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anti-Mouse (Murine) Ectodysplasin A Antikörper:
anti-Human Ectodysplasin A Antikörper:
anti-Rat (Rattus) Ectodysplasin A Antikörper:
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Human Polyclonal Ectodysplasin A Primary Antibody für IHC, ELISA - ABIN1584385
Li, Yao, Sheng, Yang, Ma: Dual-modal tracking of transplanted mesenchymal stem cells after myocardial infarction. in International journal of nanomedicine 2011
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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
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 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
Cow (Bovine) Polyclonal Ectodysplasin A Primary Antibody für WB - ABIN2773846
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 - ABIN2781905
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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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 (zeige INS Antikörper) sensitivity in obesity.
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 (zeige EGFR Antikörper)is delayed in Tabby mice, (zeige EGFR Antikörper) whereas it is restored by exogenou (zeige EGFR Antikörper)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 (zeige EDAR Antikörper) or Edaradd (zeige EDARADD Antikörper) 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 (zeige EDAR Antikörper) mutant mice and explore the pathogenic mechanisms related to glandular function, microbial and immune parameters in these lines
Wnt (zeige WNT2 Antikörper), Eda, and Shh (zeige SHH Antikörper) have roles in touch dome Merkel cell development
Using an ex vivo culture system, we show that suppression of canonical Wnt (zeige WNT2 Antikörper) signalling leads to a dose-dependent inhibition of supernumerary placodes in K14 (zeige KRT14 Antikörper)-Eda tissue explants.
Eda and activin A (zeige INHBA Antikörper) are upstream regulators of Foxi3 (zeige FOXI3 Antikörper) in skin appendage placodes
Ectodysplasin regulates activator-inhibitor balance in murine tooth development through Fgf20 (zeige FGF20 Antikörper) signaling.
NF-kappaB (zeige NFKB1 Antikörper) downstream of the TNF (zeige TNF Antikörper)-like ligand ectodysplasin (Eda) is identified as a unique regulator of embryonic and prepubertal ductal morphogenesis.
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 (zeige EGFR Antikörper) signaling pathway. (EGFR (zeige EGFR Antikörper) = epidermal growth factor receptor (zeige EGFR Antikörper))
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 (zeige EDA2R Antikörper) are overexpressed in epithelial cells of salivary glands in Sjogren's syndrome patients, in comparison with healthy individuals. The EDA-A2/XEDAR (zeige EDA2R Antikörper) system in these cells is involved in the induction of apoptosis via CASP3 (zeige CASP3 Antikörper) 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 (zeige TNF Antikörper) 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 (zeige EDAR Antikörper) 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