ArticleGenes & development2002
N-myc is essential during neurogenesis for the rapid expansion of progenitor cell populations and the inhibition of neuronal differentiation.
Article in Genes & development, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 271 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
271 citing papers in PubMed.
- Overactivation of SHH signaling induces a cascade of dedifferentiation and oncogenesis in a new mouse model for choroid plexus carcinoma.Acta neuropathologica communications · 2026Article
- Developmental timing distinguishes pediatric and adult cancers through retention and rewiring mechanisms.Nature communications · 2026Review
- Context-specific genetic effects inform endotypes and treatment in asthma.The Journal of allergy and clinical immunology · 2026Article
- Molecular Iodine/Cells · 2026Article
- Targeting the MYCN interaction network in neuroblastoma.Bioscience reports · 2026Review
- KAT6A is essential for developmental control gene expression in neural stem and progenitor cells.PLoS genetics · 2026Article
- Ubiquitin-Specific Protease 2 (USP2) as a Modulator of Energy Metabolism: A Review of Studies Using Animal and Cellular Models.Biomedicines · 2026Review
- Antidepressant-like effects of Rg1 by mycn: promotion of neurogenesis in the hippocampus.Frontiers in pharmacology · 2026Article
- CRISPR/Cas9-mediatedFrontiers in physiology · 2026Article
- Epigenetic crosstalk in neuroblastoma development and progression.Frontiers in cell and developmental biology · 2026Review
- Sequential transcriptional programs underpin activation of hippocampal stem cells.Science advances · 2025Article
- A Rapid F0 CRISPR Screen in Zebrafish to Identify Regulator Genes of Neuronal Development in the Enteric Nervous System.Neurogastroenterology and motility · 2025Article
- Targeting the MYCN-MDM2 pathways for cancer therapy: Are they druggable?Genes & diseases · 2025Review
- iFlpMosaics enable the multispectral barcoding and high-throughput comparative analysis of mutant and wild-type cells.Nature methods · 2025Article
- Review
- MYCN as an oncogene in pediatric brain tumors.Frontiers in oncology · 2025Review
- iSuRe-HadCre is an essential tool for effective conditional genetics.Nucleic acids research · 2024Article
- SAP30, an oncogenic driver of progression, poor survival, and drug resistance in neuroblastoma.Molecular therapy. Nucleic acids · 2024Article
- MYCN immunohistochemistry as surrogate marker for MYCN-amplified spinal ependymomas.Human cell · 2024Article
- Article
211 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To address the role of N-myc in neurogenesis and in nervous system tumors, it was conditionally disrupted in neuronal progenitor cells (NPCs) with a nestin-Cre transgene. Null mice display ataxia, behavioral abnormalities, and tremors that correlate with a twofold decrease in brain mass that disproportionately affects the cerebellum (sixfold reduced in mass) and the cerebral cortex, both of which show signs of disorganization. In control mice at E12.5, we observe a domain of high N-Myc protein expression in the rapidly proliferating cerebellar primordium. Targeted deletion of N-myc results in severely compromised proliferation as shown by a striking decrease in S phase and mitotic cells as well as in cells expressing the Myc target gene cyclin D2, whereas apoptosis is unaffected. Null progenitor cells also have comparatively high levels of the cdk inhibitors p27(Kip1) and p18(Ink4c), whereas p15(Ink4b), p21(Cip1), and p19(Ink4d) levels are unaffected. Many null progenitors also exhibit altered nuclear morphology and size. In addition, loss of N-myc disrupts neuronal differentiation as evidenced by ectopic staining of the neuron specific marker betaTUBIII in the cerebrum. Furthermore, in progenitor cell cultures derived from null embryonic brain, we observe a dramatic increase in neuronal differentiation compared with controls. Thus, N-myc is essential for normal neurogenesis, regulating NPC proliferation, differentiation, and nuclear size. Its effects on proliferation and differentiation appear due, at least in part, to down-regulation of a specific subset of cyclin-dependent kinase inhibitors.
Indexed as
Identifiers
What 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.