ArticleJournal of dental research2017
Modulating Wnt Signaling Rescues Palate Morphogenesis in Pax9 Mutant Mice.
Article in Journal of dental research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
What it found
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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
39 citing papers in PubMed, 64 citations in OpenAlex.
- Toward Understanding the Role of miRNAs in Cleft Palate Only: Observations from Patient Tissues and In Vitro Assays.International journal of molecular sciences · 2026Article
- Persistent Wnt/β-catenin signaling disables soft palatogenesis and palatal osteogenesis by inducing mesenchymal condensation.Frontiers in cell and developmental biology · 2026Article
- Dissecting the Genetic Contribution of Tooth Agenesis.International journal of molecular sciences · 2025Review
- Single cell spatial transcriptomics links Wnt signaling disruption to extracellular matrix development in a cleft palate model.Scientific reports · 2025Article
- Molecular Regulation of Palatogenesis and Clefting: An Integrative Analysis of Genetic, Epigenetic Networks, and Environmental Interactions.International journal of molecular sciences · 2025Review
- Spatial Multi-omics Reveals the Role of the Wnt Modulator, Dkk2, in Palatogenesis'.Journal of dental research · 2024Article
- The presence and distribution of various genes in postnatal CLP-affected palatine tissue.Maxillofacial plastic and reconstructive surgery · 2024Article
- Multimodal spatiotemporal transcriptomic resolution of embryonic palate osteogenesis.Nature communications · 2023Article
- Gene Regulatory Networks and Signaling Pathways in Palatogenesis and Cleft Palate: A Comprehensive Review.Cells · 2023Review
- PAX9 mutations and genetic synergism in familial tooth agenesis.Annals of the New York Academy of Sciences · 2023Article
- Integrated spatiotemporal transcriptomic resolution of embryonic palate osteogenesis.bioRxiv : the preprint server for biology · 2023Article
- Advances in tooth agenesis and tooth regeneration.Regenerative therapy · 2023Review
- Successful therapeutic intervention in new mouse models of frizzled 2-associated congenital malformations.Development (Cambridge, England) · 2023Article
- Article
- MSX1 Drives Tooth Morphogenesis Through Controlling Wnt Signaling Activity.Journal of dental research · 2022Article
- Revisiting the embryogenesis of lip and palate development.Oral diseases · 2022Review
- SATB2: A versatile transcriptional regulator of craniofacial and skeleton development, neurogenesis and tumorigenesis, and its applications in regenerative medicine.Genes & diseases · 2022Review
- In-frame deletion of SPECC1L microtubule association domain results in gain-of-function phenotypes affecting embryonic tissue movement and fusion events.Human molecular genetics · 2021Article
- Article
- 3D facial phenotyping by biometric sibling matching used in contemporary genomic methodologies.PLoS genetics · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Cleft palate is a common birth defect caused by disruption of palatogenesis during embryonic development. Although mutations disrupting components of the Wnt signaling pathway have been associated with cleft lip and palate in humans and mice, the mechanisms involving canonical Wnt signaling and its regulation in secondary palate development are not well understood. Here, we report that canonical Wnt signaling plays an important role in Pax9-mediated regulation of secondary palate development. We found that cleft palate pathogenesis in Pax9-deficient embryos is accompanied by significantly reduced expression of Axin2, an endogenous target of canonical Wnt signaling, in the developing palatal mesenchyme, particularly in the posterior regions of the palatal shelves. We found that expression of Dkk2, encoding a secreted Wnt antagonist, is significantly increased whereas the levels of active β-catenin protein, the essential transcriptional coactivator of canonical Wnt signaling, is significantly decreased in the posterior regions of the palatal shelves in embryonic day 13.5 Pax9-deficent embryos in comparison with control littermates. We show that small molecule-mediated inhibition of Dickkopf (DKK) activity in utero during palatal shelf morphogenesis partly rescued secondary palate development in Pax9-deficient embryos. Moreover, we found that genetic inactivation of Wise, which is expressed in the developing palatal shelves and encodes another secreted antagonist of canonical Wnt signaling, also rescued palate morphogenesis in Pax9-deficient mice. Furthermore, whereas Pax9
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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.