ArticleHuman molecular genetics2016
Regulation of neuronal morphogenesis by 14-3-3epsilon (Ywhae) via the microtubule binding protein, doublecortin.
Article in Human molecular genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 25 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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Who cites it
25 citing papers in PubMed, 57 citations in OpenAlex.
- Understanding the Molecular Basis of Miller-Dieker Syndrome.International journal of molecular sciences · 2025Review
- Deep clinical and genetic analysis of 17p13.3 region: 38 pediatric patients diagnosed using next-generation sequencing and literature review.BMC medical genomics · 2025Review
- 14-3-3ε conditional knockout mice exhibit defects in the development of the epidermis.FEBS letters · 2024Article
- Article
- The cytoplasmic localization of ADNP through 14-3-3 promotes sex-dependent neuronal morphogenesis, cortical connectivity, and calcium signaling.Molecular psychiatry · 2023Article
- Structure-Guided Prediction of the Functional Impact of DCLK1 Mutations on Tumorigenesis.Biomedicines · 2023Review
- Pyramidal neuron morphogenesis requires a septin network that stabilizes filopodia and suppresses lamellipodia during neurite initiation.Current biology : CB · 2023Article
- Further expansion and confirmation of phenotype in rare loss of YWHAE gene distinct from Miller-Dieker syndrome.American journal of medical genetics. Part A · 2023Review
- Refining the Clinical Spectrum of the 17p13.3 Microduplication Syndrome: Case-Report of a Familial Small Microduplication.Biomedicines · 2022Article
- Rpsa Signaling Regulates Cortical Neuronal Morphogenesis via Its Ligand, PEDF, and Plasma Membrane Interaction Partner, Itga6.Cerebral cortex (New York, N.Y. : 1991) · 2022Article
- Identification of Sodium Transients Through NaFrontiers in cellular neuroscience · 2022Article
- Developmental control of noradrenergic system by SLITRK1 and its implications in the pathophysiology of neuropsychiatric disorders.Frontiers in molecular neuroscience · 2022Review
- Establishing neuronal polarity: microtubule regulation during neurite initiation.Oxford open neuroscience · 2022Review
- Responsible Genes for Neuronal Migration in the Chromosome 17p13.3: BeyondBrain sciences · 2021Review
- Identification of molecular glues of the SLP76/14-3-3 protein-protein interaction.RSC medicinal chemistry · 2021Article
- High-throughput kinase inhibitor screening reveals roles for Aurora and Nuak kinases in neurite initiation and dendritic branching.Scientific reports · 2021Article
- Glutathione S-transferase Pi (Gstp) proteins regulate neuritogenesis in the developing cerebral cortex.Human molecular genetics · 2021Article
- Identification of 14-3-3 epsilon as a regulator of the neural apoptotic pathway for chronic-stress-induced depression.iScience · 2021Article
- Article
- Dysregulation of peripheral expression of the YWHA genes during conversion to psychosis.Scientific reports · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
17p13.3 microduplication syndrome is a newly identified genetic disorder characterized by duplications in the 17p13.3 chromosome locus, resulting in a variety of disorders including autism spectrum disorder (ASD). Importantly, a minimum duplication region has been defined, and this region exclusively contains the gene encoding 14-3-3ε. Furthermore, duplication of this minimum region is strongly associated with the appearance of ASD in human patients, thus implicating the overexpression of 14-3-3ε in ASD. Using in vitro and in vivo techniques, we have found that 14-3-3ε binds to the microtubule binding protein doublecortin preventing its degradation. We also found that 14-3-3ε overexpression disrupts neurite formation by preventing the invasion of microtubules into primitive neurites, which can be rescued by the knockdown of doublecortin. To analyse the function of 14-3-3ε in neurite formation, we used 14-3-3ε flox mice and found that 14-3-3ε deficiency results in an increase in neurite formation. Our findings provide the first evidence of cellular pathology in 17p13.3 microduplication syndrome.
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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.