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1  does not require paracrine support from the hypoblast.
2  formation but suppresses development of the hypoblast.
3 th a riboprobe for Crescent, a marker of the hypoblast.
4  only parietal endoderm, a derivative of the hypoblast.
5 the segmental plate, epiblast, mesoderm, and hypoblast.
6 ation development: trophoblast, epiblast and hypoblast.
7 wth factor from the extraembryonic endoderm (hypoblast, a cell layer unique to amniotes) directs the
8                To reevaluate the role of the hypoblast/ADE (lower layer) in patterning the chick ecto
9 ith or without tissue replacement), that the hypoblast/ADE (lower layer) is required and sufficient f
10                         The spreading of the hypoblast also directs cell movements in the adjacent ep
11 e failed to demonstrate a clear role for the hypoblast and anterior definitive endoderm (ADE) in patt
12 in which they are expressed, the pregastrula hypoblast and anterior lateral endoderm, respectively.
13                                              Hypoblast and endoblast (a second lower layer formed und
14 esizing retinoids are expressed in the avian hypoblast and in tissues directly involved in head patte
15 e cardiac-inducing capacities of pregastrula hypoblast and stage 5 anterior lateral endoderm.
16        Finally, the relationship between the hypoblast and the definitive endoderm was defined by fol
17  embryo, has focused on Koller's sickle, the hypoblast and the posterior marginal zone.
18 ose induced by an extraembryonic tissue, the hypoblast, and are normally expressed in the pregastrula
19 d inhibition by Cerberus from the underlying hypoblast, and finally a late inhibition from Lefty emit
20  Epiblasts were separated from the mesoderm, hypoblast, and primitive streak, dissociated to produce
21 yngeal endodermal precursors of the anterior hypoblast, anticipating both temporally and spatially th
22 s, we show that the node, head mesoderm, and hypoblast are interchangeable to begin any of these indu
23 ocysts, implying segregation of epiblast and hypoblast, as in rodent embryos.
24                           We report that the hypoblast can induce a set of very early markers that ar
25 calation at its interface with the displaced hypoblast cells.
26 udies suggest a signaling cascade in which a hypoblast-derived activin/TGFbeta signal is required pri
27 s regulating cardiac myogenesis in avians, a hypoblast-derived signal acting on epiblast and mediated
28              These findings suggest that the hypoblast-derived signal likely acts upstream of propose
29  is underway by stage 3, indicating that the hypoblast-derived signal occurs shortly before specifica
30                       A goosecoid-expressing hypoblast did not form under the induced streak, indicat
31 lium, or in the presence of the mesoderm and hypoblast, did not undergo myogenesis.
32                         In the human embryo, hypoblast differentiation has not previously been charac
33                                 However, the hypoblast does induce transient expression of the early
34                             We show that the hypoblast does not fit the criteria for a head organizer
35 sen's node as a cell monolayer that replaces hypoblast during chick gastrulation.
36 se observations indicate that segregation of hypoblast from the bipotent ICM is dependent on FGF/Erk
37 ising influences of the organiser, the chick hypoblast has been suggested to be the homologue of the
38 rdiac mesodermal precursors in the zebrafish hypoblast immediately following gastrulation.
39 n is strongly expressed in the yolk cell and hypoblast in the early gastrula, just preceding the appe
40 of Hoxa-1 message during gastrulation in the hypoblast in the head region.
41                    However, the formation of hypoblast in the human is apparently not dependent upon
42 l differences in epiblast responsiveness and hypoblast inductiveness restrict appearance of cardiac m
43                 Here we argue that the chick hypoblast is equivalent to the mouse VE, based on fate,
44                        This dual role of the hypoblast is more consistent with the Nieuwkoop model th
45 al plate or a forebrain, suggesting that the hypoblast is not a head organizer and that other signals
46 express ndr1, while ndr2 RNA is found in the hypoblast layer of the shield and later in notochord, pr
47      These cells involute to join the deeper hypoblast layer where they adopt a migratory, mesenchyma
48 iation of cells toward the trophectoderm and hypoblast lineages compared with that for control embryo
49                      After gastrulation, the hypoblast might protect prospective forebrain cells from
50 cells of the gastrula that involute into the hypoblast, motility appears wild-type.
51                         However, neither the hypoblast nor any of these factors or combinations there
52 the absence of axial-expressing cells in the hypoblast of oep mutants.
53                                          The hypoblast possessed broad capacity to induce heart muscl
54              Here we explore the role of the hypoblast (the chick equivalent of the AVE) in the early
55                         One such tissue, the hypoblast (visceral endoderm in mouse), acquired a role
56 eriments demonstrated that a signal from the hypoblast was required to induce cardiac myogenesis in t

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