ArticleNature cell biology2013
A tuberous sclerosis complex signalling node at the peroxisome regulates mTORC1 and autophagy in response to ROS.
Article in Nature cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers, 4 of them syntheses that pooled it.
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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.
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Who cites it
151 citing papers in PubMed, 4 syntheses or guidelines pooled it, 251 citations in OpenAlex.
- The interplay between oxidative stress and autophagy in chronic obstructive pulmonary disease.Frontiers in physiology · 2022Pooled it
- Selective autophagy of intracellular organelles: recent research advances.Theranostics · 2021Pooled it
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).Autophagy · 2016Guideline
- Autophagy dependent HIF1α proteostasis is compromised in models of PEX1 deficiencies.bioRxiv : the preprint server for biology · 2026Article
- Impaired Chaperone-Mediated Autophagy Accelerates Intervertebral Disc Degeneration by Inducing MIDN Accumulation to Target TSC2 for Proteasomal Degradation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Perspective: Personalized Management of Oxidative and Nitrosative Stress in Post-Exercise Recovery with a Particular Emphasis on the Potential of Micro-Immunotherapy.Sports (Basel, Switzerland) · 2026Review
- Genetically targeted mTORC1 inhibitor reveals transcriptional control by nuclear mTORC1.Nature chemical biology · 2026Article
- Protein Kinase C promotes peroxisome biogenesis and peroxisome-endoplasmic reticulum interaction.The Journal of cell biology · 2025Article
- Pexophagy and Oxidative Stress: Focus on Peroxisomal Proteins and Reactive Oxygen Species (ROS) Signaling Pathways.Antioxidants (Basel, Switzerland) · 2025Review
- mTORC1, the maestro of cell metabolism and growth.Genes & development · 2025Review
- Peroxisomes as emerging clinical targets in neuroinflammatory diseases.Frontiers in molecular neuroscience · 2025Review
- Visualization of Subcellular mTOR Complex 1 Activity with a FRET-Based Sensor (TORCAR).Methods in molecular biology (Clifton, N.J.) · 2025Article
- Research on the role and mechanism of the PI3K/Akt/mTOR signalling pathway in osteoporosis.Frontiers in endocrinology · 2025Review
- Canagliflozin as a Potential Preclinical Therapy for Tuberous Sclerosis Complex: Inhibition ofDrug design, development and therapy · 2025Article
- New insights into tuberous sclerosis complex: from structure to pathogenesis.Frontiers in cell and developmental biology · 2025Review
- Stress response regulation of mRNA translation: Implications for antioxidant enzyme expression in cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024Review
- Circulating biomarkers of kidney angiomyolipoma and cysts in tuberous sclerosis complex patients.iScience · 2024Article
- Mammalian pexophagy at a glance.Journal of cell science · 2024Review
- Integrated analysis of gut metabolome, microbiome, and exfoliome data in an equine model of intestinal injury.Microbiome · 2024Article
91 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
18 authors at 9 institutions in 3 countries.
Funding
Abstract
Subcellular localization is emerging as an important mechanism for mTORC1 regulation. We report that the tuberous sclerosis complex (TSC) signalling node, TSC1, TSC2 and Rheb, localizes to peroxisomes, where it regulates mTORC1 in response to reactive oxygen species (ROS). TSC1 and TSC2 were bound by peroxisomal biogenesis factors 19 and 5 (PEX19 and PEX5), respectively, and peroxisome-localized TSC functioned as a Rheb GTPase-activating protein (GAP) to suppress mTORC1 and induce autophagy. Naturally occurring pathogenic mutations in TSC2 decreased PEX5 binding, and abrogated peroxisome localization, Rheb GAP activity and suppression of mTORC1 by ROS. Cells lacking peroxisomes were deficient in mTORC1 repression by ROS, and peroxisome-localization-deficient TSC2 mutants caused polarity defects and formation of multiple axons in neurons. These data identify a role for the TSC in responding to ROS at the peroxisome, and identify the peroxisome as a signalling organelle involved in regulation of mTORC1.
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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.