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3D Modeling of Dendritic Spines with Synaptic Plasticity
Published on: May 18, 2020
Dysregulated Dscam levels act through Abelson tyrosine kinase to enlarge presynaptic arbors
Gabriella R Sterne1, Jung Hwan Kim1, Bing Ye1
1Life Sciences Institute, University of Michigan, Ann Arbor, United States.
Abstract:
Increased expression of Down Syndrome Cell Adhesion Molecule (Dscam) is implicated in the pathogenesis of brain disorders such as Down syndrome (DS) and fragile X syndrome (FXS). Here, we show that the cellular defects caused by dysregulated Dscam levels can be ameliorated by genetic and pharmacological inhibition of Abelson kinase (Abl) both in Dscam-overexpressing neurons and in a Drosophila model of fragile X syndrome. This study offers Abl as a potential therapeutic target for treating brain disorders associated with dysregulated Dscam expression.
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