ArticleJournal of dental research2013
The specific role of FAM20C in amelogenesis.
Article in Journal of dental research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
29 citing papers in PubMed, 32 citations in OpenAlex.
- Human Enamel Formation: A Scoping Review for Oral Health Professionals.Dentistry journal · 2026Review
- Mechanosensitive Piezo1 Channels in Enamel Cells.Calcified tissue international · 2026Article
- FAM20C: A key protein kinase in multiple diseases.Genes & diseases · 2025Review
- Gingival proteomics reveals the role of TGF beta and YAP/TAZ signaling in Raine syndrome fibrosis.Scientific reports · 2024Article
- FAM20A is a golgi-localized Type II transmembrane protein.Scientific reports · 2024Article
- Ablation of FAM20C caused short root defects via suppressing the BMP signaling pathway in mice.Journal of orofacial orthopedics = Fortschritte der Kieferorthopadie : Organ/official journal Deutsche Gesellschaft fur Kieferorthopadie · 2023Article
- Fam20C overexpression in odontoblasts regulates dentin formation and odontoblast differentiation.Journal of molecular histology · 2023Article
- The phosphorylation of serineMatrix biology : journal of the International Society for Matrix Biology · 2022Article
- Crucial Roles of microRNA-16-5p and microRNA-27b-3p in Ameloblast Differentiation Through Regulation of Genes Associated With Amelogenesis Imperfecta.Frontiers in genetics · 2022Article
- Proteolytic processing of secretory pathway kinase Fam20C by site-1 protease promotes biomineralization.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- FAM20C Overview: Classic and Novel Targets, Pathogenic Variants and Raine Syndrome Phenotypes.International journal of molecular sciences · 2021Review
- From biomineralization to tumorogenesis-the expanding insight of the physiological and pathological roles of Fam20C.Bioscience reports · 2021Article
- Two NovelGenes · 2020Article
- FAM20A is essential for amelogenesis, but is dispensable for dentinogenesis.Journal of molecular histology · 2019Article
- High-Phosphate Diet Improved the Skeletal Development of Fam20c-Deficient Mice.Cells, tissues, organs · 2019Article
- Abrogation of Fam20c altered cell behaviors and BMP signaling of immortalized dental mesenchymal cells.Experimental cell research · 2018Article
- The Importance of Serine Phosphorylation of Ameloblastin on Enamel Formation.Journal of dental research · 2016Article
- Inactivation of Fam20B in Joint Cartilage Leads to Chondrosarcoma and Postnatal Ossification Defects.Scientific reports · 2016Article
- FAM20A binds to and regulates FAM20C localization.Scientific reports · 2016Article
- Molecular Characterization of Three Canine Models of Human Rare Bone Diseases: Caffey, van den Ende-Gupta, and Raine Syndromes.PLoS genetics · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Previously, we showed that Sox2-Cre;Fam20C(fl/fl) mice in which Fam20C was ubiquitously inactivated had severe defects in dentin, enamel, and bone, along with hypophosphatemia. It remains to be determined if the enamel defects in the mice with universal inactivation of Family with sequence similarity 20-C (FAM20C) were associated with the dentin defects and whether hypophosphatemia in the knockout mice contributed to the enamel defects. In this study, we crossed Fam20C(fl/fl) mice with keratin 14-Cre (K14-Cre) transgenic mice to specifically inactivate Fam20C in the epithelial cells, including the dental epithelial cells that are responsible for forming tooth enamel. X-ray, backscattered scanning electron microscopic, and histological analyses showed that the K14-Cre;Fam20C(fl/fl) mice had severe enamel and ameloblast defects, while their dentin and alveolar bone were not significantly affected. Accordingly, serum biochemistry of the K14-Cre;Fam20C(fl/fl) mice showed normal phosphate and FGF23 levels in the circulation. Analysis of these data indicates that, while FAM20C is a molecule essential to amelogenesis, its inactivation in the dental epithelium does not significantly affect dentinogenesis. Hypophosphatemia makes no significant contribution to the enamel defects in the mice with the ubiquitous deletion of Fam20C.
Indexed as
Identifiers
What OpenQuestion holds
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.