ArticleScientific reports2016
TGF-β1 autocrine signalling and enamel matrix components.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 34 citations in OpenAlex.
- Integrative multi-omics and bioinformatic analysis ofThe Japanese dental science review · 2026Review
- Proteomic Signatures of Dental Enamel Hypomineralization: Divergent Molecular Pathways in Coal-Burning vs. Drinking-Water Fluorosis.Biological trace element research · 2026Article
- FAM20A Deficiency Drives Transcriptomic Dysregulation and Functional Impairment in Gingival Fibroblasts.Cell proliferation · 2026Article
- The Interplay of Immune Response and Dental Enamel Formation in Health and Sickness.Advances in experimental medicine and biology · 2026Review
- Roles of calcium in ameloblasts during tooth development: A scoping review.Journal of Taibah University Medical Sciences · 2025Review
- Article
- The role of the TGF-β1 signaling pathway in the process of amelogenesis.Frontiers in physiology · 2025Review
- TGF-β1/Smad3 Signaling Is Required to Alleviate Fluoride-Induced Enamel Hypomineralization.Biological trace element research · 2024Article
- Production of Proliferation- and Differentiation-Competent Porcine Myoblasts for Preclinical Studies in a Porcine Large Animal Model of Muscular Insufficiency.Life (Basel, Switzerland) · 2024Article
- The synergistic effects of TGF-β1 and RUNX2 on enamel mineralization through regulating ODAPH expression during the maturation stage.Journal of molecular histology · 2022Article
- Organoids from human tooth showing epithelial stemness phenotype and differentiation potential.Cellular and molecular life sciences : CMLS · 2022Article
- KLK4 Induces Anti-Tumor Effects in Human Xenograft Mouse Models of Orthotopic and Metastatic Prostate Cancer.Cancers · 2020Article
- Severity of oro-dental anomalies in Loeys-Dietz syndrome segregates by gene mutation.Journal of medical genetics · 2020Article
- Tooth Formation: Are the Hardest Tissues of Human Body Hard to Regenerate?International journal of molecular sciences · 2020Review
- Calcium Sets the Clock in Ameloblasts.Frontiers in physiology · 2020Article
- Amelogenic transcriptome profiling in ameloblast-like cells derived from adult gingival epithelial cells.Scientific reports · 2019Article
- The dynamics of TGF-β in dental pulp, odontoblasts and dentin.Scientific reports · 2018Article
- Differentiation of Human Amniotic Mesenchymal Stem Cells into Human Anterior Cruciate Ligament Fibroblast Cells by In Vitro Coculture.BioMed research international · 2017Article
- TGF-β and Physiological Root Resorption of Deciduous Teeth.International journal of molecular sciences · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor-β1 (TGF-β1) is present in porcine enamel extracts and is critical for proper mineralization of tooth enamel. Here, we show that the mRNA of latent TGF-β1 is expressed throughout amelogenesis. Latent TGF-β1 is activated by matrix metalloproteinase 20 (MMP20), coinciding with amelogenin processing by the same proteinase. Activated TGF-β1 binds to the major amelogenin cleavage products, particularly the neutral-soluble P103 amelogenin, to maintain its activity. The P103 amelogenin-TGF-β1 complex binds to TGFBR1 to induce TGF-β1 signalling. The P103 amelogenin-TGF-β1 complex is slowly cleaved by kallikrein 4 (KLK4), which is secreted into the transition- and maturation-stage enamel matrix, thereby reducing TGF-β1 activity. To exert the multiple biological functions of TGF-β1 for amelogenesis, we propose that TGF-β1 is activated or inactivated by MMP20 or KLK4 and that the amelogenin cleavage product is necessary for the in-solution mobility of TGF-β1, which is necessary for binding to its receptor on ameloblasts and retention of its activity.
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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.