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

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 pharmacolog...

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Detalles Bibliográficos
Autores principales: Sterne, Gabriella R, Kim, Jung Hwan, Ye, Bing
Formato: Online Artículo Texto
Lenguaje:English
Publicado: eLife Sciences Publications, Ltd 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4434255/
https://www.ncbi.nlm.nih.gov/pubmed/25988807
http://dx.doi.org/10.7554/eLife.05196
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author Sterne, Gabriella R
Kim, Jung Hwan
Ye, Bing
author_facet Sterne, Gabriella R
Kim, Jung Hwan
Ye, Bing
author_sort Sterne, Gabriella R
collection PubMed
description 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. DOI: http://dx.doi.org/10.7554/eLife.05196.001
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spelling pubmed-44342552015-05-20 Dysregulated Dscam levels act through Abelson tyrosine kinase to enlarge presynaptic arbors Sterne, Gabriella R Kim, Jung Hwan Ye, Bing eLife Neuroscience 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. DOI: http://dx.doi.org/10.7554/eLife.05196.001 eLife Sciences Publications, Ltd 2015-05-19 /pmc/articles/PMC4434255/ /pubmed/25988807 http://dx.doi.org/10.7554/eLife.05196 Text en © 2015, Sterne et al http://creativecommons.org/licenses/by/4.0/ This article is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use and redistribution provided that the original author and source are credited.
spellingShingle Neuroscience
Sterne, Gabriella R
Kim, Jung Hwan
Ye, Bing
Dysregulated Dscam levels act through Abelson tyrosine kinase to enlarge presynaptic arbors
title Dysregulated Dscam levels act through Abelson tyrosine kinase to enlarge presynaptic arbors
title_full Dysregulated Dscam levels act through Abelson tyrosine kinase to enlarge presynaptic arbors
title_fullStr Dysregulated Dscam levels act through Abelson tyrosine kinase to enlarge presynaptic arbors
title_full_unstemmed Dysregulated Dscam levels act through Abelson tyrosine kinase to enlarge presynaptic arbors
title_short Dysregulated Dscam levels act through Abelson tyrosine kinase to enlarge presynaptic arbors
title_sort dysregulated dscam levels act through abelson tyrosine kinase to enlarge presynaptic arbors
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4434255/
https://www.ncbi.nlm.nih.gov/pubmed/25988807
http://dx.doi.org/10.7554/eLife.05196
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