Receptor for EDA isoform TAA, but not for EDA isoform TA-2 (By similarity). May mediate the activation of NF-kappa-B and JNK. May promote caspase-independent cell death. Binds to EDARADD. Associates with TRAF1, TRAF2, TRAF3 and NIK. Transcripts are not detectable in the branchial arch epithelium before morphological tooth formation (10 dpc), but are highly expressed during the initiation of tooth development (11 dpc). Starting 12 dpc, expression is high and limited to the budding cells, and remains high in the fully developed enamel knot at 14 dpc, whereas all other dental cells were completely negative. During 15 dpc the enamel knot disappears largely through apoptosis, and no transcripts were detected in the tooth germs of newborns. In skin, uniformly distributed in the basal cells of the epidermis before follicle initiation. Expression becomes focally elevated before placodes become distinguishable. By 17 dpc transcripts are almost exclusively confined to maturing follicles and the recently initiated placodes. By activin A in 12 dpc dental epithelium. Defects in Edar are a cause of the downless phenotype in mice (the equivalent of anhidrotic ectodermal dysplasia in humans). The disease is characterized by sparse hair (atrichosis or hypotrichosis), abnormal or missing teeth and the inability to sweat due to the absence of sweat glands.