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X-linked ectodysplasin-A2 receptor (XEDAR) is a recently isolated member of the tumor necrosis factor receptor family that is highly expressed during embryonic development and binds to ectodysplatin-A2 (EDA-A2). Two predominantly expressed isoforms, XEDAR-s and XEDAR-L, differ by only a 21-amino region at the juxtamembrane region of the cytoplasmic domain. Neither isoform possesses a death domain and both have been shown to act mainly through TRAF3 and TRAF6 to activate the NF-kappa-B and JNK pathways. Cells transfected with XEDAR and treated with EDA-A2 cause the assembly of a secondary complex containing FADD, caspase-8 and caspase-10, leading to the activation caspase-8 and caspase-3, and finally apoptosis. The EDA-A2-induced apoptosis is dependent on caspase-9 activation, as various pharmacological and genetic inhibitors of caspase-8 blocked apoptosis following EDA-A2 treatment.
9430060M22Rik; ectodysplasin A2 isoform receptor; ectodysplasin A2 receptor; EDA2R; EDA-A2 receptor; EDAA2R; EDA-A2R; RGD1564025; Tnfrsf27; Tumor necrosis factor receptor superfamily member 27; tumor necrosis factor receptor superfamily member XEDAR; UNQ2448/PRO5727/PRO34080; X linked ectodysplasin receptor; Xedar; X-linked ectodysplasin-A2 receptor
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