ReviewCells2019
Update on the Role of the Non-Canonical Wnt/Planar Cell Polarity Pathway in Neural Tube Defects.
Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed.
- Unravelıng non-canonıcal Wnt sıgnalıng ın neural development and dısorders: a revıew of Wnt/PCP and Wnt/caMolecular biology reports · 2026Review
- Quantitative live imaging reveals PRICKLE1 controls junctional neural tube morphogenesis independent of Planar Cell Polarity.Nature communications · 2026Article
- Discovering the unexpected: Insights into the dynamics of mouse neural tube closure revealed by time-lapse imaging.Developmental biology · 2026Review
- Loss of KDM5A-mediated H3K4me3 demethylation promotes aberrant neural development by Wnt/β-catenin pathway activation.Cell death & disease · 2025Article
- Epigenetic dysregulation and the etiology of spina bifida.Neurochemistry international · 2025Review
- Mechanobiological engineering strategies for organoid culture.APL bioengineering · 2025Review
- Epithelial polarization by the planar cell polarity complex is exclusively non-cell autonomous.Science (New York, N.Y.) · 2025Article
- Inferring active and passive mechanical drivers of epithelial convergent extension.bioRxiv : the preprint server for biology · 2025Article
- Small Extracellular Vesicles Promote Axon Outgrowth by Engaging the Wnt-Planar Cell Polarity Pathway.Cells · 2025Article
- A computational dynamic systems model forCurrent research in toxicology · 2025Article
- Integrative Analysis of Key Signalling Pathways in Neural Tube Defects: From Molecular Mechanisms to Therapeutic Strategies.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2025Review
- Preconceptional and Periconceptional Folic Acid Supplementation in the Visegrad Group Countries for the Prevention of Neural Tube Defects.Nutrients · 2024Review
- Planar cell polarity zebrafish models of congenital scoliosis reveal underlying defects in notochord morphogenesis.Development (Cambridge, England) · 2024Article
- Mitochondrial metabolism in neural stem cells and implications for neurodevelopmental and neurodegenerative diseases.Journal of translational medicine · 2024Review
- Monitoring the Mechanical Evolution of Tissue During Neural Tube Closure of Chick Embryo.Journal of visualized experiments : JoVE · 2023Article
- TMEM132A regulates mouse hindgut morphogenesis and caudal development.Development (Cambridge, England) · 2023Article
- A Van Gogh/Vangl tyrosine phosphorylation switch regulates its interaction with core Planar Cell Polarity factors Prickle and Dishevelled.PLoS genetics · 2023Article
- Genetic mutations in ribosomal biogenesis gene TCOF1 identified in human neural tube defects.Molecular genetics & genomic medicine · 2023Article
- Functional interaction between Vangl2 and N-cadherin regulates planar cell polarization of the developing neural tube and cochlear sensory epithelium.Scientific reports · 2023Article
- Deficiency ofFrontiers in cell and developmental biology · 2023Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neural tube defects (NTDs), including spina bifida and anencephaly, represent the most severe and common malformations of the central nervous system affecting 0.7-3 per 1000 live births. They result from the failure of neural tube closure during the first few weeks of pregnancy. They have a complex etiology that implicate a large number of genetic and environmental factors that remain largely undetermined. Extensive studies in vertebrate models have strongly implicated the non-canonical Wnt/planar cell polarity (PCP) signaling pathway in the pathogenesis of NTDs. The defects in this pathway lead to a defective convergent extension that is a major morphogenetic process essential for neural tube elongation and subsequent closure. A large number of genetic studies in human NTDs have demonstrated an important role of PCP signaling in their etiology. However, the relative contribution of this pathway to this complex etiology awaits a better picture of the complete genetic architecture of these defects. The emergence of new genome technologies and bioinformatics pipelines, complemented with the powerful tool of animal models for variant interpretation as well as significant collaborative efforts, will help to dissect the complex genetics of NTDs. The ultimate goal is to develop better preventive and counseling strategies for families affected by these devastating conditions.
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