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1 f CDH1 and CDH2 expression does not indicate epithelial-mesenchymal transformation.
2 of valves and septa, is a classic example of epithelial-mesenchymal transformation.
3 arrangements that characterize renal tubular epithelial-mesenchymal transformation.
4 ptive myocytes at the time they initiate the epithelial-mesenchymal transformation.
5 the cardiac valves and form by a process of epithelial-mesenchymal transformation.
6 such as TGFbeta3, which are known to promote epithelial-mesenchymal transformation.
7 phenotypic plasticity resembling aspects of epithelial-mesenchymal transformation.
8 ium, although these cells did not undergo an epithelial/mesenchymal transformation.
10 inase A were co-localized to sites of active epithelial-mesenchymal transformation and basal lamina d
11 ymal cells in endocardial cushions following epithelial-mesenchymal transformation and in mature valv
12 7 phosphorylation, and activates programs of epithelial-mesenchymal transformation and metastasis.
13 that neurofibromin normally acts to modulate epithelial-mesenchymal transformation and proliferation
14 on AV cushion endocardial cells to stimulate epithelial-mesenchymal transformation and that TGFbeta m
15 ation, cells in the primitive streak undergo epithelial-mesenchymal transformation and the resulting
18 cription factor Slug/Snai2 is a regulator of epithelial-mesenchymal transformation during development
19 differentiation of cells that have undergone epithelial-mesenchymal transformation during embryogenes
20 3258 promoted PCa cell migration by inducing epithelial mesenchymal transformation (EMT) in vitro as
25 oglin and Alk5 were not directly involved in epithelial-mesenchymal transformation (EMT) in the heart
29 KO hearts that suggest defects in epicardial epithelial-mesenchymal transformation (EMT), a process t
31 programmed process consisting of endocardial epithelial-mesenchymal transformation (EMT), mesenchymal
32 y the SNAI2 gene, has been shown to modulate epithelial-mesenchymal transformation (EMT), the convers
38 t described in developing heart valves as an epithelial mesenchymal transformation, EndMT begins in r
40 type that does not require ERK activation or epithelial-mesenchymal transformation for progression.
41 role for MMPs during a specific stage of the epithelial mesenchymal transformation in the embryonic h
42 matrix glycoprotein ES/ 130 is necessary for epithelial--mesenchymal transformation in the developing
44 treatment degraded beta-catenin and induced epithelial-mesenchymal transformation in cultured mammar
45 ocardial, are required to start and complete epithelial-mesenchymal transformation in cushion-forming
46 e gelatinase A alone is sufficient to induce epithelial-mesenchymal transformation in the absence of
48 tive gelatinase A is absolutely required for epithelial-mesenchymal transformation induced by TGF-bet
53 other causes are explored, including direct epithelial-mesenchymal transformations of the lens epith
55 ignaling, completely abolished the excessive epithelial-mesenchymal transformation seen in the absenc
56 mation of the midline seam are necessary for epithelial-mesenchymal transformation to be triggered.
57 Here we show that epicardial cells undergo epithelial-mesenchymal transformation to become coronary
58 maintained squamous differentiation whereas epithelial-mesenchymal transformation was frequent in no
59 isappear and palates become confluent due to epithelial-mesenchymal transformation, while seams remai