|Application ||WB, IHC-P, E|
|Other Accession||AAQ89953, 37222208|
|Calculated MW||32759 Da|
|Application Notes||XEDAR antibody can be used for the detection of XEDAR by Western blot at 0.5 - 2 µg/mL. Antibody can also be used for immunohistochemistry starting at 10 µg/mL.|
|Other Names||XEDAR Antibody: XEDAR, EDAA2R, EDA-A2R, TNFRSF27, XEDAR, UNQ2448/PRO5727/PRO34080, Tumor necrosis factor receptor superfamily member 27, X-linked ectodysplasin-A2 receptor, EDA-A2 receptor, ectodysplasin A2 receptor|
|Reconstitution & Storage||XEDAR antibody can be stored at 4℃ for three months and -20℃, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.|
|Precautions||XEDAR Antibody is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Receptor for EDA isoform A2, but not for EDA isoform A1. Mediates the activation of the NF-kappa-B and JNK pathways. Activation seems to be mediated by binding to TRAF3 and TRAF6.|
|Cellular Location||Membrane; Single-pass type III membrane protein|
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Provided below are standard protocols that you may find useful for product applications.
XEDAR Antibody: 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-κB 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.
Yan M, Wang LC, Hymowitz SG, et al. Two-amino acid molecular switch in an epithelial morphogen that regulates binding to two distinct receptors. Science 2000; 290:523-7.
Sinha SK, Zachariah S, Quinones HI, et al. Role of TRAF3 and -6 in the activation of the NF-κB and JNK pathways by X-linked ectodermal dysplasia receptor. J. Biol. Chem. 2002; 277:44953-61.
Sinha SK and Chaudhary PM. Induction of apoptosis by X-linked ectodermal dysplasia receptor via a caspase 8-dependent mechanism. J. Biol. Chem. 2004; 41873-81.
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