ArticleLearning & memory (Cold Spring Harbor, N.Y.)2014
Activity-dependent changes in MAPK activation in the Angelman Syndrome mouse model.
Article in Learning & memory (Cold Spring Harbor, N.Y.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- A dual-reporter mouse for therapeutic discovery in Angelman syndrome.JCI insight · 2026Article
- Extracellular vesicle dysfunction contributes to synaptic and cognitive deficits in a mouse model of Angelman syndrome.Progress in neurobiology · 2026Article
- Molecular aspects of Angelman Syndrome: Defining the new path forward.Biomolecules & biomedicine · 2025Review
- Loss of UBE3A impacts both neuronal and non-neuronal cells in human cerebral organoids.Communications biology · 2025Article
- Unraveling the Roles of UBE3A in Neurodevelopment and Neurodegeneration.International journal of molecular sciences · 2025Review
- A human Angelman Syndrome class II pluripotent stem cell line with fluorescent paternalFrontiers in cell and developmental biology · 2025Article
- Regulation of MAPK Signaling Pathways by the Large HERC Ubiquitin Ligases.International journal of molecular sciences · 2023Review
- Excessive Laughter-like Vocalizations, Microcephaly, and Translational Outcomes in theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Insulin-like growth factor-2 does not improve behavioral deficits in mouse and rat models of Angelman Syndrome.Molecular autism · 2021Article
- UBE3A reinstatement as a disease-modifying therapy for Angelman syndrome.Developmental medicine and child neurology · 2021Review
- Emerging Gene and Small Molecule Therapies for the Neurodevelopmental Disorder Angelman Syndrome.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- Electrophysiological Characterization of Regular and Burst Firing Pyramidal Neurons of the Dorsal Subiculum in an Angelman Syndrome Mouse Model.Frontiers in cellular neuroscience · 2021Article
- The Noonan Syndrome-linked Raf1L613V mutation drives increased glial number in the mouse cortex and enhanced learning.PLoS genetics · 2019Article
- The Autism and Angelman Syndrome Protein Ube3A/E6AP: The Gene, E3 Ligase Ubiquitination Targets and Neurobiological Functions.Frontiers in molecular neuroscience · 2019Review
- A coding-independent function of an alternative Ube3a transcript during neuronal development.Nature neuroscience · 2015Article
- Reelin supplementation recovers synaptic plasticity and cognitive deficits in a mouse model for Angelman syndrome.The European journal of neuroscience · 2015Article
- The ubiquitin ligase UBE3A dampens ERK pathway signalling in HPV E6 transformed HeLa cells.PloS one · 2015Article
- From UBE3A to Angelman syndrome: a substrate perspective.Frontiers in neuroscience · 2015Review
- Neurodevelopmental Underpinnings of Angelman Syndrome.Journal of bioanalysis & biomedicine · 2014Article
- Disruption of the LTD dialogue between the cerebellum and the cortex in Angelman syndrome model: a timing hypothesis.Frontiers in systems neuroscience · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Angelman Syndrome (AS) is a devastating neurological disorder caused by disruption of the maternal UBE3A gene. Ube3a protein is identified as an E3 ubiquitin ligase that shows neuron-specific imprinting. Despite extensive research evaluating the localization and basal expression profiles of Ube3a in mouse models, the molecular mechanisms whereby Ube3a deficiency results in AS are enigmatic. Using in vitro and in vivo systems we show dramatic changes in the expression of Ube3a following synaptic activation. In primary neuronal culture, neuronal depolarization was found to increase both nuclear and cytoplasmic Ube3a levels. Analogous up-regulation in maternal and paternal Ube3a expression was observed in Ube3a-YFP reporter mice following fear conditioning. Absence of Ube3a led to deficits in the activity-dependent increases in ERK1/2 phosphorylation, which may contribute to reported deficits in synaptic plasticity and cognitive function in AS mice. Taken together, our findings provide novel insight into the regulation of Ube3a by synaptic activity and its potential role in kinase regulation.
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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.