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1 s isoforms of a novel transmembrane protein, ectodysplasin.
2                      Patients with defective ectodysplasin A (EDA) are affected by X-linked hypohidro
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
5                                     Impaired ectodysplasin A (EDA) receptor (EDAR) signaling affects
6 requires the action of the TNF family ligand ectodysplasin A (EDA).
7                         The highly conserved ectodysplasin A (EDA)/EDA receptor signaling pathway is
8                                     Finally, ectodysplasin A can physically interact with the extrace
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
11 ion in humans surrounds the V370A variant of Ectodysplasin A receptor (EDAR).
12                                              Ectodysplasin, a member of the tumor necrosis factor fam
13                             The gene encodes ectodysplasin, a TNF ligand family member that activates
14  in anhidrotic ectodermal dysplasia, encodes ectodysplasin, a TNF superfamily member that activates N
15                           tabby (Ta) encodes ectodysplasin-A (Eda) a type II membrane protein of the
16                       Mutations in the human ectodysplasin-A (EDA) are responsible for the most commo
17                                 Mutations in ectodysplasin-A (EDA) cause loss of hair, sweat glands,
18 nant X-linked form results from mutations in ectodysplasin-A (EDA), a TNF-like ligand.
19                       The ED-1 gene product, ectodysplasin-A (EDA), is a tumor necrosis factor (TNF)
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.
22                              The isoforms of ectodysplasin-A may correlate with differential roles du
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
25 encodes a 391-residue transmembrane protein, ectodysplasin-A, containing 19 Gly-Xaa-Yaa repeats.
26                                              Ectodysplasin-A, the protein encoded by the EDA gene, is
27 othelial-monocyte-activating polypeptide II, ectodysplasin A2, Galectin-3, chemokine (C-X-C motif) li
28 ed during embryonic development and binds to ectodysplasin-A2 (EDA-A2).
29 es during embryonic development and binds to ectodysplasin-A2 (EDA-A2).
30 nds only the related, but distinct, X-linked ectodysplasin-A2 receptor (XEDAR).
31  heterozygotes at the major underlying gene, Ectodysplasin (Eda) [5].
32                                              Ectodysplasin (Eda) and its receptor (Edar) are required
33  NF-kappaB downstream of the TNF-like ligand ectodysplasin (Eda) as a unique regulator of embryonic a
34                  Previous studies identified ectodysplasin (EDA) gene as the major locus controlling
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
38                                              Ectodysplasin (Eda), a tumor necrosis factor-like ligand
39 e existence of standing allelic variation in Ectodysplasin (Eda), the gene that underlies the major p
40 e the transgene is the only source of active ectodysplasin (Eda).
41  by and functions downstream from epithelial ectodysplasin (Eda)/Edar and Wnt/beta-Catenin signaling
42      We demonstrate that the activity of the ectodysplasin/Edar/nuclear factor kappaB pathway is rest
43                     Our results suggest that ectodysplasin is a new member in the TNF-related ligand
44 proteins and members of TNF-related ligands, ectodysplasin is a type II membrane protein and it forms
45                 The membrane localization of ectodysplasin is asymmetrical: it is found on the apical
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
48                                          The ectodysplasin pathway, comprising the ligand ectodysplas
49 act system in order to study the role of the ectodysplasin pathway.
50 der to understand better the function of the ectodysplasin protein molecule and its domains, we have
51             An adaptive variant of the human Ectodysplasin receptor, EDARV370A, is one of the stronge
52 ui et al. report on the dose and duration of ectodysplasin signaling required for the maintenance and
53 pes of skin appendages is guided by prenatal ectodysplasin signaling.
54 elates with the acquisition of autonomy from ectodysplasin stimulation.
55        EDA-A1 and EDA-A2 are two isoforms of ectodysplasin that differ only by an insertion of two am
56                  Mutations in members of the ectodysplasin (TNF-related) signalling pathway, EDA, EDA

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