ArticleExperimental & molecular medicine2025
Canonical Wnt signaling regulates Mbd3 protein stability during neurogenesis.
Article in Experimental & molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed.
- Bridging MBD3 functions in developmental biology and glioma heterogeneity to immune remodeling with future perspectives.Frontiers in immunology · 2026Review
- Regulation ofFrontiers in molecular neuroscience · 2026Article
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3 authors.
Funding
Abstract
Acquisition of neural progenitor cell (NPC) homeostasis through balancing self-renewal and differentiation is essential for brain development and function. Among the mechanisms controlling these processes, canonical Wnt signaling and the Mbd3-NuRD complex, with prominent suppressive effects on neurogenesis, have been described as crucial parts of the core regulatory circuit. Here we explored Mbd3 as a downstream element of the canonical Wnt signalosomes. Specifically, dynamic modulation of Wnt signaling through activator (Wnt3a) and inhibitor (DKK1) resulted in parallel alterations in β-catenin and Mbd3 expression patterns. Also, overexpression and depletion of GSK3β respectively promoted and attenuated Mbd3 ubiquitination, highlighting that the canonical Wnt cascade promotes Mbd3 stability. Downstream of the Wnt-β-catenin pathway, Mbd3 represses transcription of neurogenesis-associated genes by triggering NuRD complex assembly, thereby promoting NPC stemness. This new Wnt-Mbd3 axis extends the current understanding of the canonical Wnt network in directing neuronal cell-fate determination in NPCs, suggesting this pathway as a potential target for driving neural stem cell reprogramming and neuronal lineage commitment.
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Registered trials
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