ArticleScientific reports2019
Hyperactivation of mTORC1 disrupts cellular homeostasis in cerebellar Purkinje cells.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Regulatory T lymphocytes/Th17 lymphocytes imbalance in autism spectrum disorders: evidence from a meta-analysis.Molecular autism · 2021Pooled it
- Loss of YY1 in Purkinje cells triggers cerebellar ataxia via Wnt10b-mediated impairment of dendrite development.iScience · 2026Article
- A Streamlined Workflow for Purkinje Cell Labeling and High-Resolution Analyses of Dendrites and Spines in Mice.eNeuro · 2026Article
- Targeting endoplasmic reticulum export disrupts metabolic resilience in multiple myeloma.Signal transduction and targeted therapy · 2026Article
- Cerebellar microRNA-206 tunes Purkinje neuron firing dynamics to control sensorimotor gating.bioRxiv : the preprint server for biology · 2026Article
- PTEN deficiency in postnatally developing Purkinje cells disrupts metabolic signaling, leading to dendritic abnormalities and sex-specific behavioral deficits.Scientific reports · 2025Article
- Delta opioid receptor agonists activate PI3K-mTORC1 signaling in parvalbumin-positive interneurons in mouse infralimbic prefrontal cortex to exert acute antidepressant-lie effects.Molecular psychiatry · 2025Article
- Adaptive protein synthesis in genetic models of copper deficiency and childhood neurodegeneration.Molecular biology of the cell · 2025Article
- Potential of Vitamin D and l-Cysteine Co-supplementation to Downregulate Mammalian Target of Rapamycin: A Novel Therapeutic Approach to Diabetes.Metabolic syndrome and related disorders · 2025Review
- Homer-3 antibody in autoimmune cerebellar syndromes: a potentially treatable mimic of MSA-C - A review.Frontiers in immunology · 2025Review
- Cerebellar Roles in Motor and Social Functions and Implications for ASD.Cerebellum (London, England) · 2024Review
- Adaptive protein synthesis in genetic models of copper deficiency and childhood neurodegeneration.bioRxiv : the preprint server for biology · 2024Article
- Converging and Diverging Cerebellar Pathways for Motor and Social Behaviors in Mice.Cerebellum (London, England) · 2024Review
- Hyperactive mTORC1 in striatum dysregulates dopamine receptor expression and odor preference behavior.Frontiers in neuroscience · 2024Article
- Heterozygous variants in TBCK cause a mild neurologic syndrome in humans and mice.American journal of medical genetics. Part A · 2023Article
- Insight into Genetic Mutations of SZT2: Is It a Syndrome?Biomedicines · 2023Article
- The Cerebellum in Niemann-Pick C1 Disease: Mouse Versus Man.Cerebellum (London, England) · 2023Review
- GPRC6A Mediates Glucose and Amino Acid Homeostasis in Mice.Metabolites · 2022Article
- The non-essential TSC complex component TBC1D7 restricts tissue mTORC1 signaling and brain and neuron growth.Cell reports · 2022Article
- Neuronal mechanism of a BK channelopathy in absence epilepsy and dyskinesia.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mammalian target of rapamycin (mTOR) is a central regulator of cellular metabolism. The importance of mTORC1 signaling in neuronal development and functions has been highlighted by its strong relationship with many neurological and neuropsychiatric diseases. Previous studies demonstrated that hyperactivation of mTORC1 in forebrain recapitulates tuberous sclerosis and neurodegeneration. In the mouse cerebellum, Purkinje cell-specific knockout of Tsc1/2 has been implicated in autistic-like behaviors. However, since TSC1/2 activity does not always correlate with clinical manifestations as evident in some cases of tuberous sclerosis, the intriguing possibility is raised that phenotypes observed in Tsc1/2 knockout mice cannot be attributable solely to mTORC1 hyperactivation. Here we generated transgenic mice in which mTORC1 signaling is directly hyperactivated in Purkinje cells. The transgenic mice exhibited impaired synapse elimination of climbing fibers and motor discoordination without affecting social behaviors. Furthermore, mTORC1 hyperactivation induced prominent apoptosis of Purkinje cells, accompanied with dysregulated cellular homeostasis including cell enlargement, increased mitochondrial respiratory activity, and activation of pseudohypoxic response. These findings suggest the different contributions between hyperactivated mTORC1 and Tsc1/2 knockout in social behaviors, and reveal the perturbations of cellular homeostasis by hyperactivated mTORC1 as possible underlying mechanisms of neuronal dysfunctions and death in tuberous sclerosis and neurodegenerative diseases.
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