ArticleScientific reports2017
Characterization of developmental defects in the forebrain resulting from hyperactivated mTOR signaling by integrative analysis of transcriptomic and proteomic data.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Leveraging Quantitative Proteomics and Extracellular Vesicle Data to Uncover Druggable Receptor Kinases Across Cancers.Journal of extracellular vesicles · 2026Article
- Low tristetraprolin expression activates phenotypic plasticity and primes transition to lethal prostate cancer in mice.The Journal of clinical investigation · 2024Article
- Abnormal activation of Yap/Taz contributes to the pathogenesis of tuberous sclerosis complex.Human molecular genetics · 2022Article
- Hyperactivation of mTORC1 in a double hit mutant zebrafish model of tuberous sclerosis complex causes increased seizure susceptibility and neurodevelopmental abnormalities.Frontiers in cell and developmental biology · 2022Article
- Stromal androgen and hedgehog signaling regulates stem cell niches in pubertal prostate development.Development (Cambridge, England) · 2021Article
- The essential role of primary cilia in cerebral cortical development and disorders.Current topics in developmental biology · 2021Review
- Article
- Brain Proteomic Profiling in Intractable Epilepsy Caused by TSC1 Truncating Mutations: A Small Sample Study.Frontiers in neurology · 2020Article
- mTOR hyperactivation in Down Syndrome underlies deficits in autophagy induction, autophagosome formation, and mitophagy.Cell death & disease · 2019Article
- Downregulation of CENPF Remodels Prostate Cancer Cells and Alters Cellular Metabolism.Proteomics · 2019Article
Corrections and comments
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperactivated mTOR signaling in the developing brain has been implicated in multiple forms of pathology including tuberous sclerosis complex (TSC). To date, various phenotypic defects such as cortical lamination irregularity, subependymal nodule formation, dysmorphic astrocyte differentiation and dendritic malformation have been described for patients and animal models. However, downstream networks affected in the developing brain by hyperactivated mTOR signaling have yet to be characterized. Here, we present an integrated analysis of transcriptomes and proteomes generated from wild-type and Tsc1/Emx1-Cre forebrains. This led to comprehensive lists of genes and proteins whose expression levels were altered by hyperactivated mTOR signaling. Further incorporation of TSC patient data followed by functional enrichment and network analyses pointed to changes in molecular components and cellular processes associated with neuronal differentiation and morphogenesis as the key downstream events underlying developmental and morphological defects in TSC. Our results provide novel and fundamental molecular bases for understanding hyperactivated mTOR signaling-induced brain defects which can in turn facilitate identification of potential diagnostic markers and therapeutic targets for mTOR signaling-related neurological disorders.
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