ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
Aberrant growth and differentiation of oligodendrocyte progenitors in neurofibromatosis type 1 mutants.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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.
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Who cites it
42 citing papers in PubMed, 66 citations in OpenAlex.
- Genetic activation of ERK2 recapitulates core neurodevelopmental features of Rasopathy syndromes in mice.HGG advances · 2026Article
- Genetic activation of ERK2 recapitulates core neurodevelopmental features of Rasopathy syndromes in mice.bioRxiv : the preprint server for biology · 2025Article
- Quantitative T1 Mapping Indicates Elevated White Matter Myelin in Children With RASopathies.Biological psychiatry · 2025Article
- Current states in understanding oligodendroglia-mediated neurological issues in neurofibromatosis type 1 (NF1).Acta neuropathologica communications · 2025Review
- Age-related white matter alterations in children with neurofibromatosis type 1: a diffusion MRI tractography study.Frontiers in neuroscience · 2025Article
- Nf1 mutation disrupts activity-dependent oligodendroglial plasticity and motor learning in mice.Nature neuroscience · 2024Article
- Impact of pathogenic variants of the Ras-mitogen-activated protein kinase pathway on major white matter tracts in the human brain.Brain communications · 2024Article
- Interactions between Ras and Rap signaling pathways during neurodevelopment in health and disease.Frontiers in molecular neuroscience · 2024Review
- Review
- Presentation and integration of multiple signals that modulate oligodendrocyte lineage progression and myelination.Frontiers in cellular neuroscience · 2022Review
- A role for sustained MAPK activity in the mouse ventral telencephalon.Developmental biology · 2021Article
- Rnd2 differentially regulates oligodendrocyte myelination at different developmental periods.Molecular biology of the cell · 2021Article
- Generation of a Mouse Model to Study the Noonan Syndrome GeneFrontiers in cell and developmental biology · 2021Article
- Neurofibromatosis I and multiple sclerosis.Orphanet journal of rare diseases · 2020Article
- An update on the central nervous system manifestations of neurofibromatosis type 1.Acta neuropathologica · 2020Review
- Article
- The impact of RASopathy-associated mutations on CNS development in mice and humans.Molecular brain · 2019Review
- Article
- Oligodendrocyte Nf1 Controls Aberrant Notch Activation and Regulates Myelin Structure and Behavior.Cell reports · 2017Article
- The reactions and role of NG2 glia in spinal cord injury.Brain research · 2016Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Neurofibromatosis type 1 (NF1) patients are predisposed to learning disabilities, macrocephaly, and brain tumors as well as abnormalities on magnetic resonance imaging that are postulated to result from abnormal myelination. Here we show that Nf1+/- spinal cords in adult mice have more than twofold-increased numbers of NG2+ progenitor cells. Nf1-/- embryonic spinal cords have increased numbers of Olig2+ progenitors. Also, cultures from Nf1 mutant embryos with hemizygous and biallelic Nf1 mutations have dramatically increased numbers of CNS oligodendrocyte progenitor cells. In medium that allows growth of neuroepithelial cells and glial progenitors, mutant cells hyper-respond to FGF2, have increased basal and FGF-stimulated Ras-GTP, and fail to accumulate when treated with a farnesyltransferase inhibitor. Cell accumulation results in part from increased proliferation and decreased cell death. In contrast to wild-type cells, Nf1-/- progenitors express the glial differentiation marker O4 while retaining expression of the progenitor marker nestin. Nf1 mutant progenitors also abnormally coexpress the glial differentiation markers O4 and GFAP. Importantly, Nf1-/- spinal cord-derived oligodendrocyte progenitors, which are amplified 12-fold, retain the ability to form oligodendrocytes after in vivo transplantation. The data reveal a key role for neurofibromin and Ras signaling in the maintenance of CNS progenitor cell pools and also suggest a potential role for progenitor cell defects in the CNS abnormalities of NF1 patients.
Indexed as
Identifiers
12904481PMC6740670W1632311490What 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.