ArticleMatrix biology : journal of the International Society for Matrix Biology2009
A mouse model expressing a truncated form of ameloblastin exhibits dental and junctional epithelium defects.
Article in Matrix biology : journal of the International Society for Matrix Biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 84 citations in OpenAlex.
- Ameloblastin amphipathic helix motif mediates ameloblast polarization and prismatic enamel formation.International journal of oral science · 2026Article
- Ameloblastin Amphipathic Helix Motif mediates Ameloblast Polarization and Prismatic Enamel Formation via a RhoA Signaling Pathway.Research square · 2026Article
- Ameloblastin binding to biomimetic models of cell membranes - A continuum of intrinsic disorder.Archives of oral biology · 2025Article
- Deletion within ameloblastin multitargeting domain reduces its interaction with artificial cell membrane.Journal of structural biology · 2024Article
- Ameloblastin and its multifunctionality in amelogenesis: A review.Matrix biology : journal of the International Society for Matrix Biology · 2024Review
- Ganoin and acrodin formation on scales and teeth in spotted gar: A vital role of enamelin in the unique process of enamel mineralization.Journal of experimental zoology. Part B, Molecular and developmental evolution · 2023Article
- The Dynamic Interactions of a Multitargeting Domain in Ameloblastin Protein with Amelogenin and Membrane.International journal of molecular sciences · 2023Article
- Enamel Structure Defects inBiomedicines · 2023Article
- Revisiting ameloblastin; addressing the EMT-ECM axis above and beyond oral biology.Frontiers in cell and developmental biology · 2023Article
- Loss of BMP2 and BMP4 Signaling in the Dental Epithelium Causes Defective Enamel Maturation and Aberrant Development of Ameloblasts.International journal of molecular sciences · 2022Article
- Ameloblastin promotes polarization of ameloblast cell lines in a 3-D cell culture system.Matrix biology : journal of the International Society for Matrix Biology · 2022Article
- Adenovirus-Mediated LAMA3 Transduction Enhances Hemidesmosome Formation and Periodontal Reattachment during Wound Healing.Molecular therapy. Methods & clinical development · 2020Article
- An Evolutionarily Conserved Helix Mediates Ameloblastin-Cell Interaction.Journal of dental research · 2020Article
- Co-Immunoprecipitation Reveals Interactions Between Amelogenin and AmeloblastinFrontiers in physiology · 2020Article
- ENAM mutations and digenic inheritance.Molecular genetics & genomic medicine · 2019Article
- AMBN mutations causing hypoplastic amelogenesis imperfecta and Ambn knockout-NLS-lacZ knockin mice exhibiting failed amelogenesis and Ambn tissue-specificity.Molecular genetics & genomic medicine · 2019Article
- Ameloblastin Binds to Phospholipid Bilayers via a Helix-Forming Motif within the Sequence Encoded by Exon 5.ACS omega · 2019Article
- Peptide coatings enhance keratinocyte attachment towards improving the peri-implant mucosal seal.Biomaterials science · 2018Article
- DENTAL ENAMEL FORMATION AND IMPLICATIONS FOR ORAL HEALTH AND DISEASE.Physiological reviews · 2017Review
- Intrinsically disordered proteins drive enamel formation via an evolutionarily conserved self-assembly motif.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Ameloblastin (AMBN) is the second most abundant extracellular matrix protein produced by the epithelial cells called ameloblasts and is found mainly in forming dental enamel. Inactivation of its expression by gene knockout results in absence of the enamel layer and its replacement by a thin layer of dysplastic mineralized matrix. The objective of this study was to further characterize the enamel organ and mineralized matrix produced in the AMBN knockout mouse. However, in the course of our study, we unexpectedly found that this mouse is in fact a mutant that does not express the full-length protein but that produces a truncated form of AMBN. Mandibles from wild type and mutant mice were processed for morphological analyses and immunolabeling. Microdissected enamel organs and associated matrix were also prepared for molecular and biochemical analyses. In incisors from mutants, ameloblasts lost their polarized organization and the enamel organ detached from the tooth surface and became disorganized. A thin layer of dysplastic mineralized material was deposited onto dentin, and mineralized masses were present within the enamel organ. These mineralized materials generated lower backscattered electron contrast than normal enamel, and immunocytochemistry with colloidal gold revealed the presence of amelogenin, bone sialoprotein and osteopontin. In addition, the height of the alveolar bone was reduced, and the junctional epithelium lost its integrity. Immunochemical and RT-PCR results revealed that the altered enamel organ in the mutant mice produced a shorter AMBN protein that is translated from truncated RNA missing exons 5 and 6. These results indicate that absence of full-length protein and/or expression of an incomplete protein have direct/indirect effects beyond structuring of mineral during enamel formation, and highlight potential functional regions on the AMBN molecule.
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