{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,15]],"date-time":"2026-10-15T15:55:39Z","timestamp":1792079739379,"version":"4.4.0"},"reference-count":45,"publisher":"eLife Sciences Publications, Ltd","license":[{"start":{"date-parts":[[2015,5,19]],"date-time":"2015-05-19T00:00:00Z","timestamp":1431993600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2015,5,19]],"date-time":"2015-05-19T00:00:00Z","timestamp":1431993600000},"content-version":"am","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2015,5,19]],"date-time":"2015-05-19T00:00:00Z","timestamp":1431993600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health (NIH)","doi-asserted-by":"publisher","award":["R01MH091186"],"award-info":[{"award-number":["R01MH091186"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000875","name":"Pew Charitable Trusts","doi-asserted-by":"publisher","award":["2009-000359-016"],"award-info":[{"award-number":["2009-000359-016"]}],"id":[{"id":"10.13039\/100000875","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100007270","name":"University of Michigan (U-M)","doi-asserted-by":"publisher","award":["Protein Folding Disease Initiative"],"award-info":[{"award-number":["Protein Folding Disease Initiative"]}],"id":[{"id":"10.13039\/100007270","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"abstract":"<jats:p>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.<\/jats:p>","DOI":"10.7554\/elife.05196","type":"journal-article","created":{"date-parts":[[2015,5,18]],"date-time":"2015-05-18T05:16:54Z","timestamp":1431926214000},"source":"Crossref","is-referenced-by-count":33,"title":["Dysregulated Dscam levels act through Abelson tyrosine kinase to enlarge presynaptic arbors"],"prefix":"10.7554","volume":"4","author":[{"given":"Gabriella R","family":"Sterne","sequence":"first","affiliation":[{"name":"Life Sciences Institute, University of Michigan, Ann Arbor, United States"},{"name":"Department of Cell and Developmental Biology, University of Michigan, Ann Arbor, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jung Hwan","family":"Kim","sequence":"additional","affiliation":[{"name":"Life Sciences Institute, University of Michigan, Ann Arbor, United States"},{"name":"Department of Cell 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