ArticleProceedings of the National Academy of Sciences of the United States of America2016
Normalizing translation through 4E-BP prevents mTOR-driven cortical mislamination and ameliorates aberrant neuron integration.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed.
- The phosphoproteomic landscape of the neurological manifestations in tuberous sclerosis complex.Acta neuropathologica · 2026Article
- The 4E-BPs as Translational Regulators in Neurological Disorders: Molecular Mechanisms and Therapeutic Potential.Molecular neurobiology · 2025Review
- Orchestrating Neural Development Through mRNA Translation Regulation.Journal of neurochemistry · 2025Review
- Hippocampal Inhibitory Interneuron-Specific DREADDs Treatment Alters mTORC1-4E-BP Signaling and Impairs Memory Formation.Journal of neurochemistry · 2025Article
- Focal postnatal deletion ofFrontiers in molecular neuroscience · 2025Article
- Increased translation in adult mouse striatum is sufficient to induce motor dysfunction.Brain communications · 2025Article
- Reducing Filamin A Restores Cortical Synaptic Connectivity and Early Social Communication Following Cellular Mosaicism in Autism Spectrum Disorder Pathways.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- The mTOR pathway geneseLife · 2024Article
- The mTOR pathway genesbioRxiv : the preprint server for biology · 2024Article
- Article
- Modeling genetic mosaicism of the mammalian target of rapamycin pathway in the cerebral cortex.Frontiers in mammal science · 2023Article
- Treatment-Resistant Epilepsy and Tuberous Sclerosis Complex: Treatment, Maintenance, and Future Directions.Neuropsychiatric disease and treatment · 2023Review
- 4E-BP1 expression in embryonic postmitotic neurons mitigates mTORC1-induced cortical malformations and behavioral seizure severity but does not prevent epilepsy in mice.Frontiers in neuroscience · 2023Article
- Pathological Networks Involving Dysmorphic Neurons in Type II Focal Cortical Dysplasia.Neuroscience bulletin · 2022Article
- Synaptic hyperexcitability of cytomegalic pyramidal neurons contributes to epileptogenesis in tuberous sclerosis complex.Cell reports · 2022Article
- Expression of 4E-BP1 in juvenile mice alleviates mTOR-induced neuronal dysfunction and epilepsy.Brain : a journal of neurology · 2022Article
- The Role of Zinc in Axon Formation via the mTORC1 Pathway.Molecular neurobiology · 2022Article
- PTEN Regulates Dendritic Arborization by Decreasing Microtubule Polymerization Rate.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Review
- Preimplantation factor modulates oligodendrocytes by H19-induced demethylation of NCOR2.JCI insight · 2021Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Hyperactive mammalian target of rapamycin complex 1 (mTORC1) is a shared molecular hallmark in several neurodevelopmental disorders characterized by abnormal brain cytoarchitecture. The mechanisms downstream of mTORC1 that are responsible for these defects remain unclear. We show that focally increasing mTORC1 activity during late corticogenesis leads to ectopic placement of upper-layer cortical neurons that does not require altered signaling in radial glia and is accompanied by changes in layer-specific molecular identity. Importantly, we found that decreasing cap-dependent translation by expressing a constitutively active mutant of the translational repressor eukaryotic initiation factor 4E-binding protein 1 (4E-BP1) prevents neuronal misplacement and soma enlargement, while partially rescuing dendritic hypertrophy induced by hyperactive mTORC1. Furthermore, overactivation of translation alone through knockdown of 4E-BP2 was sufficient to induce neuronal misplacement. These data show that many aspects of abnormal brain cytoarchitecture can be prevented by manipulating a single intracellular process downstream of mTORC1, cap-dependent translation.
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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 Socratic graph.