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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 een stickleback lateral plate phenotypes and Ectodysplasin A (Eda) genotypes to infer changes in alle
4 he tumor necrosis factor (TNF) family ligand ectodysplasin A (EDA) is produced as 2 full-length splic
5 based on the interaction between the WNT and Ectodysplasin A (EDA) pathways.
6 otypes could be produced by gradually adding ectodysplasin A (EDA) protein in culture to tooth explan
7                                     Impaired ectodysplasin A (EDA) receptor (EDAR) signaling affects
8 n as a cytoplasmic accessory protein for the Ectodysplasin A (EDA) signalling pathway.
9 ent in chicken feathers involves a spreading Ectodysplasin A (EDA) wave and Fibroblast Growth Factor
10 mation is imposed by expanding expression of Ectodysplasin A (EDA), which initiates the expression of
11 requires the action of the TNF family ligand ectodysplasin A (EDA).
12                         The highly conserved ectodysplasin A (EDA)/EDA receptor signaling pathway is
13                                     Finally, ectodysplasin A can physically interact with the extrace
14 e core hair morphogenetic program, including ectodysplasin A receptor (EDAR) and the Wnt and Shh path
15  associated with a functional variant in the Ectodysplasin A receptor (EDAR) gene, a key regulator of
16                                              Ectodysplasin A receptor (EDAR) is a death receptor in t
17   In flighted birds, the key role of the EDA/Ectodysplasin A receptor (EDAR) pathway in vertebrate sk
18 ion in humans surrounds the V370A variant of Ectodysplasin A receptor (EDAR).
19                                      Loss of Ectodysplasin A signaling alters the morphology of dMCs
20  Merkel cell maturation program and identify Ectodysplasin A signaling as a key regulator of Merkel c
21                                              Ectodysplasin, a member of the tumor necrosis factor fam
22                             The gene encodes ectodysplasin, a TNF ligand family member that activates
23  in anhidrotic ectodermal dysplasia, encodes ectodysplasin, a TNF superfamily member that activates N
24                           tabby (Ta) encodes ectodysplasin-A (Eda) a type II membrane protein of the
25                       Mutations in the human ectodysplasin-A (EDA) are responsible for the most commo
26                                 Mutations in ectodysplasin-A (EDA) cause loss of hair, sweat glands,
27 nant X-linked form results from mutations in ectodysplasin-A (EDA), a TNF-like ligand.
28                       The ED-1 gene product, ectodysplasin-A (EDA), is a tumor necrosis factor (TNF)
29  components, the downstream effectors of the ectodysplasin-A (EDA)/ ectodysplasin-A receptor (EDAR)/N
30 naling does control EDA gene expression, but ectodysplasin-A does not feedback on the Wnt pathway.
31                              The isoforms of ectodysplasin-A may correlate with differential roles du
32 ream effectors of the ectodysplasin-A (EDA)/ ectodysplasin-A receptor (EDAR)/NF-kappaB signaling casc
33 s now been identified in one of these genes, ectodysplasin-A receptor, in the teleost fish Medaka, th
34 encodes a 391-residue transmembrane protein, ectodysplasin-A, containing 19 Gly-Xaa-Yaa repeats.
35                                              Ectodysplasin-A, the protein encoded by the EDA gene, is
36 ing growth factor-beta binding protein 2 and ectodysplasin A2 receptor showed the strongest mediation
37 mpared with sarcomeric DCM, including EDA2R (ectodysplasin A2 receptor; per log2 fold change in relat
38 minal pro-brain natriuretic peptide], EDA2R [ectodysplasin A2 receptor], NPPB [B-type natriuretic pep
39 othelial-monocyte-activating polypeptide II, ectodysplasin A2, Galectin-3, chemokine (C-X-C motif) li
40 ed during embryonic development and binds to ectodysplasin-A2 (EDA-A2).
41 es during embryonic development and binds to ectodysplasin-A2 (EDA-A2).
42 diabetes, result in heightened levels of the Ectodysplasin-A2 ligand.
43 nds only the related, but distinct, X-linked ectodysplasin-A2 receptor (XEDAR).
44      Our findings suggest that targeting the Ectodysplasin-A2 surface receptor represents a promising
45 ing-associated increase of the transmembrane Ectodysplasin-A2-Receptor is a prominent tissue-independ
46            We show that strengthening of the Ectodysplasin-A2-Receptor signalling axis in myogenic pr
47  heterozygotes at the major underlying gene, Ectodysplasin (Eda) [5].
48                                              Ectodysplasin (Eda) and its receptor (Edar) are required
49  NF-kappaB downstream of the TNF-like ligand ectodysplasin (Eda) as a unique regulator of embryonic a
50                  Previous studies identified ectodysplasin (EDA) gene as the major locus controlling
51  The products of alternative splicing of the ectodysplasin (EDA) gene, EDA-A1 and EDA-A2 differ by an
52 nt therapy, which acts as an agonist for the ectodysplasin (Eda) pathway, can resolve cleft palate de
53 TNF receptor subfamily and a mediator of the ectodysplasin (EDA) pathway.
54 encing, and transgenic studies show that the Ectodysplasin (EDA) signaling pathway plays a key role i
55 e detected a single, large-effect locus near Ectodysplasin (Eda), a gene having an ancient freshwater
56                                              Ectodysplasin (Eda), a tumor necrosis factor-like ligand
57 e existence of standing allelic variation in Ectodysplasin (Eda), the gene that underlies the major p
58 e the transgene is the only source of active ectodysplasin (Eda).
59 h the addition of a single signaling ligand, Ectodysplasin (Eda).
60  by and functions downstream from epithelial ectodysplasin (Eda)/Edar and Wnt/beta-Catenin signaling
61 ungs like humans, and disrupted the gene for ectodysplasin (EDA-KO), which initiates SMG development.
62      We demonstrate that the activity of the ectodysplasin/Edar/nuclear factor kappaB pathway is rest
63                     Our results suggest that ectodysplasin is a new member in the TNF-related ligand
64 proteins and members of TNF-related ligands, ectodysplasin is a type II membrane protein and it forms
65                 The membrane localization of ectodysplasin is asymmetrical: it is found on the apical
66 ectodysplasin pathway, comprising the ligand ectodysplasin, its receptor Edar and a dedicated death d
67 These results suggest that activation of the ectodysplasin pathway may be permissive for activating s
68                                          The ectodysplasin pathway, comprising the ligand ectodysplas
69 act system in order to study the role of the ectodysplasin pathway.
70 der to understand better the function of the ectodysplasin protein molecule and its domains, we have
71             An adaptive variant of the human Ectodysplasin receptor, EDARV370A, is one of the stronge
72 ui et al. report on the dose and duration of ectodysplasin signaling required for the maintenance and
73 ermal appendages along the trunk and loss of Ectodysplasin signaling, which prevents dermal appendage
74 pes of skin appendages is guided by prenatal ectodysplasin signaling.
75 elates with the acquisition of autonomy from ectodysplasin stimulation.
76        EDA-A1 and EDA-A2 are two isoforms of ectodysplasin that differ only by an insertion of two am
77                  Mutations in members of the ectodysplasin (TNF-related) signalling pathway, EDA, EDA