ArticleCell reports2013
Genetic reduction of the α1 subunit of Na/K-ATPase corrects multiple hippocampal phenotypes in Angelman syndrome.
Article in Cell reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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44 citing papers in PubMed, 77 citations in OpenAlex.
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- Insights into the structure and function of the hippocampus: implications for the pathophysiology and treatment of autism spectrum disorder.Frontiers in psychiatry · 2024Review
- UBE3A: The Role in Autism Spectrum Disorders (ASDs) and a Potential Candidate for Biomarker Studies and Designing Therapeutic Strategies.Diseases (Basel, Switzerland) · 2023Review
- Immunoproximity biotinylation reveals the axon initial segment proteome.Nature communications · 2023Article
- Neonatal immune challenge poses a sex-specific risk for epigenetic microglial reprogramming and behavioral impairment.Nature communications · 2023Article
- Article
- The Hippocampal Response to Acute Corticosterone Elevation Is Altered in a Mouse Model for Angelman Syndrome.International journal of molecular sciences · 2022Article
- An Association Study of DNA Methylation and Gene Expression in Angelman Syndrome: A Bioinformatics Approach.International journal of molecular sciences · 2022Article
- Article
- UBE3A reinstatement as a disease-modifying therapy for Angelman syndrome.Developmental medicine and child neurology · 2021Review
- Age-dependent shift in the de novo proteome accompanies pathogenesis in an Alzheimer's disease mouse model.Communications biology · 2021Article
- Chronic α1-Na/K-ATPase inhibition reverses the elongation of the axon initial segment of the hippocampal CA1 pyramidal neurons in Angelman syndrome model mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Article
- Aberrant aggressive behavior in a mouse model of Angelman syndrome.Scientific reports · 2021Article
- Electrophysiological Characterization of Regular and Burst Firing Pyramidal Neurons of the Dorsal Subiculum in an Angelman Syndrome Mouse Model.Frontiers in cellular neuroscience · 2021Article
- Novel Insights into the Role of UBE3A in Regulating Apoptosis and Proliferation.Journal of clinical medicine · 2020Article
- Translational outcomes in a full gene deletion of ubiquitin protein ligase E3A rat model of Angelman syndrome.Translational psychiatry · 2020Article
- AdultThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Neuromodulation of Axon Terminals.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
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7 authors at 3 institutions in 2 countries.
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Abstract
Angelman syndrome (AS) is associated with symptoms that include autism, intellectual disability, motor abnormalities, and epilepsy. We recently showed that AS model mice have increased expression of the alpha1 subunit of Na/K-ATPase (α1-NaKA) in the hippocampus, which was correlated with increased expression of axon initial segment (AIS) proteins. Our developmental analysis revealed that the increase in α1-NaKA expression preceded that of the AIS proteins. Therefore, we hypothesized that α1-NaKA overexpression drives AIS abnormalities and that by reducing its expression these and other phenotypes could be corrected in AS model mice. Herein, we report that the genetic normalization of α1-NaKA levels in AS model mice corrects multiple hippocampal phenotypes, including alterations in the AIS, aberrant intrinsic membrane properties, impaired synaptic plasticity, and memory deficits. These findings strongly suggest that increased expression of α1-NaKA plays an important role in a broad range of abnormalities in the hippocampus of AS model mice.
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