ArticleScientific reports2015
IRF6 is the mediator of TGFβ3 during regulation of the epithelial mesenchymal transition and palatal fusion.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 52 citations in OpenAlex.
- Next-Generation Sequencing Data and Clinical Features in Patients with Cleft Palate and Tooth Agenesis: A Systematic Literature Review.Dentistry journal · 2026Review
- A Novel Nonsense Variant in TBX15 Transcription Factor Suggests an Expanded Genetic Spectrum Of Submucous Cleft Palate.International dental journal · 2026Article
- Non-Syndromic or Anomaly-Associated Genes (MYH3, GREM1, IRF6) and Their Proteins in Unilateral Right Cleft Tissue.International journal of molecular sciences · 2026Article
- IRF6 regulates adherens junction proteins and inflammatory cytokines in salivary acinar cells and its expression is elevated in Sjӧgren's syndrome.Archives of oral biology · 2025Article
- The developmental bases of cleft lip and cleft palate: cellular and molecular mechanisms.Anatomy & cell biology · 2025Review
- Proteomic-based stemness score measures oncogenic dedifferentiation and enables the identification of druggable targets.Cell genomics · 2025Article
- Molecular Regulation of Palatogenesis and Clefting: An Integrative Analysis of Genetic, Epigenetic Networks, and Environmental Interactions.International journal of molecular sciences · 2025Review
- TheFrontiers in medicine · 2025Review
- A novelFrontiers in genetics · 2024Article
- Case report and functional verification of a novel mutation in the interferon regulatory transcription factor 6 gene in a family with orofacial clefts.American journal of translational research · 2024Article
- Unraveling the Molecular Puzzle: Exploring Gene Networks across Diverse EMT Status of Cell Lines.International journal of molecular sciences · 2023Review
- Review
- Gene Regulatory Networks and Signaling Pathways in Palatogenesis and Cleft Palate: A Comprehensive Review.Cells · 2023Review
- MiRNA-470-5p suppresses epithelial-mesenchymal transition of embryonic palatal shelf epithelial cells by targetingExperimental biology and medicine (Maywood, N.J.) · 2023Article
- Revisiting the embryogenesis of lip and palate development.Oral diseases · 2022Review
- Consistent downregulation of the cleft lip/palate-associated genesFrontiers in oncology · 2022Article
- Identification of EMT signaling cross-talk and gene regulatory networks by single-cell RNA sequencing.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Expression Analysis ofBiology · 2021Article
- FACEts of mechanical regulation in the morphogenesis of craniofacial structures.International journal of oral science · 2021Review
- Lack of IRF6 Disrupts Human Epithelial Homeostasis by Altering Colony Morphology, Migration Pattern, and Differentiation Potential of Keratinocytes.Frontiers in cell and developmental biology · 2021Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutation in interferon regulatory factor 6 (IRF6) is known to cause syndromic and non-syndromic cleft lip/palate in human. In this study, we investigated the molecular mechanisms related to IRF6 during palatal fusion using palatal shelves organ culture. The results showed that ablation of Irf6 resulted in a delay in TGFβ3-regulated palatal fusion. Ectopic expression of IRF6 was able to promote palatal fusion and rescue shTgfβ3-induced fusion defect. These findings indicate that IRF6 is involved in TGFβ3-mediated palatal fusion. Molecular analysis revealed that ectopic expression of IRF6 increased the expression of SNAI2, an epithelial mesenchymal transition (EMT) regulator, and diminished the expression of various epithelial markers, such as E-cadherin, Plakophilin and ZO-1. In addition, knockdown of Irf6 expression decreased SNAI2 expression, and restored the expression of ZO-1 and Plakophilin that were diminished by TGFβ3. Blocking of Snai2 expression delayed palatal fusion and abolished the IRF6 rescuing effect associated with shTgfβ3-induced fusion defect. These findings indicate that TGFβ3 increases IRF6 expression and subsequently regulates SNAI2 expression, and IRF6 appears to regulate EMT during palatal fusion via SNAI2. Taken together, this study demonstrates that IRF6 is a mediator of TGFβ3, which regulates EMT and fusion process during the embryonic palate development.
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