ArticleStem cell reports2023
Mowat-Wilson syndrome factor ZEB2 controls early formation of human neural crest through BMP signaling modulation.
Article in Stem cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Craniofacial development: genetics, signaling pathways, teratogenic mechanisms, and clinal significance.Molecular biomedicine · 2026Review
- TGFβ signaling is required during human and chick Neural Crest formation.Developmental biology · 2026Article
- Whole Genome Sequencing Reveals amedRxiv : the preprint server for health sciences · 2026Article
- Enrichment of Neural Crest Cells by Antibody Labeling and Flow Cytometry for Single-Cell Transcriptomics in a Lizard.Evolution & development · 2026Article
- Transcription factor ZEB2 is essential for ureteral smooth muscle cell differentiation.PLoS genetics · 2026Article
- Epithelial-to-mesenchymal transition transcription factors: New strategies for mesenchymal tissue regeneration.Cytokine & growth factor reviews · 2025Review
- Mesenchymal stem cells derived from hPSC via neural crest attenuate chemotherapy-induced premature ovarian insufficiency by ameliorating apoptosis and oxidative stress in granulosa cells.Stem cell research & therapy · 2025Article
- TheFrontiers in medicine · 2025Review
- Clinical and Genetic Correlation in Neurocristopathies: Bridging a Precision Medicine Gap.Journal of clinical medicine · 2024Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Mowat-Wilson syndrome is caused by mutations in ZEB2, with patients exhibiting characteristics indicative of neural crest (NC) defects. We examined the contribution of ZEB2 to human NC formation using a model based on human embryonic stem cells. We found ZEB2 to be one of the earliest factors expressed in prospective human NC, and knockdown revealed a role for ZEB2 in establishing the NC state while repressing pre-placodal and non-neural ectoderm genes. Examination of ZEB2 N-terminal mutant NC cells demonstrates its requirement for the repression of enhancers in the NC gene network and proper NC cell terminal differentiation into osteoblasts and peripheral neurons and neuroglia. This ZEB2 mutation causes early misexpression of BMP signaling ligands, which can be rescued by the attenuation of BMP. Our findings suggest that ZEB2 regulates early human NC specification by modulating proper BMP signaling and further elaborate the molecular defects underlying Mowat-Wilson syndrome.
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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 Socratic graph.