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anti-Human Ectodysplasin A Antikörper:
anti-Mouse (Murine) Ectodysplasin A Antikörper:
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Human Polyclonal Ectodysplasin A Primary Antibody für IHC (p), ELISA - ABIN545790
Tarpey, Pemberton, Stockton, Das, Ninis, Edkins, Andrew Futreal, Wooster, Kamath, Nayak, Stratton, Patel: A novel Gln358Glu mutation in ectodysplasin A associated with X-linked dominant incisor hypodontia. in American journal of medical genetics. Part A 2007
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Cow (Bovine) Polyclonal Ectodysplasin A Primary Antibody für WB - ABIN2781905
Zhao, Watt, Battle, Li, Bondow, Duncan: Loss of both GATA4 and GATA6 blocks cardiac myocyte differentiation and results in acardia in mice. in Developmental biology 2008
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Cow (Bovine) Polyclonal Ectodysplasin A Primary Antibody für WB - ABIN2773846
Zhao, Hua, Zhao, Meng, Ao, Liu, Shang, Sun, Lo, Zhang: Three novel mutations of the EDA gene in Chinese patients with X-linked hypohidrotic ectodermal dysplasia. in The British journal of dermatology 2008
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Human Polyclonal Ectodysplasin A Primary Antibody für IF (p), IHC (p) - ABIN1713994
Sisto, Barca, Lofrumento, Lisi: Downstream activation of NF-κB in the EDA-A1/EDAR signalling in Sjögren's syndrome and its regulation by the ubiquitin-editing enzyme A20. in Clinical and experimental immunology 2016
Human Polyclonal Ectodysplasin A Primary Antibody für WB - ABIN3042668
Ning, Chen, Li, Wu, Wu, Li, Feng: X-irradiation for inhibiting glial scar formation in injured spinal cord. in Neural regeneration research 2014
Human Monoclonal Ectodysplasin A Primary Antibody für ELISA - ABIN2752205
Arbat-Plana, Cobianchi, Herrando-Grabulosa, Navarro, Udina: Endogenous Modulation of Trkb Signaling by Treadmill Exercise After Peripheral Nerve Injury. in Neuroscience 2016
Human Polyclonal Ectodysplasin A Primary Antibody für IF (p), IHC (p) - ABIN738381
Oya, Yokoyama, Kokuryo, Uno, Yamauchi, Nagino: Inhibition of Toll-like receptor 4 suppresses liver injury induced by biliary obstruction and subsequent intraportal lipopolysaccharide injection. in American journal of physiology. Gastrointestinal and liver physiology 2014
The new EDA variants expand the mutational pro fi le of hypohidrotic ectodermal dysplasia, and in two patients, a de novo mutation was identi fi ed.
One novel mutation (c.441_442insACTCT) and three reported mutations (c.252delT, c.463C>T, and c.1013C>T) in EDA were identified in families with ectodermal dysplasia. The novel EDA mutation was co-segregated with phenotype.
The EDA mutations of c.878 T > G, c.663-697del and c.587-615del may be responsible for the pathogenesis of autosomal recessive hypohidrotic ectodermal dysplasia in their pedigrees.
rs132630321 (c.1013C>T) in EDA gene was found in non-syndromic X-linked oligodontia male patients. Heterozygous female carriers for this EDA mutation may present a highly variable and milder dental phenotype. Replacement of T338 native (hydrophilic) by an M338 mutated residue (hydrophobic) was predicted to alter the conformation of the 337-342 loop leading to a potential impact on EDA-A1 receptor binding properties.
EDA gene expression contributes to the maintenance of epithelial barrier function.
Mutations were identified in all seven families, including four previously reported missense mutations (p.M1T, p.R156C, p.G299S, and p.A349T) and three novel mutations; missense mutation (p.Q358 L), indel (P228Tfs*52), as well as a large deletion.
A novel functional skipping-splicing EDA mutation was considered to be the cause of HED in the two pedigrees reported here.
Case Report: EDA mutation causing hypohidrotic ectodermal dysplasia with hyperplasia of the sebaceous glands in a Chinese patient.
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 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 signaling pathway. (EGFR = epidermal growth factor receptor)
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 are overexpressed in epithelial cells of salivary glands in Sjogren's syndrome patients, in comparison with healthy individuals. The EDA-A2/XEDAR system in these cells is involved in the induction of apoptosis via CASP3 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 homology domain were correlated with fewer missing teeth.
hemizygous frame-shift mutation c. 731delG (p.R244Qfs*36) underlies hypohidrotic ectodermal dysplasia in a Japanese family
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.
novel nonsense mutation in Chinese family
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
A single point mutation within this gene disrupts correct splicing at two different splice sites and leads to anhidrotic ectodermal dysplasia in cattle
Eda and edar are not required for early development but are specific for the development of adult skeletal and dental structures.
results indicate that EDA/NKX2-3 signaling is essential for enamel knot formation during tooth morphogenesis in mice
loss of Fgf20 delays formation of Eda-induced supernumerary mammary buds and normalizes the embryonic and postnatal hyperbranching phenotype of Eda overexpressing mice.
Eda initiates a signaling cascade and recruits a BAF complex to specific gene loci to facilitate transcription during organogenesis.
Gain- and loss-of-function approaches reveal that liver-derived EDA regulates systemic glucose metabolism, suggesting that EDA is a hepatokine that can contribute to impaired skeletal muscle insulin sensitivity in obesity.
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 is delayed in Tabby mice, whereas it is restored by exogenous 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 or Edaradd 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 mutant mice and explore the pathogenic mechanisms related to glandular function, microbial and immune parameters in these lines
Wnt, Eda, and Shh have roles in touch dome Merkel cell development
Using an ex vivo culture system, we show that suppression of canonical Wnt signalling leads to a dose-dependent inhibition of supernumerary placodes in K14-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 signaling.
NF-kappaB downstream of the TNF-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 via transcription factor NF-kappaB in the epithelium, and that the hedgehog pathway is an important mediator of Eda/NF-kappaB.
Dkk4 affects an auxiliary pathway for Eda-independent development of secondary hair
Treatment of Eda-/- minor salivary gland explants with EDA A1 rescues minor salivary gland induction.
The ectodysplasin-A gene plays a role in normal bone development in mice.
Eda and 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.
Gene expression profiling data are consistent with the regulation of the NF-kappa B and JNK pathways by EDA
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.
X-linked anhidroitic ectodermal dysplasia protein
, oligodontia 1
, ectodysplasin A
, ectodermal dysplasia 1, anhidrotic
, ectodermal dysplasia protein
, EDA protein homolog
, ectodysplasin A1