ArticleNature communications2021
Neurofibromin regulates metabolic rate via neuronal mechanisms in Drosophila.
Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 34 citations in OpenAlex.
- Excessive activation of the RAS/MAPK pathway triggers adult-onset motor axonal degeneration.iScience · 2026Article
- Genetic activation of ERK2 recapitulates core neurodevelopmental features of Rasopathy syndromes in mice.HGG advances · 2026Article
- Article
- Metabolic and behavioral effects of neurofibromin result from differential recruitment of MAPK and mTOR signaling.PLoS genetics · 2026Article
- Genetic activation of ERK2 recapitulates core neurodevelopmental features of Rasopathy syndromes in mice.bioRxiv : the preprint server for biology · 2025Article
- Energy Deficit Is a Key Driver of Sleep Homeostasis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Burden of disease and unmet needs associated with scoliosis in neurofibromatosis type 1: a systematic literature review.JBMR plus · 2025Article
- Cognition and behavior in neurofibromatosis type 1: report and perspective from the Cognition and Behavior in NF1 (CABIN) Task Force.Genes & development · 2025Article
- Anthropometric measurements of children with neurofibromatosis type I: impact of plexiform neurofibroma volume and treatment.Pediatric research · 2025Article
- Neurofibromin Deficiency Alters the Patterning and Prioritization of Motor Behaviors in a State-Dependent Manner.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Inhibition of autophagy as a novel treatment for neurofibromatosis type 1 tumors.Molecular oncology · 2025Article
- SERUM LncRNA SNHG16: A Biomarker for Diagnosing Childhood Obesity and Predicting Its Progression to Metabolic Syndrome.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Unraveling neuronal and metabolic alterations in neurofibromatosis type 1.Journal of neurodevelopmental disorders · 2024Review
- Neurofibromin deficiency alters the patterning and prioritization of motor behaviors in a state-dependent manner.bioRxiv : the preprint server for biology · 2024Article
- Do metabolic deficits contribute to sleep disruption in monogenic intellectual disability syndromes?Trends in neurosciences · 2024Review
- PET Imaging of Neurofibromatosis Type 1 with a Fluorine-18 Labeled Tryptophan Radiotracer.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Modeling neurodegenerative and neurodevelopmental disorders in theLearning & memory (Cold Spring Harbor, N.Y.) · 2024Review
- Review
- Neurofibromin 1 mediates sleep depth in Drosophila.PLoS genetics · 2023Article
- Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
Neurofibromatosis type 1 is a chronic multisystemic genetic disorder that results from loss of function in the neurofibromin protein. Neurofibromin may regulate metabolism, though the underlying mechanisms remain largely unknown. Here we show that neurofibromin regulates metabolic homeostasis in Drosophila via a discrete neuronal circuit. Loss of neurofibromin increases metabolic rate via a Ras GAP-related domain-dependent mechanism, increases feeding homeostatically, and alters lipid stores and turnover kinetics. The increase in metabolic rate is independent of locomotor activity, and maps to a sparse subset of neurons. Stimulating these neurons increases metabolic rate, linking their dynamic activity state to metabolism over short time scales. Our results indicate that neurofibromin regulates metabolic rate via neuronal mechanisms, suggest that cellular and systemic metabolic alterations may represent a pathophysiological mechanism in neurofibromatosis type 1, and provide a platform for investigating the cellular role of neurofibromin in metabolic homeostasis.
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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.