ArticleNeurogenetics2016
Transgenic rescue of phenotypic deficits in a mouse model of alternating hemiplegia of childhood.
Article in Neurogenetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
The trial behind it
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
7 citing papers in PubMed.
- ATP1A3-related neurological disorders: updated insights into clinical heterogeneity, molecular mechanisms and precision therapeutics.Neurogenetics · 2026Review
- Sensational site: the sodium pump ouabain-binding site and its ligands.American journal of physiology. Cell physiology · 2024Review
- Genetically altered animal models for ATP1A3-related disorders.Disease models & mechanisms · 2021Article
- Sensitivity to expression levels underlies differential dominance of a putative null allele of the Drosophila tβh gene in behavioral phenotypes.PLoS biology · 2021Article
- Adeno-Associated Virus-Mediated Gene Therapy in the Mashlool,Human gene therapy · 2021Article
- Deficits in social behavioral tests in a mouse model of alternating hemiplegia of childhood.Journal of neurogenetics · 2016Article
- Insights into the Pathology of the α2-Na(+)/K(+)-ATPase in Neurological Disorders; Lessons from Animal Models.Frontiers in physiology · 2016Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Missense mutations in ATP1A3 encoding Na(+),K(+)-ATPase α3 are the primary cause of alternating hemiplegia of childhood (AHC). Most ATP1A3 mutations in AHC lie within a cluster in or near transmembrane α-helix TM6, including I810N that is also found in the Myshkin mouse model of AHC. These mutations all substantially reduce Na(+),K(+)-ATPase α3 activity. Herein, we show that Myshkin mice carrying a wild-type Atp1a3 transgene that confers a 16 % increase in brain-specific total Na(+),K(+)-ATPase activity show significant phenotypic improvements compared with non-transgenic Myshkin mice. Interventions to increase the activity of wild-type Na(+),K(+)-ATPase α3 in AHC patients should be investigated further.
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Registered trials
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