ArticleeLife2015
Dysregulated Dscam levels act through Abelson tyrosine kinase to enlarge presynaptic arbors.
Article in eLife, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- Future Directions for Studying the Potential of Mammalian Dscam in Autism Spectrum Disorder and Alzheimer's Disease: Insights from Dose Sensitivity.Molecular neurobiology · 2025Review
- Exploring perspectives of Dscam for cognitive deficits: a review of multifunction for regulating neural wiring in homeostasis.Frontiers in molecular neuroscience · 2025Review
- The role of Down syndrome cell adhesion molecule in Down syndrome.Medical review (2021) · 2024Review
- Synaptic cell adhesion molecules contribute to the pathogenesis and progression of fragile X syndrome.Frontiers in cellular neuroscience · 2024Review
- Lamivudine modulates the expression of neurological impairment-related genes and LINE-1 retrotransposons in brain tissues of a Down syndrome mouse model.Frontiers in aging neuroscience · 2024Article
- The Drosophila homolog of APP promotes Dscam expression to drive axon terminal growth, revealing interaction between Down syndrome genes.Disease models & mechanisms · 2023Article
- A systematic CRISPR screen reveals redundant and specific roles for Dscam1 isoform diversity in neuronal wiring.PLoS biology · 2023Article
- Article
- DSCAM gene triplication causes excessive GABAergic synapses in the neocortex in Down syndrome mouse models.PLoS biology · 2023Article
- Dscam1 overexpression impairs the function of the gut nervous system in Drosophila.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Article
- Dual Leucine Zipper Kinase Regulates Dscam Expression through a Noncanonical Function of the Cytoplasmic Poly(A)-Binding Protein.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- DSCAM Deficiency Leads to Premature Spine Maturation and Autism-like Behaviors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Generation and validation of pX-UASTattB for dose-dependent misexpression studies inmicroPublication biology · 2022Article
- All Creatures Great and Small: New Approaches for Understanding Down Syndrome Genetics.Trends in genetics : TIG · 2021Review
- isoTarget: A Genetic Method for Analyzing the Functional Diversity of Splicing Isoforms In Vivo.Cell reports · 2020Article
- The first quarter of the C-terminal domain of Abelson regulates the WAVE regulatory complex and Enabled in axon guidance.Neural development · 2020Article
- Nuclear import of the DSCAM-cytoplasmic domain drives signaling capable of inhibiting synapse formation.The EMBO journal · 2019Article
- The Role of Apoptotic Signaling in Axon Guidance.Journal of developmental biology · 2018Review
- Modeling Fragile X Syndrome inFrontiers in molecular neuroscience · 2018Review
- Multifarious Functions of the Fragile X Mental Retardation Protein.Trends in genetics : TIG · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.