ArticlePloS one2015
Transcriptional factor DLX3 promotes the gene expression of enamel matrix proteins during amelogenesis.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 39 citations in OpenAlex.
- Soluble Notch agonist enables human ameloblast maturation and enamel-like tissue formation for tooth regeneration.International journal of oral science · 2026Article
- Genetic and environmental determinants of dental fluorosis: a case‒control study of DLX3, ESR1, and ESR2 variants in a high-fluoride region of Mexico.BMC oral health · 2025Article
- The circadian clock in enamel development.International journal of oral science · 2024Review
- MAST4 regulates stem cell maintenance with DLX3 for epithelial development and amelogenesis.Experimental & molecular medicine · 2024Article
- Enam expression is regulated by Msx2.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Article
- Effects of Early Life Adversity on Tooth Enamel Formation.Frontiers in dental medicine · 2022Article
- MutantPeerJ · 2020Article
- Store-operated CaJCI insight · 2017Article
- Tricho-dento-osseous syndrome and precocious eruption.Journal of clinical and experimental dentistry · 2017Article
- DLX3-Dependent Regulation of Ion Transporters and Carbonic Anhydrases is Crucial for Enamel Mineralization.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2017Article
- Amelogenesis Imperfecta; Genes, Proteins, and Pathways.Frontiers in physiology · 2017Review
- Distribution of Cathepsin K in Late Stage of Tooth Germ Development and Its Function in Degrading Enamel Matrix Proteins in Mouse.PloS one · 2017Article
- An Nfic-hedgehog signaling cascade regulates tooth root development.Development (Cambridge, England) · 2015Article
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Authors and funding
8 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Mutation of distal-less homeobox 3 (DLX3) is responsible for human tricho-dento-osseous syndrome (TDO) with amelogenesis imperfecta, indicating a crucial role of DLX3 in amelogenesis. However, the expression pattern of DLX3 and its specific function in amelogenesis remain largely unknown. The aim of this study was to investigate the effects of DLX3 on enamel matrix protein (EMP) genes. By immunohistochemistry assays of mouse tooth germs, stronger immunostaining of DLX3 protein was identified in ameloblasts in the secretory stage than in the pre-secretory and maturation stages, and the same pattern was found for Dlx3 mRNA using Realtime PCR. In a mouse ameloblast cell lineage, forced expression of DLX3 up-regulated the expression of the EMP genes Amelx, Enam, Klk4, and Odam, whereas knockdown of DLX3 down-regulated these four EMP genes. Further, bioinformatics, chromatin immunoprecipitation, and luciferase assays revealed that DLX3 transactivated Enam, Amelx, and Odam through direct binding to their enhancer regions. Particularly, over-expression of mutant-DLX3 (c.571_574delGGGG, responsible for TDO) inhibited the activation function of DLX3 on expression levels and promoter activities of the Enam, Amelx, and Odam genes. Together, our data show that DLX3 promotes the expression of the EMP genes Amelx, Enam, Klk4, and Odam in amelogenesis, while mutant-DLX3 disrupts this regulatory function, thus providing insights into the molecular mechanisms underlying the enamel defects of TDO disease.
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