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

eLife

Jung Hwan Kim¹  Gabriella R Sterne²  Bing Ye² 

[1] Department of Cell and Developmental Biology, University of Michigan, Ann Arbor, United States;Life Sciences Institute, University of Michigan, Ann Arbor, United States;

关键词: Dscam;    Abl;    fragile X syndrome;    tyrosine kinase inhibitor;    presynaptic terminal;    neuronal development;   

DOI  :  10.7554/eLife.05196

来源: DOAJ

【 摘 要 】

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.

【 授权许可】

Unknown