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Elife. 2015 May 19;4. doi: 10.7554/eLife.05196.

Dysregulated Dscam levels act through Abelson tyrosine kinase to enlarge presynaptic arbors.

Author information

1
Life 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.

KEYWORDS:

Abl; D. melanogaster; Dscam; fragile X syndrome; neuronal development; neuroscience; presynaptic terminals; tyrosine kinase inhibitors

PMID:
25988807
PMCID:
PMC4434255
DOI:
10.7554/eLife.05196
[Indexed for MEDLINE]
Free PMC Article

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