Dysregulated Dscam levels act through Abelson tyrosine kinase to enlarge presynaptic arbors.
basic_science · Level V
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- Record sourced from PubMed, PMID 25988807.
- Also identified by DOI 10.7554/eLife.05196 and PMC identifier 4434255.
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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.
Medical subject headings
- Cell Adhesion Molecules
- Drosophila Proteins
- Fragile X Syndrome
- Neuronal Plasticity
- Presynaptic Terminals
- Protein-Tyrosine Kinases