ArticleiScience2024
Cullin-RING E3 ubiquitin ligase 4 regulates neurite morphogenesis during neurodevelopment.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Recessive variants in WSB2 encoding a substrate receptor of E3 ubiquitin ligase underlie a neurodevelopmental syndrome.European journal of human genetics : EJHG · 2026Article
- Neddylation regulates the development and function of glutamatergic neurons.Communications biology · 2025Article
- Cullin-RING Ubiquitin Ligases in Neurodevelopment and Neurodevelopmental Disorders.Biomedicines · 2025Review
- The Hao-Fountain syndrome protein USP7 regulates neuronal connectivity in the brain via a novel p53-independent ubiquitin signaling pathway.Cell reports · 2025Article
- Emerging roles for E3 ubiquitin ligases in neural development and disease.Frontiers in cell and developmental biology · 2025Review
- The X-linked intellectual disability gene CUL4B is critical for memory and synaptic function.Acta neuropathologica communications · 2024Article
- Antidepressant Effect of Enzymatic Porcine Placenta Hydrolysate in Repeated Immobilization Stress-Induced Ovariectomized Female Mice.Current issues in molecular biology · 2024Article
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Authors and funding
6 authors.
Funding
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Abstract
Neuritogenesis is crucial for establishing proper neuronal connections during brain development; its failure causes neurodevelopmental defects. Cullin-RING E3 ubiquitin ligase complexes participate in various neurodevelopmental processes by regulating protein stability. We demonstrated the regulatory function of Cullin-RING E3 ubiquitin ligase 4 (CRL4) in neurite morphogenesis during early neurodevelopment. Cul4a and Cul4b, the core scaffold proteins of CRL4, exhibit high expression and activation within the cytosol of developing neurons, regulated by neuronal stimulation through N-methyl D-aspartate (NMDA) receptor signaling. CRL4 also interacts with cytoskeleton-regulating proteins involved in neurite morphogenesis. Notably, genetic depletion and inhibition of cytosolic CRL4 enhance neurite extension and branching in developing neurons. Conversely, Cul4a overexpression suppresses basal and NMDA-enhanced neuritogenesis. Furthermore, CRL4 and its substrate adaptor regulate the polyubiquitination and proteasomal degradation of doublecortin protein. Collectively, our findings suggest that CRL4 ensures proper neurite morphogenesis in developing neurons by regulating cytoskeleton-regulating proteins.
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