ArticleThe Journal of biological chemistry2014
Generation and characterization of function-blocking anti-ectodysplasin A (EDA) monoclonal antibodies that induce ectodermal dysplasia.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Decoding sebaceous gland functions and diseases: insights from domestic animals.Veterinary research communications · 2026Review
- Unique and redundant roles of mouse BCMA, TACI, BAFF, APRIL, and IL-6 in supporting antibody-producing cells in different tissues.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- A Causal Treatment for X-Linked Hypohidrotic Ectodermal Dysplasia: Long-Term Results of Short-Term Perinatal Ectodysplasin A1 Replacement.International journal of molecular sciences · 2023Article
- Advances in tooth agenesis and tooth regeneration.Regenerative therapy · 2023Review
- Ectodysplasin A1 Deficiency Leads to Osteopetrosis-like Changes in Bones of the Skull Associated with Diminished Osteoclastic Activity.International journal of molecular sciences · 2022Article
- The EDA-deficient mouse has Zymbal's gland hypoplasia and acute otitis externa.Disease models & mechanisms · 2022Article
- Elevated EDAR signalling promotes mammary gland tumourigenesis with squamous metaplasia.Oncogene · 2022Article
- Article
- Anti-USAG-1 therapy for tooth regeneration through enhanced BMP signaling.Science advances · 2021Article
- Correction of Vertebral Bone Development in Ectodysplasin A1-Deficient Mice by Prenatal Treatment With a Replacement Protein.Frontiers in genetics · 2021Article
- EDA and EDAR expression at different stages of hair follicle development in cashmere goats and effects on expression of related genes.Archives animal breeding · 2020Article
- Role of ectodysplasin signalling in middle ear and nasal pathology in rat and mouse models of hypohidrotic ectodermal dysplasia.Disease models & mechanisms · 2019Article
- Article
- Modeling Edar expression reveals the hidden dynamics of tooth signaling center patterning.PLoS biology · 2019Article
- Conservation analysis and pathogenicity prediction of mutant genes of ectodysplasin a.BMC medical genetics · 2018Article
- A loop region of BAFF controls B cell survival and regulates recognition by different inhibitors.Nature communications · 2018Article
- Pharmacological stimulation of Edar signaling in the adult enhances sebaceous gland size and function.The Journal of investigative dermatology · 2015Article
- Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Development of ectodermal appendages, such as hair, teeth, sweat glands, sebaceous glands, and mammary glands, requires the action of the TNF family ligand ectodysplasin A (EDA). Mutations of the X-linked EDA gene cause reduction or absence of many ectodermal appendages and have been identified as a cause of ectodermal dysplasia in humans, mice, dogs, and cattle. We have generated blocking antibodies, raised in Eda-deficient mice, against the conserved, receptor-binding domain of EDA. These antibodies recognize epitopes overlapping the receptor-binding site and prevent EDA from binding and activating EDAR at close to stoichiometric ratios in in vitro binding and activity assays. The antibodies block EDA1 and EDA2 of both mammalian and avian origin and, in vivo, suppress the ability of recombinant Fc-EDA1 to rescue ectodermal dysplasia in Eda-deficient Tabby mice. Moreover, administration of EDA blocking antibodies to pregnant wild type mice induced in developing wild type fetuses a marked and permanent ectodermal dysplasia. These function-blocking anti-EDA antibodies with wide cross-species reactivity will enable study of the developmental and postdevelopmental roles of EDA in a variety of organisms and open the route to therapeutic intervention in conditions in which EDA may be implicated.
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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.