ReviewOncogene2005
Tuberous sclerosis complex: linking growth and energy signaling pathways with human disease.
Review in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.
What it found
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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.
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.
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Who cites it
77 citing papers in PubMed, 210 citations in OpenAlex.
- Physiologic mechanisms underlying polycystic kidney disease.Physiological reviews · 2025Review
- Neuroprotective Roles of Daidzein Through Extracellular Signal-Regulated Kinases Dependent Pathway In Chronic Unpredictable Mild Stress Mouse Model.Molecular neurobiology · 2025Article
- Translationally Controlled Tumor Protein (TCTP) and Growth Regulation in the Drosophila Model.Advances in experimental medicine and biology · 2025Article
- Quality of life and disease burden in tuberous sclerosis and comparison with the population with idiopathic autism spectrum disorder: an investigation conducted through questionnaires and clinical data collection in the pediatric population.Frontiers in psychiatry · 2025Article
- Beyond Protein Synthesis; The Multifaceted Roles of Tuberin in Cell Cycle Regulation.Frontiers in cell and developmental biology · 2021Review
- Recombinant Tumor Suppressor TSC1 Differentially Interacts withACS omega · 2020Article
- Chronic Sulforaphane Administration Inhibits Resistance to the mTOR-Inhibitor Everolimus in Bladder Cancer Cells.International journal of molecular sciences · 2020Article
- Neural Mechanisms Underlying Repetitive Behaviors in Rodent Models of Autism Spectrum Disorders.Frontiers in cellular neuroscience · 2020Review
- Tuberous sclerosis complex: new insights into clinical and therapeutic approach.Journal of nephrology · 2019Review
- Metabolism and mitochondria in polycystic kidney disease research and therapy.Nature reviews. Nephrology · 2018Review
- Two novel TSC2 mutations in pediatric patients with tuberous sclerosis complex: Case report.Medicine · 2018Article
- Molecular genetic diagnostics of tuberous sclerosis complex in Bulgaria: six novel mutations in theJournal of genetics · 2018Article
- Inhibition of ERK1/2 Restores GSK3β Activity and Protein Synthesis Levels in a Model of Tuberous Sclerosis.Scientific reports · 2017Article
- Article
- [Two novel TSC2 frameshift mutations in tuberous sclerosis complex].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2017Article
- Article
- Reprogramming towards anabolism impedes degeneration in a preclinical model of retinitis pigmentosa.Human molecular genetics · 2016Article
- Triterpenes in cancer: significance and their influence.Molecular biology reports · 2016Review
- Hypothalamic roles of mTOR complex I: integration of nutrient and hormone signals to regulate energy homeostasis.American journal of physiology. Endocrinology and metabolism · 2016Review
- Restoration of Normal Cerebral Oxygen Consumption with Rapamycin Treatment in a Rat Model of Autism-Tuberous Sclerosis.Neuromolecular medicine · 2015Article
17 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The most exciting advances in the tuberous sclerosis complex (TSC) field occurred in 1993 and 1997 with the cloning of the TSC2 and TSC1 genes, respectively, and in 2003 with the identification of Rheb as the target of tuberin's (TSC2) GTPase activating protein (GAP) domain. Rheb has a dual role: it activates mTOR and inactivates B-Raf. Activation of mTOR leads to increased protein synthesis through phosphorylation of p70S6K and 4E-BP1. Upon insulin or growth factor stimulation, tuberin is phosphorylated by several kinases, including AKT/PKB, thereby suppressing its GAP activity and activating mTOR. Phosphorylation of hamartin (TSC1) by CDK1 also negatively regulates the activity of the hamartin/tuberin complex. Despite these biochemical advances, exactly how mutations in TSC1 or TSC2 lead to the clinical manifestations of TSC is far from being understood. Two of the most unusual phenotypes in TSC are the apparent metastasis of benign cells carrying TSC1 and TSC2 mutations, resulting in pulmonary lymphangiomyomatosis, and the ability of cells with TSC1 or TSC2 mutations to differentiate into the separate components of renal angiomyolipomas (vessels, smooth muscle and fat). We will discuss how the TSC signaling pathways are affected by mutations in TSC1 or TSC2, focusing on how these mutations may lead to the renal and pulmonary manifestations of TSC.
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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.