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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 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)
Top mentioned proteins: HAIR, NF-kappaB, Aga, ED1, V1a
Papers on XEDAR
X-linked ectodermal dysplasia receptor (XEDAR) gene silencing prevents caspase-3-mediated apoptosis in Sjögren's syndrome.
Lisi et al., Bari, Italy. In Clin Exp Med, Jan 2016
Ectodysplasin-A2 (EDA-A2) is a recently isolated member of the tumor necrosis factor superfamily that binds to X-linked ectodermal dysplasia receptor (XEDAR).
XEDAR activates the non-canonical NF-κB pathway.
Beyaert et al., Gent, Belgium. In Biochem Biophys Res Commun, Oct 2015
The X-linked ectodermal dysplasia receptor (XEDAR; also known as EDA2R or TNFRSF27) is a member of the TNFR superfamily that is highly expressed in ectodermal derivatives during embryonic development and binds to ectodysplasin-A2 (EDA-A2), a member of the TNF family that is encoded by the anhidrotic ectodermal dysplasia (EDA) gene.
Gene expression profiling in non-human primate jejunum, ileum and colon after total-body irradiation: a comparative study of segment-specific molecular and cellular responses.
Hauer-Jensen et al., Little Rock, United States. In Bmc Genomics, 2014
In addition to the identification a marked increase of TNFα cascade, this study also identified radiation induced strikingly up-regulated tight junction gene CLDN2 (196-fold after 7.4-Gy TBI), matrix degradation genes such as MMP7 (increased 11- and 41-fold after 6.7-Gy and 7.4-Gy TBI), and anoikis mediated gene EDA2R that mediate mucosal shedding and barrier disruption.
Investigation of four novel male androgenetic alopecia susceptibility loci: no association with female pattern hair loss.
Betz et al., Bonn, Germany. In Arch Dermatol Res, 2014
Our recent findings indicate that the major AGA locus, an X-chromosome region containing the androgen receptor and the ectodysplasin A2 receptor (EDA2R) genes, may represent a common genetic factor underlying both early-onset FPHL and AGA.
Information compression exploits patterns of genome composition to discriminate populations and highlight regions of evolutionary interest.
Reverter et al., Brisbane, Australia. In Bmc Bioinformatics, 2013
We also identified a set of previously unidentified loci with high population-specific CE scores including the chromatin remodeler SCMH1 in Africans and EDA2R in Asians.
Poor survival with wild-type TP53 ovarian cancer?
Gershenson et al., Houston, United States. In Gynecol Oncol, 2013
Using RNAseq data, it was found that EDA2R gene, a direct target of wild-type TP53, was highly up-regulated in samples with wild-type TP53 in comparison to samples with either nonsense or missense TP53 mutations.
A tale of two haplotypes: the EDA2R/AR Intergenic region is the most divergent genomic segment between Africans and East Asians in the human genome.
Feldman et al., Stanford, United States. In Hum Biol, 2012
The longest run of SNPs with an allele frequency difference of one between the Yoruba of Nigeria and the Han Chinese is found on the long arm of the X chromosome in the intergenic region separating the EDA2R and AR genes.
Genetic variants at 20p11 confer risk to androgenetic alopecia in the Chinese Han population.
Zhang et al., Hefei, China. In Plos One, 2012
Several susceptibility genes/loci, such as AR/EDA2R, HDAC9 and 20p11, have been identified as being involved in its development in European populations.
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.
Genome-wide detection and characterization of positive selection in human populations.
Stewart et al., Cambridge, United States. In Nature, 2007
Examination of these candidates highlights three cases in which two genes in a common biological process have apparently undergone positive selection in the same population:LARGE and DMD, both related to infection by the Lassa virus, in West Africa;SLC24A5 and SLC45A2, both involved in skin pigmentation, in Europe; and EDAR and EDA2R, both involved in development of hair follicles, in Asia.
Edar signaling in the control of hair follicle development.
Fessing et al., Boston, United States. In J Investig Dermatol Symp Proc, 2005
Ectodysplasin receptor Edar and its ligand Eda A1, as well as their related receptor Xedar and ligand Eda A2, are recently discovered members of the tumor necrosis factor superfamily that signal predominantly through the nuclear factor-kappaB and c-jun N-terminal kinases pathways.
CYLD is a deubiquitinating enzyme that negatively regulates NF-kappaB activation by TNFR family members.
Mosialos et al., Greece. In Nature, 2003
CYLD inhibits activation of NF-kappaB by the TNFR family members CD40, XEDAR and EDAR in a manner that depends on the deubiquitinating activity of CYLD.
Ectodysplasin signaling in development.
Thesleff et al., Helsinki, Finland. In Cytokine Growth Factor Rev, 2003
Two closely related isoforms of ectodysplasin, Eda-A1 and Eda-A2, have been described which bind to and activate two different receptors, Edar and X-linked Eda-A2 receptor (Xedar), respectively.
Permanent correction of an inherited ectodermal dysplasia with recombinant EDA.
Schneider et al., Lausanne, Switzerland. In Nat Med, 2003
Two main splice variants of Eda, encoding EDA1 and EDA2, engage the tumor necrosis factor (TNF) family receptors EDAR and XEDAR, respectively.
Recent advances in understanding of the molecular basis of anhidrotic ectodermal dysplasia: discovery of a ligand, ectodysplasin A and its two receptors.
Kobielak et al., Poznań, Poland. In J Appl Genet, 2001
The role of an alternative EDA receptor, localised on the X chromosome (XEDAR) in the developmental control of the differentiation of skin appendages, is discussed.
Two-amino acid molecular switch in an epithelial morphogen that regulates binding to two distinct receptors.
Dixit et al., San Francisco, United States. In Science, 2000
This insertion functions to determine receptor binding specificity, such that EDA-A1 binds only the receptor EDAR, whereas EDA-A2 binds only the related, but distinct, X-linked ectodysplasin-A2 receptor (XEDAR).
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