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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 08 Dec 2016.

Ectodysplasin A2 receptor

XEDAR, EDA2R, X-linked ectodysplasin-A2 receptor
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.[provided by RefSeq, May 2011] (from NCBI)
Papers on XEDAR
Investigation of the male pattern baldness major genetic susceptibility loci AR/EDA2R and 20p11 in female pattern hair loss.
Betz et al., Bonn, Germany. In Br J Dermatol, 2012
The results suggest that EDA2R confers susceptibility to early onset female pattern hair loss
Analysis of genetic polymorphisms in skeletal Class I crowding.
Rabie et al., Hong Kong, Hong Kong. In Am J Orthod Dentofacial Orthop, 2011
association in dental crowding in the Hong Kong Chinese population
Crosstalk of EDA-A2/XEDAR in the p53 signaling pathway.
Matsuda et al., Tokyo, Japan. In Mol Cancer Res, 2010
A crucial role of the EDA-A2/ectodysplasin A2 (XEDAR) interaction is revealed in the p53-signaling pathway.
Fine mapping of the human AR/EDA2R locus in androgenetic alopecia.
Nöthen et al., In Br J Dermatol, 2010
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
XEDAR as a putative colorectal tumor suppressor that mediates p53-regulated anoikis pathway.
Matsuda et al., Tokyo, Japan. In Oncogene, 2009
XEDAR is a putative tumor suppressor that could prevent malignant transformation and tumor progression by regulating apoptosis and anoikis.
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