loss of the maternal allele largely eliminates neuronal expression of UBE3A protein. However, recent studies suggest that paternal Ube3a may escape silencing in certain neuron populations, allowing for persistent expression of paternal UBE3A protein. Here we extend evidence in AS model mice (Ube3a(m-/p+)) of paternal UBE3A expression within the suprachiasmatic nucleus (SCN), the master circadian pacemaker. Paternal UBE3A-positive cells in the SCN show partial colocalization with the neuropeptide arginine vasopressin (AVP) and clock proteins (PER2 and BMAL1), supporting that paternal UBE3A expression in the SCN is often of neuronal origin. Paternal UBE3A also partially colocalizes with a marker of neural progenitors, SOX2, implying that relaxed or incomplete imprinting of paternal Ube3a reflects an overall immature molecular phenotype. Our findings highlight the complexity of Ube3a imprinting in the brain and illuminate a subpopulation of SCN neurons as a focal point for future studies aimed at understanding the mechanisms of Ube3a imprinting.
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