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1 s isoforms of a novel transmembrane protein, ectodysplasin.
3 he tumor necrosis factor (TNF) family ligand ectodysplasin A (EDA) is produced as 2 full-length splic
4 otypes could be produced by gradually adding ectodysplasin A (EDA) protein in culture to tooth explan
9 e core hair morphogenetic program, including ectodysplasin A receptor (EDAR) and the Wnt and Shh path
10 associated with a functional variant in the Ectodysplasin A receptor (EDAR) gene, a key regulator of
14 in anhidrotic ectodermal dysplasia, encodes ectodysplasin, a TNF superfamily member that activates N
20 components, the downstream effectors of the ectodysplasin-A (EDA)/ ectodysplasin-A receptor (EDAR)/N
21 naling does control EDA gene expression, but ectodysplasin-A does not feedback on the Wnt pathway.
23 ream effectors of the ectodysplasin-A (EDA)/ ectodysplasin-A receptor (EDAR)/NF-kappaB signaling casc
24 s now been identified in one of these genes, ectodysplasin-A receptor, in the teleost fish Medaka, th
27 othelial-monocyte-activating polypeptide II, ectodysplasin A2, Galectin-3, chemokine (C-X-C motif) li
33 NF-kappaB downstream of the TNF-like ligand ectodysplasin (Eda) as a unique regulator of embryonic a
35 The products of alternative splicing of the ectodysplasin (EDA) gene, EDA-A1 and EDA-A2 differ by an
36 nt therapy, which acts as an agonist for the ectodysplasin (Eda) pathway, can resolve cleft palate de
37 encing, and transgenic studies show that the Ectodysplasin (EDA) signaling pathway plays a key role i
39 e existence of standing allelic variation in Ectodysplasin (Eda), the gene that underlies the major p
41 by and functions downstream from epithelial ectodysplasin (Eda)/Edar and Wnt/beta-Catenin signaling
44 proteins and members of TNF-related ligands, ectodysplasin is a type II membrane protein and it forms
46 ectodysplasin pathway, comprising the ligand ectodysplasin, its receptor Edar and a dedicated death d
47 These results suggest that activation of the ectodysplasin pathway may be permissive for activating s
50 der to understand better the function of the ectodysplasin protein molecule and its domains, we have
52 ui et al. report on the dose and duration of ectodysplasin signaling required for the maintenance and
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