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This is the first analysis of the role of Eda in the root, showing a direct role for this pathway during postnatal mouse development, and it suggests that changes in proliferation and angle of HERS may underlie taurodontism in a range of syndromes.
Data suggest that corneal epithelial integrity is defective and the thickness is reduced in Eda mutant Tabby mice at early postnatal stage (4-week-old); corneal epithelial cell proliferation is decreased and epithelial wound healing (show EGFR ELISA Kits)is delayed in Tabby mice, (show EGFR ELISA Kits) whereas it is restored by exogenou (show EGFR ELISA Kits)s Eda. Tabby mice are a model for X-linked hypohidrotic ectodermal dysplasia and can be treated with recombinant Eda.
Murine nasal submucosal glands express EDA during embryonic development. EDA signalling is essential for Lateral Nasal Gland and Medial Nasal Gland budding and ductal morphogenesis.
Mouse models with HED also carry Eda, Edar (show EDAR ELISA Kits) or Edaradd (show EDARADD ELISA Kits) mutations and have defects that map to the same structures.We report that otitis media, rhinitis and nasopharyngitis occur at high frequency in Eda and Edar (show EDAR ELISA Kits) mutant mice and explore the pathogenic mechanisms related to glandular function, microbial and immune parameters in these lines
Wnt (show WNT2 ELISA Kits), Eda, and Shh (show SHH ELISA Kits) have roles in touch dome Merkel cell development
Using an ex vivo culture system, we show that suppression of canonical Wnt (show WNT2 ELISA Kits) signalling leads to a dose-dependent inhibition of supernumerary placodes in K14 (show KRT14 ELISA Kits)-Eda tissue explants.
Eda and activin A are upstream regulators of Foxi3 in skin appendage placodes
Ectodysplasin regulates activator-inhibitor balance in murine tooth development through Fgf20 (show FGF20 ELISA Kits) signaling.
NF-kappaB (show NFKB1 ELISA Kits) downstream of the TNF (show TNF ELISA Kits)-like ligand ectodysplasin (Eda) is identified as a unique regulator of embryonic and prepubertal ductal morphogenesis.
Data found that Eda regulates growth and branching of the SMG (show SNRPG ELISA Kits) via transcription factor NF-kappaB (show NFKB1 ELISA Kits) in the epithelium, and that the hedgehog (show SHH ELISA Kits) pathway is an important mediator of Eda/NF-kappaB (show NFKB1 ELISA Kits).
Data suggest that EDA is highly expressed in meibomian glands and is detectible in human tears but not serum; EDA protein is secreted from meibomian glands and promotes corneal epithelial cell proliferation through regulation of EGFR (show EGFR ELISA Kits) signaling pathway. (EGFR (show EGFR ELISA Kits) = epidermal growth factor receptor (show EGFR ELISA Kits))
EDA is an important candidate gene for two developmental diseases sharing the common feature of the congenital lack of teeth. In addition, these results can support the hypothesis that X-linked HED and EDA-related NTA are the same disease with different degrees of severity.
EDA-A2 and its receptor XEDAR (show EDA2R ELISA Kits) are overexpressed in epithelial cells of salivary glands in Sjogren's syndrome patients, in comparison with healthy individuals. The EDA-A2/XEDAR (show EDA2R ELISA Kits) system in these cells is involved in the induction of apoptosis via CASP3 (show CASP3 ELISA Kits) activation.
Based on a computerized protein structure analysis, we suggest that the change p.Arg289His in EDA impairs protein stabilization and thus might possibly be involved in the development of oligodontia concomitant with a mild ED phenotype.
we identified a novel and three reported EDA missense mutations in four of six patients with X-linked hypohidrotic ectodermal dysplasia. Missense mutations and the mutations affecting the tumor necrosis factor (show TNF ELISA Kits) homology domain were correlated with fewer missing teeth.
Our findings indicate that a novel mutation (c.878T>G) of EDA is associated with XLHED and adds to the repertoire of EDA mutations.
We found a novel missense mutation in exon 1 of the EDA1 gene in a putative Mayan family from Mexico with XL-HED.
A novel missense mutation in the EDA gene in a Chinese family with X-linked hypohidrotic ectodermal dysplasia.
dentified a novel deletion mutation located in exon 1 which if expressed would produce a highly truncated protein in a Chinese Han family with X-linked hypohidrotic ectodermal dysplasia
Authors identifya mutation, never described before, that changes the regulation of alternative splicing in the EDA gene and causes ectodermal dysplasia in cattle.
The 161-bp-long LINE1-derived-pseudoexon introduces a shift in reading frame and a premature stop codon early in EDA exon 2 and is probably the cause of XHED in this Danish Red Holstein family.
describe a novel mutation of the EDA gene in which a 19 bp deletion in exon 1 in male Holstein calves demonstrated the phenotypic features of EDA
Eda and edar (show EDAR ELISA Kits) are not required for early development but are specific for the development of adult skeletal and dental structures.
The protein encoded by this gene is a type II membrane protein that can be cleaved by furin to produce a secreted form. The encoded protein, which belongs to the tumor necrosis factor family, acts as a homotrimer and may be involved in cell-cell signaling during the development of ectodermal organs. Defects in this gene are a cause of ectodermal dysplasia, anhidrotic, which is also known as X-linked hypohidrotic ectodermal dysplasia. Several transcript variants encoding many different isoforms have been found for this gene.
, embryonic development factor 1
, protein CWC15 homolog
, spliceosome-associated protein CWC15 homolog
, X-linked anhidroitic ectodermal dysplasia protein
, oligodontia 1
, ectodysplasin A1
, ectodermal dysplasia 1, anhidrotic
, ectodermal dysplasia protein
, EDA protein homolog