Recombinant Human EDAR

Ectodysplasin A receptor (EDAR), also known as ED1R, is a cell surface receptor of the tumor necrosis factor receptor (TNFR) family. Defects in EDAR are a cause of hypohidrotic ectodermal dysplasia (HED).¹ It is characterized by abnormalities in the hair, teeth and sweat glands. EDAR is also the genetic determinant of hair fiber thickness variation among Asian populations.² EDA has two splice variants, EDA-A1 and EDA-A2, which differ by only two amino acids. Despite this minor difference, EDAR only binds to EDA-A1, whereas EDA-A2 binds to XEDAR. It mediates the activation of NF-κB and JNK and may promote caspase independent cell death.³