ArticleJournal of molecular neuroscience : MN2018
Abundant Focal Adhesion Kinase Causes Aberrant Neuronal Migration Via Its Phosphorylation at Tyr925.
Article in Journal of molecular neuroscience : MN, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 8 citations in OpenAlex.
- Loss of non-motor kinesin KIF26A causes congenital brain malformations via dysregulated neuronal migration and axonal growth as well as apoptosis.Developmental cell · 2022Article
- Prenatal exposure to valproic acid alters Reelin, NGF expressing neuron architecture and impairs social interaction in their autistic-like phenotype male offspring.Experimental brain research · 2022Article
- Phosphorylation of Focal Adhesion Kinase at Y925: Role in Glia-Dependent and Independent Migration through Regulating Cofilin and N-Cadherin.Molecular neurobiology · 2022Article
- Integrin αVβ3 Function Influences Citalopram Immobility Behavior in the Tail Suspension Test.Frontiers in neuroscience · 2019Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
The process of neuronal migration is precisely regulated by different molecules during corticogenesis. The FAK (focal adhesion kinase) plays a critical role in embryogenesis and is involved in cell motility through focal adhesions, but the underlying mechanisms on inordinate expression are unclear. To investigate the effect of FAK overexpression on neuronal migration spatiotemporally, mice FAK was transfected into the neurons in vivo by electroporation. Results showed that exogenous FAK distributed in the cytoplasm (in vivo) and co-localized with vinculin (in vitro) and induced aberrant neuronal migration via phosphorylation of FAK at Tyr925 during cerebral cortex development. Meanwhile, FAK Y925F mutant also induced aberrant neuronal migration like inordinate FAK/GFP phenotype. All these results implied that FAK-induced abnormal phenotype depended on phosphorylation of FAK at Tyr925, and this demonstrated that the overexpression of FAK impaired neuronal migration through its phosphorylation and activity of FAK during corticogenesis.
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Registered trials
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