ArticleProceedings of the National Academy of Sciences of the United States of America2007
BM88/CEND1 coordinates cell cycle exit and differentiation of neuronal precursors.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 72 citations in OpenAlex.
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- Neuronal differentiation regulator CEND1 coordinately suppresses tumor growth and energetics via AMPK signaling in brain glioma.Cell & bioscience · 2025Article
- Modeling glioma intratumoral heterogeneity with primary human neural stem and progenitor cells.Stem cell reports · 2025Article
- The regulatory role of cell cycle exit and neuronal differentiation 1 in the pathogenesis of Parkinson's disease by regulating the nuclear factor kappa B pathway.Neuroreport · 2025Article
- Rapid and Effective Neuronal Conversion of Human Glioblastoma In Vitro and In Vivo Using Potent Small Molecules.Cell proliferation · 2025Article
- Sex-dependent differences in the ability of nicotine to modulate discrimination learning and cognitive flexibility in mice.Journal of neurochemistry · 2025Article
- ADAR3 modulates neuronal differentiation and regulates mRNA stability and translation.Nucleic acids research · 2024Article
- Mirk/Dyrk1B controls ventral spinal cord development via Shh pathway.Cellular and molecular life sciences : CMLS · 2024Article
- Human amygdala involvement in Alzheimer's disease revealed by stereological and dia-PASEF analysis.Brain pathology (Zurich, Switzerland) · 2023Article
- SnRNA-seq reveals the heterogeneity of spinal ventral horn and mechanism of motor neuron axon regeneration.iScience · 2023Article
- Glaucoma-Associated CDR1 Peptide Promotes RGC Survival in Retinal Explants through Molecular Interaction with Acidic Leucine Rich Nuclear Phosphoprotein 32A (ANP32A).Biomolecules · 2023Article
- Down-Regulation of CEND1 Expression Contributes to The Progression and Temozolomide Resistance of Glioma.Cell journal · 2023Article
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- CEND1 deficiency induces mitochondrial dysfunction and cognitive impairment in Alzheimer's disease.Cell death and differentiation · 2022Article
- ATP13A1 prevents ERAD of folding-competent mislocalized and misoriented proteins.Molecular cell · 2022Article
- Cell cycle exit and neuronal differentiation 1-engineered embryonic neural stem cells enhance neuronal differentiation and neurobehavioral recovery after experimental traumatic brain injury.Neural regeneration research · 2022Article
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- Prox1 inhibits neurite outgrowth during central nervous system development.Cellular and molecular life sciences : CMLS · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During development, coordinate regulation of cell cycle exit and differentiation of neuronal precursors is essential for generation of appropriate number of neurons and proper wiring of neuronal circuits. BM88 is a neuronal protein associated in vivo with terminal neuron-generating divisions, marking the exit of proliferative cells from the cell cycle. Here, we provide functional evidence that BM88 is sufficient to initiate the differentiation of spinal cord neural precursors toward acquisition of generic neuronal and subtype-specific traits. Gain-of-function approaches show that BM88 negatively regulates proliferation of neuronal precursors, driving them to prematurely exit the cell cycle, down-regulate Notch1, and commit to a neuronal differentiation pathway. The combined effect on proliferation and differentiation results in precocious induction of neurogenesis and generation of postmitotic neurons within the ventricular zone. The dual action of BM88 is not recapitulated by the cell cycle inhibitor p27Kip1, suggesting that cell cycle exit does not induce differentiation by default. Mechanistically, induction of endogenous BM88 by forced expression of the proneural gene Mash1 indicates that BM88 is part of the differentiation program activated by proneural genes. Furthermore, BM88 gene silencing conferred by small interfering RNA in spinal cord neural progenitor cells enhances cell cycle progression and impairs neuronal differentiation. Our results implicate BM88 in the synchronization of cell cycle exit and differentiation of neuronal precursors in the developing nervous system.
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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.