ArticleThe Journal of biological chemistry2011
Molecular and therapeutic characterization of anti-ectodysplasin A receptor (EDAR) agonist monoclonal antibodies.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 35 citations in OpenAlex.
- Two mutations at KRT74 and EDAR synergistically drive the fine-wool production in Chinese sheep.Journal of advanced research · 2024Article
- Protein Interaction Analysis by Surface Plasmon Resonance.Methods in molecular biology (Clifton, N.J.) · 2023Article
- The Role of Ectodysplasin A on the Ocular Surface Homeostasis.International journal of molecular sciences · 2022Review
- 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
- Development of tooth regenerative medicine strategies by controlling the number of teeth using targeted molecular therapy.Inflammation and regeneration · 2020Review
- Role of ectodysplasin signalling in middle ear and nasal pathology in rat and mouse models of hypohidrotic ectodermal dysplasia.Disease models & mechanisms · 2019Article
- Article
- Small-molecule Wnt agonists correct cleft palates inDevelopment (Cambridge, England) · 2017Article
- Anti-EDAR Agonist Antibody Therapy Resolves Palate Defects in Pax9Journal of dental research · 2017Article
- Antibodies That Block or Activate Mouse B Cell Activating Factor of the Tumor Necrosis Factor (TNF) Family (BAFF), Respectively, Induce B Cell Depletion or B Cell Hyperplasia.The Journal of biological chemistry · 2016Article
- Ectodysplasin signalling deficiency in mouse models of hypohidrotic ectodermal dysplasia leads to middle ear and nasal pathology.Human molecular genetics · 2016Article
- Ectodysplasin A Pathway Contributes to Human and Murine Skin Repair.The Journal of investigative dermatology · 2016Article
- Article
- Pharmacological stimulation of Edar signaling in the adult enhances sebaceous gland size and function.The Journal of investigative dermatology · 2015Article
- Therapeutic blockade of LIGHT interaction with herpesvirus entry mediator and lymphotoxin β receptor attenuates in vivo cytotoxic allogeneic responses.Transplantation · 2014Article
- Generation and characterization of function-blocking anti-ectodysplasin A (EDA) monoclonal antibodies that induce ectodermal dysplasia.The Journal of biological chemistry · 2014Article
- Pharmacological activation of the EDA/EDAR signaling pathway restores salivary gland function following radiation-induced damage.PloS one · 2014Article
- Understanding cytokine and growth factor receptor activation mechanisms.Critical reviews in biochemistry and molecular biologyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
The TNF family ligand ectodysplasin A (EDA) and its receptor EDAR are required for proper development of skin appendages such as hair, teeth, and eccrine sweat glands. Loss of function mutations in the Eda gene cause X-linked hypohidrotic ectodermal dysplasia (XLHED), a condition that can be ameliorated in mice and dogs by timely administration of recombinant EDA. In this study, several agonist anti-EDAR monoclonal antibodies were generated that cross-react with the extracellular domains of human, dog, rat, mouse, and chicken EDAR. Their half-life in adult mice was about 11 days. They induced tail hair and sweat gland formation when administered to newborn EDA-deficient Tabby mice, with an EC(50) of 0.1 to 0.7 mg/kg. Divalency was necessary and sufficient for this therapeutic activity. Only some antibodies were also agonists in an in vitro surrogate activity assay based on the activation of the apoptotic Fas pathway. Activity in this assay correlated with small dissociation constants. When administered in utero in mice or at birth in dogs, agonist antibodies reverted several ectodermal dysplasia features, including tooth morphology. These antibodies are therefore predicted to efficiently trigger EDAR signaling in many vertebrate species and will be particularly suited for long term treatments.
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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.