ArticleScientific reports2015
N-myc is a key switch regulating the proliferation cycle of postnatal cerebellar granule cell progenitors.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Article
- Article
- Article
- Reduced Granule Cell Proliferation and Molecular Dysregulation in the Cerebellum of Lysosomal Acid Phosphatase 2 (ACP2) Mutant Mice.International journal of molecular sciences · 2021Article
- Otx2 promotes granule cell precursor proliferation and Shh-dependent medulloblastoma maintenance in vivo.Oncogenesis · 2018Article
- The Role of MicroRNAs in Cerebellar Development and Autism Spectrum Disorder During Embryogenesis.Molecular neurobiology · 2017Review
- Nanog-driven cell-reprogramming and self-renewal maintenance in Ptch1Scientific reports · 2017Article
- Reprogramming Medulloblastoma-Propagating Cells by a Combined Antagonism of Sonic Hedgehog and CXCR4.Cancer research · 2017Article
- Notch/Hes signaling and miR-9 engage in complex feedback interactions controlling neural progenitor cell proliferation and differentiation.Neurogenesis (Austin, Tex.) · 2017Review
- Ex vivo miRNome analysis in Ptch1+/- cerebellum granule cells reveals a subset of miRNAs involved in radiation-induced medulloblastoma.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N-myc plays an important role in early cerebellar development; however, the role of N-myc in postnatal cerebellar development is still unknown. In this study, inducible and reversible N-myc mouse models (Nmyc(TRE/TRE):tTS and Nmyc(EGFP/TRE):tTS) are used to regulate and track the expression of endogenous N-myc in vivo. Loss of N-myc at the neonatal stage results in reduced proliferation of granule cell precursors (GCPs) and reduced cerebellar volume/mass. Restoration of N-myc expression no later than postnatal day 4 can rescue the cerebellar developmental defect caused by the absence of N-myc after birth. During cerebellar postnatal development, N-myc acts as a key switch, regulating the proliferation cycle of postnatal granule cell progenitors. Loss of N-myc significantly impairs the Sonic hedgehog signalling pathway, and disrupts the expression of cell cycle effectors with a significant reduction of Ccnd2. More importantly, N-myc negatively regulates the expression of microRNA-9 during postnatal cerebellar development. Our findings demonstrate that over-expression of miR-9 can inhibit the proliferation of GCPs. The regulation of these factors by N-myc is at least partly responsible for the switch role of N-myc in the proliferation cycle of GCPs.
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