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EDA-A1 and EDA-A2 are two isoforms of ectodysplasin that are encoded by the anhidrotic ectodermal dysplasia (EDA) gene. Additionally we are shipping Ectodysplasin A2 Receptor Proteins (19) and Ectodysplasin A2 Receptor Kits (4) and many more products for this protein.
Showing 10 out of 90 products:
Human Polyclonal Ectodysplasin A2 Receptor Primary Antibody for WB - ABIN2477154
Embi, Suhaimi, Mohamed, Ismail: Prevalence of antibodies to Pseudomonas pseudomallei exotoxin and whole cell antigens in military personnel in Sabah and Sarawak, Malaysia. in Microbiology and immunology 1993
Show all 3 Pubmed References
Human Polyclonal Ectodysplasin A2 Receptor Primary Antibody for WB - ABIN528408
Staropoli, Li, Chun, Allaire, Cullen, Thai, Fleet, Hua, Bennett, Krainer, Kerr, McCampbell, Rigo, Carulli: Rescue of gene-expression changes in an induced mouse model of spinal muscular atrophy by an antisense oligonucleotide that promotes inclusion of SMN2 exon 7. in Genomics 2015
We found evidence for AR but not EDA2R as the candidate gene at the androgenetic alopecia risk locus on chromosome X.
EDA-A2 (show EDA Antibodies) and its receptor XEDAR are overexpressed in epithelial cells of salivary glands in Sjogren's syndrome patients, in comparison with healthy individuals. The EDA-A2 (show EDA Antibodies)/XEDAR system in these cells is involved in the induction of apoptosis via CASP3 (show CASP3 Antibodies) activation.
XEDAR activates the non-canonical NF-kappaB (show NFKB1 Antibodies) pathway.
To investigate the evolutionary history of the EDA2R/AR intergenic region, we characterized the haplotype structure of 52 of its highly differentiated SNPs. Nearly all human X chromosomes carry one of two modal haplotypes for these 52 SNPs.
The results suggest that EDA2R confers susceptibility to early onset female pattern hair loss
A crucial role of the EDA-A2 (show EDA Antibodies)/ectodysplasin A2 (XEDAR) interaction is revealed in the p53 (show TP53 Antibodies)-signaling pathway.
because no frequent variant other than rs1385699 has been reported in EDA2R in the European population, it is probable that the causative variant(s) modifies the expression of one or more flanking genes, i.e. AR and EDA2R
Results establish a major role of TRAF3 (show TRAF3 Antibodies) and -6 in X-linked ectodermal dysplasia receptor (show EDAR Antibodies) (XEDAR) signaling and in the process of ectodermal differentiation.
XEDAR belongs to a novel class of death receptors that lack a discernible death domain but are capable of activating apoptosis in a caspase 8- and FADD-dependent fashion
isoforms of EDA (show EDA Antibodies)-A5 and A5',activated NF-kappaB (show NFKB1 Antibodies) through receptors EDAR (show EDAR Antibodies) and XEDAR
EDA-A2 (show EDA Antibodies) transgenic mice exhibited multifocal myodegeneration; this phenotype was not observed in the absence of XEDAR
EDA-A1 and EDA-A2 are two isoforms of ectodysplasin that are encoded by the anhidrotic ectodermal dysplasia (EDA) gene. Mutations in EDA give rise to a clinical syndrome characterized by loss of hair, sweat glands, and teeth. The protein encoded by this gene specifically binds to EDA-A2 isoform. This protein is a type III transmembrane protein of the TNFR (tumor necrosis factor receptor) superfamily, and contains 3 cysteine-rich repeats and a single transmembrane domain but lacks an N-terminal signal peptide. Alternatively spliced transcript variants have been found for this gene.
X-linked ectodysplasin receptor
, tumor necrosis factor receptor superfamily member 27
, ectodysplasin A2 receptor
, EDA-A2 receptor
, X-linked ectodysplasin-A2 receptor
, tumor necrosis factor receptor superfamily member XEDAR
, X linked ectodysplasin receptor
, ectodysplasin A2 isoform receptor