ArticlePloS one2012
Targeted overexpression of amelotin disrupts the microstructure of dental enamel.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 67 citations in OpenAlex.
- A novelFrontiers in physiology · 2026Article
- Conditioned medium from cultured cementoblasts upregulates amelotin gene expression via the SOCS3 signaling pathway.Journal of periodontal & implant science · 2025Article
- Functions of secretory calcium-binding phosphoproteins in dental mineralization.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2025Review
- The Rogdi knockout mouse is a model for Kohlschütter-Tönz syndrome.Scientific reports · 2024Article
- Odontogenesis-Associated Phosphoprotein (ODAPH) Overexpression in Ameloblasts Disrupts Enamel Formation via Inducing Abnormal Mineralization of Enamel in Secretory Stage.Calcified tissue international · 2022Article
- Coemergence of the Amphipathic Helix on Ameloblastin With Mammalian Prismatic Enamel.Molecular biology and evolution · 2022Article
- Amelotin Promotes Mineralization and Adhesion in Collagen-Based Systems.Cellular and molecular bioengineering · 2022Article
- Promoting mineralization at biological interfacesMaterials today. Bio · 2022Article
- Uniaxial Hydroxyapatite Growth on a Self-Assembled Protein Scaffold.International journal of molecular sciences · 2021Article
- Discovery of novel molecular characteristics and cellular biological properties in ameloblastoma.Cancer medicine · 2020Article
- Amelogenin phosphorylation regulates tooth enamel formation by stabilizing a transient amorphous mineral precursor.The Journal of biological chemistry · 2020Article
- Article
- Co-Immunoprecipitation Reveals Interactions Between Amelogenin and AmeloblastinFrontiers in physiology · 2020Article
- Canine models of human amelogenesis imperfecta: identification of novel recessive ENAM and ACP4 variants.Human genetics · 2019Article
- C/EBPβ and YY1 bind and interact with Smad3 to modulate lipopolysaccharide-induced amelotin gene transcription in mouse gingival epithelial cells.FEBS open bio · 2019Article
- Transcriptional regulation of human amelotin gene by interleukin-1β.FEBS open bio · 2018Article
- Tumor necrosis factor-α stimulates human amelotin gene transcription in gingival epithelial cells.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Article
- Article
- MiR-153 Regulates Amelogenesis by Targeting Endocytotic and Endosomal/lysosomal Pathways-Novel Insight into the Origins of Enamel Pathologies.Scientific reports · 2017Article
- Amelogenesis Imperfecta; Genes, Proteins, and Pathways.Frontiers in physiology · 2017Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
We have previously identified amelotin (AMTN) as a novel protein expressed predominantly during the late stages of dental enamel formation, but its role during amelogenesis remains to be determined. In this study we generated transgenic mice that produce AMTN under the amelogenin (Amel) gene promoter to study the effect of AMTN overexpression on enamel formation in vivo. The specific overexpression of AMTN in secretory stage ameloblasts was confirmed by Western blot and immunohistochemistry. The gross histological appearance of ameloblasts or supporting cellular structures as well as the expression of the enamel proteins amelogenin (AMEL) and ameloblastin (AMBN) was not altered by AMTN overexpression, suggesting that protein production, processing and secretion occurred normally in transgenic mice. The expression of Odontogenic, Ameloblast-Associated (ODAM) was slightly increased in secretory stage ameloblasts of transgenic animals. The enamel in AMTN-overexpressing mice was much thinner and displayed a highly irregular surface structure compared to wild type littermates. Teeth of transgenic animals underwent rapid attrition due to the brittleness of the enamel layer. The microstructure of enamel, normally a highly ordered arrangement of hydroxyapatite crystals, was completely disorganized. Tomes' process, the hallmark of secretory stage ameloblasts, did not form in transgenic mice. Collectively our data demonstrate that the overexpression of amelotin has a profound effect on enamel structure by disrupting the formation of Tomes' process and the orderly growth of enamel prisms.
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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.