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anti-Human EDAR Antibodies:
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These data suggest differential roles for Eda (show EDA Antibodies)-Edar signaling in the induction and growth of scales and teeth and support the intrinsic odontogenic competence of the rostral endoderm in medaka.
Eda (show EDA Antibodies) and edar are not required for early development but are specific for the development of adult skeletal and dental structures.
Results suggested that SNPs in EDAR could be a pathogenic factor for non-syndromic tooth agenesis. Furthermore, EDAR can be regarded as a marker gene for the risk of tooth agenesis.
To evaluate the relative contribution of these variants, we performed a second genome-wide scan in 709 samples from the Uyghur, an admixed population with both eastern and western Eurasian ancestries. In Uyghurs, both EDAR (rs3827760: P = 1.92 x 10(-12)) and TCHH (show TCHH Antibodies) (rs11803731: P = 1.46 x 10(-3)) are associated with hair straightness, but EDAR (OR 0.415) has a greater effect than TCHH (show TCHH Antibodies) (OR 0.575).
Four traits of ear pinna anatomic variation are associated with a functional variant in the EDAR gene, a key regulator of embryonic skin appendage development.
Individuals with a c.1072C > T mutation in the EDAR-gene displayed more hair shaft deformations confirming the role of EDAR for human hair follicle development and postnatal hair follicle cycling.
Individuals with a c.1072C > T mutation in the EDAR-gene displayed a typical pattern of congenitally missing teeth in the frontal area with functional consequences.
Using whole-exome sequencing we describe a novel homozygous missense mutation in EDAR causing autosomal recessive HED (show EDA Antibodies) associated with palmoplantar hyperkeratosis and the absence of breasts.
Study generated a knockin mouse model and found that, as in humans, hair thickness is increased in EDAR370A mice; new biological targets affected by the mutation were identified, including mammary and eccrine glands. Building on these results EDAR370A was found to be associated with an increased number of active eccrine glands in the Han Chinese.
This is the first report of a founder EDAR mutation and of a significantly high frequency of autosomal recessive HED (show EDA Antibodies).
WNT10A (show WNT10A Antibodies) and EDAR were each responsible for 16% of hypohidrotic/anhidrotic ectodermal dysplasia cases.
screening of all the 12 exons and splice junctions of gene EDAR revealed a novel missense mutation (c.1163T>C; p.Ile388Thr) in family A and a novel insertion mutation (c.1014insA; p.V339SfsX6) in family B.
EDAR protein signaling pathway plays an important role in wound healing in mice and human.
Mouse models with HED (show EDA Antibodies) also carry Eda (show EDA Antibodies), Edar or Edaradd (show EDARADD Antibodies) mutations and have defects that map to the same structures.We report that otitis media, rhinitis and nasopharyngitis occur at high frequency in Eda (show EDA Antibodies) and Edar mutant mice and explore the pathogenic mechanisms related to glandular function, microbial and immune parameters in these lines
Edar is expressed in the developing ear. Edar-deficient mice have an abnormally shaped pinna.
Edar signalling has pleiotropic effects on craniofacial and cutaneous glands
Edar expression is confined to the ectoderm and occurs in a pattern that suggests a role of ectodysplasin/Edar signaling in the interactions between the ectodermal compartments and the formation and function of hair placodes.
Analysis of expression patterns of eda (show EDA Antibodies), edar and tnfrsf19 (show TNFRSF19 Antibodies) in mouse embryogenesis.
Data show that Edar misexpression disrupts tooth patterning and differentiation.
isoforms of EDA (show EDA Antibodies)-A5 and A5',activated NF-kappaB (show NFKB1 Antibodies) through receptors EDAR and XEDAR (show EDA2R Antibodies)
demonstrate that epidermal NF-kappaB (show NFKB1 Antibodies) activity is first observed in placodes of primary guard hair follicles at day E14.5, and that in vivo NF-kappaB (show NFKB1 Antibodies) signalling is activated downstream of Eda A1 (show EDA Antibodies) and EdaR
Data show that ectodysplasin receptor (Edar)-bone morphogenetic protein (BMP)-4 and -7 signaling and transcriptional interactions are central to generation of the primary hair follicle pattern.
This gene encodes a member of the tumor necrosis factor receptor family. The encoded transmembrane protein is a receptor for the soluble ligand ectodysplasin A, and can activate the nuclear factor-kappaB, JNK, and caspase-independent cell death pathways. It is required for the development of hair, teeth, and other ectodermal derivatives. Mutations in this gene result in autosomal dominant and recessive forms of hypohidrotic ectodermal dysplasia.
, protein reduced scale-3
, tumor necrosis factor receptor superfamily member EDAR
, ectodysplasin receptor
, ectodysplasin A receptor
, tumor necrosis factor receptor superfamily member EDAR-like
, EDA-A1 receptor
, anhidrotic ectodysplasin receptor 1
, downless homolog
, downless, mouse, homolog of
, ectodermal dysplasia receptor
, ectodysplasin 1, anhidrotic receptor
, ectodysplasin-A receptor
, ectodysplasin A1 receptor