ArticleGenes & development2014
NF1 regulation of RAS/ERK signaling is required for appropriate granule neuron progenitor expansion and migration in cerebellar development.
Article in Genes & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 2 of them syntheses 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
41 citing papers in PubMed, 2 syntheses or guidelines pooled it, 61 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
- Blood transcriptomic comparison of individuals with and without autism spectrum disorder: A combined-samples mega-analysis.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2017Pooled it
- Comprehensive mapping of Neurofibromin (NF1) expression in developing mouse brain.Brain structure & function · 2026Article
- Comprehensive mapping of Neurofibromin (NF1) expression in developing mouse brain.bioRxiv : the preprint server for biology · 2026Article
- A Multi-parametric MRI and Machine Learning Study of Cerebellar Structure in Youth with Neurofibromatosis Type 1.Cerebellum (London, England) · 2026Article
- Alterations of plasma neural-derived extracellular vesicles microRNAs in patients with bipolar disorder.Psychological medicine · 2025Article
- The potential ameliorative effect of mesenchymal stem cells-derived exosomes on cerebellar histopathology and their modifying role on PI3k-mTOR signaling in rat model of autism spectrum disorder.Journal of molecular histology · 2025Article
- Characterizing molecular and behavioral changes arising from ROMK potassium channel deficiency in the cerebellum.Frontiers in behavioral neuroscience · 2025Article
- An EED/PRC2-H19 Loop Regulates Cerebellar Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mechanisms of brain overgrowth in autism spectrum disorder with macrocephaly.Frontiers in neuroscience · 2025Review
- Developmental mechanisms underlying pediatric epilepsy.Frontiers in neurology · 2025Review
- NF1Clinical and translational science · 2024Article
- Urine miRNA signature as potential non-invasive diagnostic biomarker for Hirschsprung's disease.Frontiers in molecular neuroscience · 2024Article
- Loss ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Cerebellum-dependent associative learning is not impaired in a mouse model of neurofibromatosis type 1.Scientific reports · 2022Article
- Rac-deficient cerebellar granule neurons die before they migrate to the internal granule layer.Scientific reports · 2022Article
- Article
- Review
- Patient-derived iPSC-cerebral organoid modeling of the 17q11.2 microdeletion syndrome establishes CRLF3 as a critical regulator of neurogenesis.Cell reports · 2021Article
- Temporarily Epigenetic Repression in Bergmann Glia Regulates the Migration of Granule Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Cerebellar development is regulated by a coordinated spatiotemporal interplay between granule neuron progenitors (GNPs), Purkinje neurons, and glia. Abnormal development can trigger motor deficits, and more recent data indicate important roles in aspects of memory, behavior, and autism spectrum disorders (ASDs). Germline mutation in the NF1 tumor suppressor gene underlies Neurofibromatosis type 1, a complex disease that enhances susceptibility to certain cancers and neurological disorders, including intellectual deficits and ASD. The NF1 gene encodes for neurofibromin, a RAS GTPase-activating protein, and thus negatively regulates the RAS signaling pathway. Here, using mouse models to direct conditional NF1 ablation in either embryonic cerebellar progenitors or neonatal GNPs, we show that neurofibromin is required for appropriate development of cerebellar folia layering and structure. Remarkably, neonatal administration of inhibitors of the ERK pathway reversed the morphological defects. Thus, our findings establish a critical cell-autonomous role for the NF1-RAS-ERK pathway in the appropriate regulation of cerebellar development and provide a basis for using neonatal ERK inhibitor-based therapies to treat NF1-induced cerebellar disorders.
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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.