ArticleExperimental neurology2017
Hypersociability in the Angelman syndrome mouse model.
Article in Experimental neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Under or Absent Reporting of Light Stimuli in Testing of Anxiety-Like Behaviors in Rodents: The Need for Standardization.Frontiers in molecular neuroscience · 2022Pooled it
- Environmental context modulates sociability in ube3a zebrafish mutants via alterations in sensory pathways.Molecular psychiatry · 2026Article
- Courtship and distress ultrasonic vocalizations are altered in a mouse model of Angelman syndrome.Journal of neurodevelopmental disorders · 2025Article
- A preclinical pig model of Angelman syndrome mirrors the early developmental trajectory of the human condition.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- IGF2 in memory, neurodevelopmental disorders, and neurodegenerative diseases.Trends in neurosciences · 2023Review
- Imbalanced expression of cation-chloride cotransporters as a potential therapeutic target in an Angelman syndrome mouse model.Scientific reports · 2023Article
- Adolescent Parvalbumin Expression in the Left Orbitofrontal Cortex Shapes Sociability in Female Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Biallelic PAX5 mutations cause hypogammaglobulinemia, sensorimotor deficits, and autism spectrum disorder.The Journal of experimental medicine · 2022Article
- Role of the DUB enzyme USP7 in dendritic arborization, neuronal migration, and autistic-like behaviors in mice.iScience · 2022Article
- Aberrant aggressive behavior in a mouse model of Angelman syndrome.Scientific reports · 2021Article
- Communication-related assessments in an Angelman syndrome mouse model.Brain and behavior · 2021Article
- Behavioral Evaluation of Angelman Syndrome Mice at Older Ages.Neuroscience · 2020Article
- Evaluation of a TrkB agonist on spatial and motor learning in theLearning & memory (Cold Spring Harbor, N.Y.) · 2020Article
- PKA and Ube3a regulate SK2 channel trafficking to promote synaptic plasticity in hippocampus: Implications for Angelman Syndrome.Scientific reports · 2020Article
- The sociability spectrum: evidence from reciprocal genetic copy number variations.Molecular autism · 2020Review
- Generation of a Novel Rat Model of Angelman Syndrome with a Complete Ube3a Gene Deletion.Autism research : official journal of the International Society for Autism Research · 2020Article
- STXBP1-associated neurodevelopmental disorder: a comparative study of behavioural characteristics.Journal of neurodevelopmental disorders · 2019Article
- A placental mammal-specific microRNA cluster acts as a natural brake for sociability in mice.EMBO reports · 2019Article
- The other side of the coin: Hypersociability.Genes, brain, and behavior · 2019Review
- Enhanced Operant Extinction and Prefrontal Excitability in a Mouse Model of Angelman Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Deletions and reciprocal triplications of the human chromosomal 15q11-13 region cause two distinct neurodevelopmental disorders. Maternally-derived deletions or inactivating mutations of UBE3A, a 15q11-13 gene expressed exclusively from the maternal allele in neurons, cause Angelman syndrome, characterized by intellectual disability, motor deficits, seizures, and a characteristic increased social smiling, laughing, and eye contact. Conversely, maternally-derived triplications of 15q11-13 cause a behavioral disorder on the autism spectrum with clinical features that include decreased sociability that we recently reconstituted in mice with Ube3a alone. Based on the unique sociability features reported in Angelman syndrome and the repressed sociability observed when Ube3a gene dosage is increased, we hypothesized that mice with neuronal UBE3A loss that models Angelman syndrome would display evidence of hypersocial behavior. We report that mice with maternally-inherited Ube3a gene deletion (Ube3a
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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.