ArticleEuropean journal of oral sciences2015
Inactivation of Fam20B in the dental epithelium of mice leads to supernumerary incisors.
Article in European journal of oral sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed.
- The phenotypic characterization of mouse floxedRegenerative therapy · 2025Article
- Recent Advances in Enzymes and Chemoenzymatic Synthesis of Tetrasaccharide Linkage Region of Proteoglycans.Chembiochem : a European journal of chemical biology · 2025Review
- FAM20B-Catalyzed Glycosylation Regulates the Chondrogenic and Osteogenic Differentiation of the Embryonic Condyle by Controlling IHH Diffusion and Release.International journal of molecular sciences · 2025Article
- Imaging analysis of 1 138 supernumerary teeth by using cone-beam computed tomography.Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2023Article
- Deficiency ofInternational journal of molecular sciences · 2023Article
- Tooth number abnormality: from bench to bedside.International journal of oral science · 2023Review
- An in situ hybridization study of syndecan family during the late stages of developing mouse molar tooth germ.Anatomical science international · 2022Article
- Analysis of the distribution of supernumerary teeth and the characteristics of mesiodens in Bengbu, China: a retrospective study.Oral radiology · 2021Article
- Chondrodysplasias With Multiple Dislocations Caused by Defects in Glycosaminoglycan Synthesis.Frontiers in genetics · 2021Review
- FAM20B-catalyzed glycosaminoglycans control murine tooth number by restricting FGFR2b signaling.BMC biology · 2020Article
- The spatiotemporal expression pattern of Syndecans in murine embryonic teeth.Gene expression patterns : GEP · 2020Article
- Article
- Inactivation of FAM20B causes cell fate changes in annulus fibrosus of mouse intervertebral disc and disc defects via the alterations of TGF-β and MAPK signaling pathways.Biochimica et biophysica acta. Molecular basis of disease · 2019Article
- Thinking outside of the cell: Secreted protein kinases in bacteria, parasites, and mammals.IUBMB life · 2019Review
- Lack of association between PAX6/SOSTDC1/FAM20B gene polymorphisms and mesiodens.BMC oral health · 2019Article
- Inactivation of Fam20b in the neural crest-derived mesenchyme of mouse causes multiple craniofacial defects.European journal of oral sciences · 2018Article
- Structure and evolution of the Fam20 kinases.Nature communications · 2018Article
- The importance of a potential phosphorylation site in enamelin on enamel formation.International journal of oral science · 2017Article
- The epidemiology of supernumerary teeth and the associated molecular mechanism.Organogenesis · 2017Review
- Inactivation of Fam20B in Joint Cartilage Leads to Chondrosarcoma and Postnatal Ossification Defects.Scientific reports · 2016Article
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9 authors.
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Abstract
Tooth formation is tightly regulated by epithelial-mesenchymal interactions via hierarchic cascades of signaling molecules. The glycosaminoglycan (GAG) chains covalently attached to the core protein of proteoglycans (PGs) provide docking sites for signaling molecules and their receptors during the morphogenesis of tissues and organs. Although PGs are believed to play important roles in tooth formation, little is known about their exact functions in this developmental process and the relevant molecular basis. Family with sequence similarity member 20-B (FAM20B) is a newly identified kinase that phosphorylates the xylose in the common linkage region connecting the GAG with the protein core of PGs. The phosphorylation of xylose is essential for elongation of the common linkage region and the subsequent GAG assembly. In this study, we generated a Fam20B-floxed allele in mice and found that inactivating Fam20B in the dental epithelium leads to supernumerary maxillary and mandibular incisors. This finding highlights the pivotal role of PGs in tooth morphogenesis and opens a new window for understanding the regulatory mechanism of PG-mediated signaling cascades during tooth formation.
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