ArticleThe Journal of biological chemistry2009
Critical role of heparin binding domains of ameloblastin for dental epithelium cell adhesion and ameloblastoma proliferation.
Article in The Journal of biological chemistry, 2009. 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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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
34 citing papers in PubMed, 58 citations in OpenAlex.
- 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
- Homeobox Genes in Odontogenic Lesions: A Scoping Review.Head and neck pathology · 2023Article
- Coemergence of the Amphipathic Helix on Ameloblastin With Mammalian Prismatic Enamel.Molecular biology and evolution · 2022Article
- Article
- Potential Biomarkers and Signaling Pathways Associated with the Pathogenesis of Primary Ameloblastoma: A Systems Biology Approach.International journal of dentistry · 2022Article
- A narrative review of the roles of muscle segment homeobox transcription factor family in cancer.Annals of translational medicine · 2021Review
- New insight into dental epithelial stem cells: Identification, regulation, and function in tooth homeostasis and repair.World journal of stem cells · 2020Review
- An Evolutionarily Conserved Helix Mediates Ameloblastin-Cell Interaction.Journal of dental research · 2020Article
- Ameloblastin Binds to Phospholipid Bilayers via a Helix-Forming Motif within the Sequence Encoded by Exon 5.ACS omega · 2019Article
- Article
- Ameloblastin induces tumor suppressive phenotype and enhances chemosensitivity to doxorubicin via Src-Stat3 inactivation in osteosarcoma.Scientific reports · 2017Article
- Phosphorylation Modulates Ameloblastin Self-assembly and CaFrontiers in physiology · 2017Article
- Ameloblastin Peptides Modulates the Osteogenic Capacity of Human Mesenchymal Stem Cells.Frontiers in physiology · 2017Article
- Bioinformatics Analysis Reveals Genes Involved in the Pathogenesis of Ameloblastoma and Keratocystic Odontogenic Tumor.International journal of molecular and cellular medicine · 2016Article
- Bmp2 deletion causes an amelogenesis imperfecta phenotype via regulating enamel gene expression.Journal of cellular physiology · 2015Article
- Evolutionary analysis of selective constraints identifies ameloblastin (AMBN) as a potential candidate for amelogenesis imperfecta.BMC evolutionary biology · 2015Article
- Deletion of ameloblastin exon 6 is associated with amelogenesis imperfecta.Human molecular genetics · 2014Article
- MSX2 in ameloblast cell fate and activity.Frontiers in physiology · 2014Review
- Tracking endogenous amelogenin and ameloblastin in vivo.PloS one · 2014Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
AMBN (ameloblastin) is an enamel matrix protein that regulates cell adhesion, proliferation, and differentiation of ameloblasts. In AMBN-deficient mice, ameloblasts are detached from the enamel matrix, continue to proliferate, and form a multiple cell layer; often, odontogenic tumors develop in the maxilla with age. However, the mechanism of AMBN functions in these biological processes remains unclear. By using recombinant AMBN proteins, we found that AMBN had heparin binding domains at the C-terminal half and that these domains were critical for AMBN binding to dental epithelial cells. Overexpression of full-length AMBN protein inhibited proliferation of human ameloblastoma AM-1 cells, but overexpression of heparin binding domain-deficient AMBN protein had no inhibitory effect. In full-length AMBN-overexpressing AM-1 cells, the expression of Msx2, which is involved in the dental epithelial progenitor phenotype, was decreased, whereas the expression of cell proliferation inhibitors p21 and p27 was increased. We also found that the expression of enamelin, a marker of differentiated ameloblasts, was induced, suggesting that AMBN promotes odontogenic tumor differentiation. Thus, our results suggest that AMBN promotes cell binding through the heparin binding sites and plays an important role in preventing odontogenic tumor development by suppressing cell proliferation and maintaining differentiation phenotype through Msx2, p21, and p27.
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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.