ArticleHuman molecular genetics2006
Effect of neurofibromatosis type I mutations on a novel pathway for adenylyl cyclase activation requiring neurofibromin and Ras.
Article in Human molecular genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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.
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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
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.
- Clinical features and surgical treatments of scoliosis in neurofibromatosis type 1: a systemic review and meta-analysis.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2024Pooled it
- Zebrafish neurofibromatosis type 1 mutants show disruption of sleep but not of circadian rhythms.Sleep · 2026Article
- Metabolic and behavioral effects of neurofibromin result from differential recruitment of MAPK and mTOR signaling.PLoS genetics · 2026Article
- Inhibition of Cxcr4 chemokine receptor signaling improves habituation learning in a zebrafish model of neurofibromatosis.Disease models & mechanisms · 2026Article
- Review
- Unraveling neuronal and metabolic alterations in neurofibromatosis type 1.Journal of neurodevelopmental disorders · 2024Review
- Modeling neurodegenerative and neurodevelopmental disorders in theLearning & memory (Cold Spring Harbor, N.Y.) · 2024Review
- Review
- Molecular diversity in isocitrate dehydrogenase-wild-type glioblastoma.Brain communications · 2024Review
- Neurofibromin 1 mediates sleep depth in Drosophila.PLoS genetics · 2023Article
- Existing and Developing Preclinical Models for Neurofibromatosis Type 1-Related Cutaneous Neurofibromas.The Journal of investigative dermatology · 2023Review
- The therapeutic potential of neurofibromin signaling pathways and binding partners.Communications biology · 2023Review
- Mechanistic insights from animal models of neurofibromatosis type 1 cognitive impairment.Disease models & mechanisms · 2022Review
- Hypophosphatemic osteomalacia in neurofibromatosis 1 associated with intracranial gliomas and congenital renal agenesis: A rare case report and review of the literature.Journal of orthopaedic case reports · 2022Article
- Current Aspects on the Pathophysiology of Bone Metabolic Defects during Progression of Scoliosis in Neurofibromatosis Type 1.Journal of clinical medicine · 2022Review
- Neurofibromin 1 in mushroom body neurons mediates circadian wake drive through activating cAMP-PKA signaling.Nature communications · 2021Article
- Associative Learning Requires Neurofibromin to Modulate GABAergic Inputs to Drosophila Mushroom Bodies.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Modeling human brain tumors in flies, worms, and zebrafish: From proof of principle to novel therapeutic targets.Neuro-oncology · 2021Review
- Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Neurofibromatosis type I (NFI) is a common genetic disorder that causes nervous system tumors, and learning and memory defects in humans, and animal models. We identify a novel growth factor stimulated adenylyl cyclase (AC) pathway in the Drosophila brain, which is disrupted by mutations in the epidermal growth factor receptor (EGFR), neurofibromin (NF1) and Ras, but not Galpha(s). This is the first demonstration in a metazoan that a receptor tyrosine kinase (RTK) pathway, acting independently of the heterotrimeric G-protein subunit Galpha(s), can activate AC. We also show that Galpha(s) is the major Galpha isoform in fly brains, and define a second AC pathway stimulated by serotonin and histamine requiring NF1 and Galpha(s), as well as a third, classical Galpha(s)-dependent AC pathway, which is stimulated by Phe-Met-Arg-Phe-amide (FMRFamide) and dopamine. Using mutations and deletions of the human NF1 protein (hNF1) expressed in Nf1 mutant flies, we show that Ras activation by hNF1 is essential for growth factor stimulation of AC activity. Further, we demonstrate that sequences in the C-terminal region of hNF1 are sufficient for NF1/Galpha(s)-dependent neurotransmitter stimulated AC activity, and for rescue of body size defects in Nf1 mutant flies.
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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.