ArticleAnnals of clinical and translational neurology2018
Depdc5 knockdown causes mTOR-dependent motor hyperactivity in zebrafish.
Article in Annals of clinical and translational neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
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Who cites it
30 citing papers in PubMed, 51 citations in OpenAlex.
- Early death and neuronal abnormalities inbioRxiv : the preprint server for biology · 2025Article
- Focal DEPDC5 loss without disruption to cerebral cortical neuron migration recapitulates DEPDC5-related focal epilepsy.JCI insight · 2025Article
- Sephin1 reduces TDP-43 cytoplasmic mislocalization and improves motor neuron survival in ALS models.Life science alliance · 2025Article
- DEPDC5 regulates the strength of excitatory synaptic transmission by interacting with ubiquitin-specific protease 46.Neurobiology of disease · 2025Article
- kcnb1 loss of function in zebrafish causes neurodevelopmental and epileptic disorders associated with γ-aminobutyric acid dysregulation.Epilepsia · 2025Article
- Neuronal cell type specific roles for Nprl2 in neurodevelopmental disorder-relevant behaviors.Neurobiology of disease · 2025Article
- Molecular Insights of Drug Resistance in Epilepsy: Multi-omics Unveil.Molecular neurobiology · 2025Review
- Poly-GP accumulation due to C9orf72 loss of function induces motor neuron apoptosis through autophagy and mitophagy defects.Autophagy · 2024Article
- Zebrafish models of candidate human epilepsy-associated genes provide evidence of hyperexcitability.iScience · 2024Article
- Zebrafish models of candidate human epilepsy-associated genes provide evidence of hyperexcitability.bioRxiv : the preprint server for biology · 2024Article
- Zebrafish as an Innovative Tool for Epilepsy Modeling: State of the Art and Potential Future Directions.International journal of molecular sciences · 2023Review
- Developing Novel Experimental Models of m-TORopathic Epilepsy and Related Neuropathologies: Translational Insights from Zebrafish.International journal of molecular sciences · 2023Review
- TFG mutation induces haploinsufficiency and drives axonal Charcot-Marie-Tooth disease by causing neurite degeneration.CNS neuroscience & therapeutics · 2022Article
- NPRL3 loss alters neuronal morphology, mTOR localization, cortical lamination and seizure threshold.Brain : a journal of neurology · 2022Article
- Modelling Autism Spectrum Disorder (ASD) and Attention-Deficit/Hyperactivity Disorder (ADHD) Using Mice and Zebrafish.International journal of molecular sciences · 2022Review
- Increased glycine contributes to synaptic dysfunction and early mortality in Nprl2 seizure model.iScience · 2022Article
- Zebrafish Is a Powerful Tool for Precision Medicine Approaches to Neurological Disorders.Frontiers in molecular neuroscience · 2022Review
- ubtor Mutation Causes Motor Hyperactivity by Activating mTOR Signaling in Zebrafish.Neuroscience bulletin · 2021Article
- Investigation on the Anticonvulsant Potential of Luteolin and Micronized Luteolin in Adult Zebrafish (Danio rerio).Neurochemical research · 2021Article
- SEA and GATOR 10 Years Later.Cells · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objective
methodsZebrafish represents a vertebrate model suitable for genetic analysis and drug screening in epilepsy-related disorders. In this study, we defined the expression of
resultsHere we report a zebrafish model of Depdc5 loss-of-function that displays a measurable behavioral phenotype, including hyperkinesia, circular swimming, and increased neuronal activity. These phenotypic features persisted throughout embryonic development and were significantly reduced upon treatment with the mTORC1 inhibitor, rapamycin, as well as overexpression of human WT
interpretationThis study demonstrates that Depdc5 knockdown leads to early-onset phenotypic features related to motor and neuronal hyperactivity. Restoration of phenotypic features by WT but not epilepsy-associated Depdc5 mutants, as well as by mTORC1 inhibition confirm the role of Depdc5 in the mTORC1-dependent molecular cascades, defining this pathway as a potential therapeutic target for
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.