ArticleeLife2014
Transient inhibition of the ERK pathway prevents cerebellar developmental defects and improves long-term motor functions in murine models of neurofibromatosis type 1.
Article in eLife, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Social Communication in Ras Pathway Disorders: A Comprehensive Review From Genetics to Behavior in Neurofibromatosis Type 1 and Noonan Syndrome.Biological psychiatry · 2025Pooled it
- Genetic activation of ERK2 recapitulates core neurodevelopmental features of Rasopathy syndromes in mice.HGG advances · 2026Article
- A Multi-parametric MRI and Machine Learning Study of Cerebellar Structure in Youth with Neurofibromatosis Type 1.Cerebellum (London, England) · 2026Article
- Genetic activation of ERK2 recapitulates core neurodevelopmental features of Rasopathy syndromes in mice.bioRxiv : the preprint server for biology · 2025Article
- Current states in understanding oligodendroglia-mediated neurological issues in neurofibromatosis type 1 (NF1).Acta neuropathologica communications · 2025Review
- FUT8 Regulates Cerebellar Neurogenesis and Development Through Maintaining the Level of Neural Cell Adhesion Molecule Cntn2.Molecular neurobiology · 2025Article
- Deficiency of FABP7 Triggers Premature Neural Differentiation in Idiopathic Normocephalic Autism Organoids.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- NF1Clinical and translational science · 2024Article
- Cerebellum-dependent associative learning is not impaired in a mouse model of neurofibromatosis type 1.Scientific reports · 2022Article
- MEK inhibitors for neurofibromatosis type 1 manifestations: Clinical evidence and consensus.Neuro-oncology · 2022Review
- Mechanistic insights from animal models of neurofibromatosis type 1 cognitive impairment.Disease models & mechanisms · 2022Review
- Dexmedetomidine improved one-lung ventilation-induced cognitive dysfunction in rats.BMC anesthesiology · 2022Article
- Allostery, and how to define and measure signal transduction.Biophysical chemistry · 2022Review
- MEK inhibition ameliorates social behavior phenotypes in a Spred1 knockout mouse model for RASopathy disorders.Molecular autism · 2021Article
- Cell Type-specific Knockout withExperimental neurobiology · 2021Article
- Temporarily Epigenetic Repression in Bergmann Glia Regulates the Migration of Granule Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Article
- Deletion ofFrontiers in cell and developmental biology · 2020Article
- Neuronal Migration During Development of the Cerebellum.Frontiers in cellular neuroscience · 2018Review
- Pediatric low-grade gliomas: implications of the biologic era.Neuro-oncology · 2017Review
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 1 country.
Funding
Abstract
Individuals with neurofibromatosis type 1 (NF1) frequently exhibit cognitive and motor impairments and characteristics of autism. The cerebellum plays a critical role in motor control, cognition, and social interaction, suggesting that cerebellar defects likely contribute to NF1-associated neurodevelopmental disorders. Here we show that Nf1 inactivation during early, but not late stages of cerebellar development, disrupts neuronal lamination, which is partially caused by overproduction of glia and subsequent disruption of the Bergmann glia (BG) scaffold. Specific Nf1 inactivation in glutamatergic neuronal precursors causes premature differentiation of granule cell (GC) precursors and ectopic production of unipolar brush cells (UBCs), indirectly disrupting neuronal migration. Transient MEK inhibition during a neonatal window prevents cerebellar developmental defects and improves long-term motor performance of Nf1-deficient mice. This study reveals essential roles of Nf1 in GC/UBC migration by generating correct numbers of glia and controlling GC/UBC fate-specification/differentiation, identifying a therapeutic prevention strategy for multiple NF1-associcated developmental abnormalities.
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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.