ArticleNature communications2022
Raptor downregulation rescues neuronal phenotypes in mouse models of Tuberous Sclerosis Complex.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
28 citing papers in PubMed, 39 citations in OpenAlex.
- Article
- PTEN Regulates Microtubule Polymerization via mTORC2, But Not mTORC1, in Peripheral Sensory Neurons.eNeuro · 2026Article
- Cell-Intrinsic Regulation of Epilepsy-Associated Pathology by mTORC1 and mTORC2.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Metabolic dysregulation reshapes the immune landscape: The gut microbiota-mTOR axis in respiratory viral infection immunity.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Review
- Tuberous sclerosis complex.Nature reviews. Disease primers · 2026Review
- NEAT1 Promotes Epileptogenesis in Tuberous Sclerosis Complex.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Cell Type-Specific mTORC1 Signaling and Translational Control in Synaptic Plasticity and Memory.Journal of neurochemistry · 2025Review
- TSC2-mTORC1 axis regulates morphogenesis and neurological function of Gli1Molecular biology of the cell · 2025Article
- Multiparameter quantitative analyses of diagnostic cells in brain tissues from tuberous sclerosis complex.Cytometry. Part B, Clinical cytometry · 2025Article
- The steroid hormone 20-hydroxyecdysone inhibits RAPTOR expression by repressing Hox gene transcription to induce autophagy.The Journal of biological chemistry · 2025Article
- Experimental and clinical tests of FDA-approved kinase inhibitors for the treatment of neurological disorders (update 2024).Exploration of drug science · 2025Article
- mTORC1-selective inhibitors rescue cellular phenotypes in TSC iPSC-derived neurons.Frontiers in neuroscience · 2025Article
- Genetic and pharmacological targeting of mTORC1 in mouse models of arteriovenous malformation expose non-cell autonomous signalling in HHT.Angiogenesis · 2024Article
- USP9X-mediated deubiquitination of Raptor contributes to autophagy impairment and memory deficits in P301S mice.Cell communication and signaling : CCS · 2024Article
- A role of dentate gyrus mechanistic target of rapamycin activation in epileptogenesis in a mouse model of posttraumatic epilepsy.Epilepsia · 2024Article
- The role of TSC1 and TSC2 proteins in neuronal axons.Molecular psychiatry · 2024Review
- Zebrafish raptor mutation inhibits the activity of mTORC1, inducing craniofacial defects due to autophagy-induced neural crest cell death.Development (Cambridge, England) · 2024Article
- Hyperactivity of mTORC1- and mTORC2-dependent signaling mediates epilepsy downstream of somatic PTEN loss.eLife · 2024Article
- The mTOR pathway geneseLife · 2024Article
- The mTORC2 signaling network: targets and cross-talks.The Biochemical journal · 2024Review
Corrections and comments
- Commented on by
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Tuberous Sclerosis Complex (TSC) is a neurodevelopmental disorder caused by mutations in the TSC1 or TSC2 genes, which encode proteins that negatively regulate mTOR complex 1 (mTORC1) signaling. Current treatment strategies focus on mTOR inhibition with rapamycin and its derivatives. While effective at improving some aspects of TSC, chronic rapamycin inhibits both mTORC1 and mTORC2 and is associated with systemic side-effects. It is currently unknown which mTOR complex is most relevant for TSC-related brain phenotypes. Here we used genetic strategies to selectively reduce neuronal mTORC1 or mTORC2 activity in mouse models of TSC. We find that reduction of the mTORC1 component Raptor, but not the mTORC2 component Rictor, rebalanced mTOR signaling in Tsc1 knock-out neurons. Raptor reduction was sufficient to improve several TSC-related phenotypes including neuronal hypertrophy, macrocephaly, impaired myelination, network hyperactivity, and premature mortality. Raptor downregulation represents a promising potential therapeutic intervention for the neurological manifestations of TSC.
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.