ArticleMolecular genetics & genomic medicine2019
The Enamel Phenotype in Homozygous Fam83h Truncation Mice.
Article in Molecular genetics & genomic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- Multiomics Data Synthesis of FAM83H in Amelogenesis Imperfecta.International dental journal · 2026Pooled it
- Pre-eruptive Coronal Resorptions as a Clinical Feature of FAM83H-Related Amelogenesis Imperfecta: Insights from Two Brazilian Families.Calcified tissue international · 2026Article
- Amelogenesis imperfecta in a Chinese family resulting from a FAM83H variation and the effect of FAM83H on the secretion of enamel matrix proteins.Clinical oral investigations · 2023Article
- CRISPR/Cas9-mediated deletion of Fam83h induces defective tooth mineralization and hair development in rabbits.Journal of cellular and molecular medicine · 2022Article
- Enamel defects in Acp4Scientific reports · 2022Article
- The phosphorylation of serineMatrix biology : journal of the International Society for Matrix Biology · 2022Article
- Identification of a NovelChildren (Basel, Switzerland) · 2022Article
- A RecurrentChildren (Basel, Switzerland) · 2022Article
- Mouse Dspp frameshift model of human dentinogenesis imperfecta.Scientific reports · 2021Article
- The gain-of-function FAM83H mutation caused hypocalcification amelogenesis imperfecta in a Chinese family.Clinical oral investigations · 2021Article
- Article
- Odontogenesis-associated phosphoprotein truncation blocks ameloblast transition into maturation in OdaphScientific reports · 2021Article
- Characterisation of the biochemical and cellular roles of native and pathogenic amelogenesis imperfecta mutants of FAM83H.Cellular signalling · 2020Article
- The Enamel Phenotype in Homozygous Fam83h Truncation Mice.Molecular genetics & genomic medicine · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
Abstract
backgroundTruncation FAM83H mutations cause human autosomal dominant hypocalcified amelogenesis imperfecta (ADHCAI), an inherited disorder characterized by severe hardness defects in dental enamel. No enamel defects were observed in Fam83h null mice suggesting that Fam83h truncation mice would better replicate human mutations.
methodsWe generated and characterized a mouse model (Fam83h
resultsDay 14 and 7-week Fam83h
conclusionsConsidering Fam83h
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.