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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Ectodysplasin A receptor

ectodysplasin receptor
Top mentioned proteins: HAIR, FATE, Ubiquitin, A20, AP-1
Papers on ectodysplasin receptor
Downstream activation of NF-κB in the EDA-A1/EDAR signalling in Sjögren's syndrome and its regulation by the ubiquitin-editing enzyme A20.
New
Lisi et al., Bari, Italy. In Clin Exp Immunol, Feb 2016
Since A20 negatively controls the ectodysplasin-A1 (EDA-A1)/ectodysplasin receptor (EDAR) signalling, and the deletion of A20 results in excessive EDA1-induced NF-κB signalling, this work investigates the expression levels of EDA-A1 and EDAR in SS human salivary glands epithelial cells (SGEC) and evaluates the hypothesis that SS SGEC-specific deregulation of A20 results in excessive EDA1-induced NF-κB signalling in SS.
Carcinogenesis of nasopharyngeal carcinoma: an alternate hypothetical mechanism.
New
Wee et al., Singapore, Singapore. In Ai Zheng, Dec 2015
This claim is indirectly supported by observations that the East Asian phenotype shares the characteristics of an increased susceptibility to NPC and immature salivary gland morphogenesis, the latter of which is influenced by the association of salivary gland morphogenesis with an evolutionary variant of the human ectodysplasin receptor gene (EDAR), EDARV370A.
Pharmacological activation of the EDA/EDAR signaling pathway restores salivary gland function following radiation-induced damage.
Limesand et al., Tucson, United States. In Plos One, 2013
During embryogenesis, the ectodysplasin/ectodysplasin receptor (EDA/EDAR) signaling pathway is a critical element in the development and growth of salivary glands.
Keratinocyte-specific ablation of the NF-κB regulatory protein A20 (TNFAIP3) reveals a role in the control of epidermal homeostasis.
van Loo et al., Gent, Belgium. In Cell Death Differ, 2011
This phenotype resembles that of mice overexpressing ectodysplasin-A1 (EDA-A1) or the ectodysplasin receptor (EDAR), suggesting that A20 negatively controls EDAR signaling.
Analysis of genes isolated from plated hemocytes of the Pacific oyster, Crassostreas gigas.
Goetz et al., Seattle, United States. In Mar Biotechnol (ny), 2009
Several genes observed in the library were significantly upregulated by bacterial challenge including interleukin 17, astacin, cystatin B, the EP4 receptor for prostaglandin E, the ectodysplasin receptor, c-jun, and the p100 subunit of nuclear factor-kB.
Zebrafish eda and edar mutants reveal conserved and ancestral roles of ectodysplasin signaling in vertebrates.
GeneRIF
Nüsslein-Volhard et al., Tübingen, Germany. In Plos Genet, 2007
Eda and edar are not required for early development but are specific for the development of adult skeletal and dental structures.
Abortive placode formation in the feather tract of the scaleless chicken embryo.
Morgan et al., United States. In Dev Dyn, 2007
An exception is the ectodysplasin receptor gene Edar, which is expressed at lower levels in mutant feather buds.
Generation of the primary hair follicle pattern.
Headon et al., Manchester, United Kingdom. In Proc Natl Acad Sci U S A, 2006
We find that ectodysplasin receptor (Edar)-bone morphogenetic protein (BMP) signaling and transcriptional interactions are central to generation of the primary hair follicle pattern, with restriction of responsiveness, rather than localization of an inducing ligand, being the key driver in this process.
TRAF6-deficient mice display hypohidrotic ectodermal dysplasia.
Inoue et al., Tokyo, Japan. In Proc Natl Acad Sci U S A, 2002
TRAF6 does not associate with the cytoplasmic tail of the dl protein (DL)/ectodysplasin receptor (EDAR) receptor, which, when mutated, results in hypohidrotic (anhidrotic) ectodermal dysplasia.
X-linked anhidrotic ectodermal dysplasia with immunodeficiency is caused by impaired NF-kappaB signaling.
Impact
Casanova et al., Paris, France. In Nat Genet, 2001
We also show that the ectodysplasin receptor, DL, triggers NF-kappaB through the NEMO protein, indicating that EDA results from impaired NF-kappaB signaling.
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