ArticlePloS one2016
RETRACTED: Functional Study of Ectodysplasin-A Mutations Causing Non-Syndromic Tooth Agenesis.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers.
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
15 citing papers in PubMed, 24 citations in OpenAlex.
- Ectodysplasin-A (EDA) Signaling Cross-Talk in Skeletogenesis.Calcified tissue international · 2026Review
- Retraction: Functional Study of Ectodysplasin-A Mutations Causing Non-Syndromic Tooth Agenesis.PloS one · 2026Article
- EDA1 variants inhibit the odontogenic differentiation and proliferation of human dental pulp stem cells.BMC oral health · 2025Article
- Transcriptome analysis identifies EDA1 variants disrupt FOSB-mediated regulation of odontogenic epithelial cell behaviors during dental germ development.Frontiers in cell and developmental biology · 2025Article
- Genotype-phenotype analysis and functional study of three novelFrontiers in genetics · 2025Article
- A novel mutation in the collagen domain of EDA results in hypohidrotic ectodermal dysplasia by impacting the receptor-binding capability.Molecular genetics & genomic medicine · 2023Article
- The EDA/EDAR/NF-κB pathway in non-syndromic tooth agenesis: A genetic perspective.Frontiers in genetics · 2023Review
- Analyses of oligodontia phenotypes and genetic etiologies.International journal of oral science · 2021Article
- Article
- A novel EDAR missense mutation identified by whole-exome sequencing with non-syndromic tooth agenesis in a Chinese family.Molecular genetics & genomic medicine · 2021Article
- Article
- Tooth Regeneration: Insights from Tooth Development and Spatial-Temporal Control of Bioactive Drug Release.Stem cell reviews and reports · 2020Review
- Genetic diagnosis for X-linked hypohidrotic ectodermal dysplasia family with a novel Ectodysplasin A gene mutation.Journal of clinical laboratory analysis · 2018Article
- Review
- Mutations in TSPEAR, Encoding a Regulator of Notch Signaling, Affect Tooth and Hair Follicle Morphogenesis.PLoS genetics · 2016Article
Corrections and comments
- Retraction · 2026-06-17Concerns/Issues about Image · Duplication of/in Image · Euphemisms for Duplication · Investigation by Journal/Publisher · Objections by Author(s) · Unreliable Results and/or Conclusions · · See also: https://pubpeer.com/publications/3134149866F26FAC14938D2D7C38B9
- Retracted
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have demonstrated that ectodysplasin-A (EDA) mutations are associated with non-syndromic tooth agenesis. Indeed, we were the first to report three novel EDA mutations (A259E, R289C and R334H) in sporadic non-syndromic tooth agenesis. We studied the mechanism linking EDA mutations and non-syndromic tooth agenesis in human embryonic kidney 293T cells and mouse ameloblast-derived LS8 cells transfected with mutant isoforms of EDA. The receptor binding capability of the mutant EDA1 protein was impaired in comparison to wild-type EDA1. Although the non-syndromic tooth agenesis-causing EDA1 mutants possessed residual binding capability, the transcriptional activation of the receptor's downstream target, nuclear factor κB (NF-κB), was compromised. We also analyzed the changes of selected genes in other signaling pathways, such as WNT and BMP, after EDA mutation. We found that non-syndromic tooth agenesis-causing EDA1 mutant proteins upregulate BMP4 (bone morphogenetic protein 4) mRNA expression and downregulate WNT10A and WNT10B (wingless-type MMTV integration site family member 10A and 10B) mRNA expression. Our results indicated that non-syndromic tooth agenesis causing EDA mutations (A259E, R289C and R334H) were loss-of-function, and suggested that EDA may regulate the expression of WNT10A, WNT10B and BMP4 via NF-κB during tooth development. The results from our study may help to understand the molecular mechanism linking specific EDA mutations with non-syndromic tooth agenesis.
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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.