ArticleNature communications2023
Structural insights into pathogenic mechanism of hypohidrotic ectodermal dysplasia caused by ectodysplasin A variants.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- A growth-adjusted digital prosthetic protocol for a child with X-linked hypohidrotic ectodermal dysplasia: a 5-year longitudinal clinical report.BMC oral health · 2026Article
- Racial and Ethnic Disparities in Persistent Chemotherapy-Induced Alopecia Among Women With Breast Cancer.JAMA network open · 2026Article
- Article
- The Roles of EDA2R in Ageing and Disease.Aging cell · 2025Review
- A novel EDA variant that causes X-linked hypohidrotic ectodermal dysplasia in a Chinese family.BMC pregnancy and childbirth · 2025Article
- FOXO4-SP6 axis controls surface epithelium commitment by mediating epigenomic remodeling.Stem cell reports · 2025Article
- Dental Implant Rehabilitation in Patients Carrying WNT10A Mutations With Different Molecular Statuses and Phenotypes: A Retrospective Cohort Study.Clinical oral implants research · 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
- Retinoic acid drives surface epithelium fate determination through the TCF7-MSX2 axis.Cellular and molecular life sciences : CMLS · 2024Article
- Article
- Critical Considerations in Calling Disease-CausingJournal of clinical medicine · 2024Article
- Skin Development and Disease: A Molecular Perspective.Current issues in molecular biology · 2024Review
- Spatial and Temporal Expression of Ectodysplasin-A Signaling Pathway Members During Mandibular Condylar Development in Postnatal Mice.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2023Article
- The EDA/EDAR/NF-κB pathway in non-syndromic tooth agenesis: A genetic perspective.Frontiers in genetics · 2023Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
EDA is a tumor necrosis factor (TNF) family member, which functions together with its cognate receptor EDAR during ectodermal organ development. Mutations of EDA have long been known to cause X-linked hypohidrotic dysplasia in humans characterized by primary defects in teeth, hair and sweat glands. However, the structural information of EDA interaction with EDAR is lacking and the pathogenic mechanism of EDA variants is poorly understood. Here, we report the crystal structure of EDA C-terminal TNF homology domain bound to the N-terminal cysteine-rich domains of EDAR. Together with biochemical, cellular and mouse genetic studies, we show that different EDA mutations lead to varying degrees of ectodermal developmental defects in mice, which is consistent with the clinical observations on human patients. Our work extends the understanding of the EDA signaling mechanism, and provides important insights into the molecular pathogenesis of disease-causing EDA variants.
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