ArticleThe EMBO journal2023
N4BP1 mediates RAM domain-dependent notch signaling turnover during neocortical development.
Article in The EMBO journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- LAMP2A-dependent chaperone mediated autophagy regulates Notch signaling and controls neural stem cell differentiation.Cellular and molecular life sciences : CMLS · 2026Article
- miR-151-5p regulates neural stem cell fate by targeting APH1A to modulate Notch signaling gradients.Stem cell reports · 2026Article
- N4BP1 acts as a potent negative regulator of IL-17 signaling by blocking the translation of Act1 mRNA.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- The human intelligence evolved from proximalQuantitative biology (Beijing, China) · 2025Article
- Posttranscriptional Control of Neural Progenitors Temporal Dynamics During Neocortical Development by Syncrip.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Enteroviral 3C protease cleaves N4BP1 to impair the host inflammatory response.Journal of virology · 2025Article
- N4BP1 mediates RAM domain-dependent notch signaling turnover during neocortical development.The EMBO journal · 2023Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Notch signaling pathway activity, particularly fluctuations in the biologically active effector fragment NICD, is required for rapid and efficient dynamic regulation of proper fate decisions in stem cells. In this study, we identified NEDD4-binding protein 1 (N4BP1), which is highly expressed in the developing mouse cerebral cortex, as a negative modulator of Notch signaling dynamics in neural progenitor cells. Intriguingly, N4BP1 regulated NICD stability specifically after Notch1 S3 cleavage through ubiquitin-mediated degradation that depended on its RAM domain, not its PEST domain, as had been extensively and previously described. The CoCUN domain in N4BP1, particularly the "Phe-Pro" motif (862/863 amino acid), was indispensable for mediating NICD degradation. The Ring family E3 ligase Trim21 was, in contrast to other NEDD4 family members, required for N4BP1-regulated NICD degradation. Overexpression of N4BP1 in cortical neural progenitors promoted neural stem cell differentiation, whereas neural progenitor cells lacking N4BP1 were sensitized to Notch signaling, resulting in the maintenance of stem-like properties in neural progenitor cells and lower production of cortical neurons.
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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.