ArticleThe Journal of biological chemistry2013
α3Na+/K+-ATPase deficiency causes brain ventricle dilation and abrupt embryonic motility in zebrafish.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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
22 citing papers in PubMed, 41 citations in OpenAlex.
- ATP1A3-related neurological disorders: updated insights into clinical heterogeneity, molecular mechanisms and precision therapeutics.Neurogenetics · 2026Review
- Congenital hydrocephalus: a review of recent advances in genetic etiology and molecular mechanisms.Military Medical Research · 2024Review
- Navigating the Complexity of Alternating Hemiplegia in Childhood: A Comprehensive Review.Rambam Maimonides medical journal · 2024Review
- The genetic basis of hydrocephalus: genes, pathways, mechanisms, and global impact.Fluids and barriers of the CNS · 2024Review
- Article
- The zebrafish mutanteLife · 2023Article
- Genome-wide alternative splicing profile in the posterior kidney of brown trout (Salmo trutta) during proliferative kidney disease.BMC genomics · 2022Article
- The genetics of adaptation in freshwater Eurasian shad (Ecology and evolution · 2022Article
- Genetically altered animal models for ATP1A3-related disorders.Disease models & mechanisms · 2021Article
- ATP1A3-Related Disorders: An Ever-Expanding Clinical Spectrum.Frontiers in neurology · 2021Review
- Neural innervation as a potential trigger of morphological color change and sexual dimorphism in cichlid fish.Scientific reports · 2020Article
- Molecular and mechanical signals determine morphogenesis of the cerebral hemispheres in the chicken embryo.Development (Cambridge, England) · 2019Article
- Recessive Inheritance of Congenital Hydrocephalus With Other Structural Brain Abnormalities Caused by Compound Heterozygous Mutations inFrontiers in cellular neuroscience · 2019Article
- HCN2 Rescues brain defects by enforcing endogenous voltage pre-patterns.Nature communications · 2018Article
- Development of brain ventricular system.Cellular and molecular life sciences : CMLS · 2018Review
- Zebrafish as an Animal Model for Drug Discovery in Parkinson's Disease and Other Movement Disorders: A Systematic Review.Frontiers in neurology · 2018Article
- Sodium pump regulation of locomotor control circuits.Journal of neurophysiology · 2017Review
- The expanding spectrum of neurological phenotypes in children with ATP1A3 mutations, Alternating Hemiplegia of Childhood, Rapid-onset Dystonia-Parkinsonism, CAPOS and beyond.Pediatric neurology · 2015Review
- Local and long-range endogenous resting potential gradients antagonistically regulate apoptosis and proliferation in the embryonic CNS.The International journal of developmental biology · 2015Article
- Distinct neurological disorders with ATP1A3 mutations.The Lancet. Neurology · 2014Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Na(+)/K(+)-ATPases are transmembrane ion pumps that maintain ion gradients across the basolateral plasma membrane in all animal cells to facilitate essential biological functions. Mutations in the Na(+)/K(+)-ATPase α3 subunit gene (ATP1A3) cause rapid-onset dystonia-parkinsonism, a rare movement disorder characterized by sudden onset of dystonic spasms and slow movements. In the brain, ATP1A3 is principally expressed in neurons. In zebrafish, the transcripts of the two ATP1A3 orthologs, Atp1a3a and Atp1a3b, show distinct expression in the brain. Surprisingly, targeted knockdown of either Atp1a3a or Atp1a3b leads to brain ventricle dilation, a likely consequence of ion imbalances across the plasma membrane that cause accumulation of cerebrospinal fluid in the ventricle. The brain ventricle dilation is accompanied by a depolarization of spinal Rohon-Beard neurons in Atp1a3a knockdown embryos, suggesting impaired neuronal excitability. This is further supported by Atp1a3a or Atp1a3b knockdown results where altered responses to tactile stimuli as well as abnormal motility were observed. Finally, proteomic analysis identified several protein candidates highlighting proteome changes associated with the knockdown of Atp1a3a or Atp1a3b. Our data thus strongly support the role of α3Na(+)/K(+)-ATPase in zebrafish motility and brain development, associating for the first time the α3Na(+)/K(+)-ATPase deficiency with brain ventricle dilation.
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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.