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1 canonical Wnt pathway at different stages of valve formation.
2 to defective lymphatic vessel patterning and valve formation.
3 ort cardiac jelly deposition at the onset of valve formation.
4 se in integrin alpha9 expression at sites of valve formation.
5 cellular matrix organization, key factors in valve formation.
6 tion protein Cx37 are required for lymphatic valve formation.
7 ed by the morphogenetic events that initiate valve formation.
8 Sema3A-Nrp1-PlexinA1 signaling in lymphatic valve formation.
9 formation, which is essential to subsequent valve formation.
10 aphorin3A (Sema3A) plays a role in lymphatic valve formation.
11 normal thoracic duct development, including valve formation.
12 for the specification of the AV boundary and valve formation.
13 sed OFT mesenchyme with failure of semilunar valve formation.
14 icular cushion (AVC) is an important step in valve formation.
15 ndocardium during a critical window of heart valve formation.
16 eoclast RANKL function are not shared during valve formation.
17 ocardial expression of RANKL and Ctsk during valve formation.
18 ng a previously unappreciated step during AV valve formation.
19 of the developing heart, a critical step in valve formation.
20 c field to initiate and perpetuate embryonic valve formation.
21 l gene mutations are known to affect cardiac valve formation.
22 yocardium underlying the site of prospective valve formation.
23 ird chamber, diminished looping and impaired valve formation.
24 ment of the AVC and subsequent septation and valve formation.
25 ich are deficient in the initiation of heart valve formation.
26 xpression in lymphocytes and control cardiac valve formation.
27 her multiple TGFbeta isoforms participate in valve formation.
28 uction processes required for normal cardiac valve formation.
29 stress (WSS), such as are found at sites of valve formation.
30 uce underlying endocardial cells to initiate valve formation.
31 phatic mTORC1 in vivo promoted supernumerary valve formation.
32 cardiac morphogenesis as well as in cardiac valve formation.
33 generate positional information and control valve formation.
34 e of mechanical forces and blood flow during valve formation.
35 lymphatic sprouting, migration and lymphatic valve formation.
36 embryos exhibited abnormal atrioventricular valve formation, a phenotype never seen in ECE-1 single
37 ad increased crypt presence, abnormal mitral valve formation and alterations in the compaction proces
38 These opposing defects are evident before valve formation and are the result of distinct gene misr
39 whose inactivation leads to bicuspid aortic valve formation and calcific aortic valve disease, but k
40 advances in the molecular genetics of aortic valve formation and calcification have recently been ide
42 utant enzymes were unable to restore cardiac valve formation and could only partially rescue cardiac
45 . further define the mechanisms of lymphatic valve formation and implicate oscillatory shear stress i
46 es a unique morphogenetic program during OFT valve formation and places Piezo as a central modulator
47 gata6 specifically impacts atrioventricular valve formation and recruitment of epicardium, with a pr
48 h signaling is required for proper lymphatic valve formation and regulates integrin alpha9 and fibron
49 llular processes and molecules that regulate valve formation and remodeling is required to develop ef
50 levant target to stimulate de novo lymphatic valve formation and rescue defective valves in congenita
52 flow plays in fibrous ECM expression during valve formation and to test the underlying cellular mech
56 ults suggest that FOG-2 functions in cardiac valve formation as an attenuator of EMT by repressing GA
57 cardial Klf2 deficiency results in defective valve formation associated with loss of Wnt9b expression
58 To gain mechanistic understanding of cardiac valve formation at single-cell resolution and insights i
59 endocardial cells and is required for normal valve formation, but its role in the fate of valve endoc
60 ing pathway is crucial for primitive cardiac valve formation by epithelial-mesenchymal transition, an
61 tion factor, Foxo1, that repressed lymphatic valve formation by inhibiting the expression of valve-fo
62 Using a zebrafish model of defective heart valve formation caused by morpholino oligonucleotide kno
65 ion of several genes known to be involved in valve formation (Foxc2, Connexin37, EphrinB2, and Neurop
66 VEGF) signaling is one pathway implicated in valve formation, however its specific spatial and tempor
68 alone or in combination result in defective valve formation in lymphatic collecting vessels, lymphed
70 ablation of Foxo1 in LECs induced additional valve formation in postnatal and adult mice in multiple
78 f collecting lymphatic vessels and lymphatic valve formation, uncovering an important role for fluid
79 terations in cardiomyocyte maturation, heart valve formation, vascular development, skeletal muscle d
80 Sema3A is selectively required for lymphatic valve formation, via interaction with Nrp1 and PlexinA1.
82 ema3a(-/-) mice exhibit defects in lymphatic valve formation, which are not due to abnormal lymphatic
83 entrains sequential chamber contraction; and valve formation, which prevents retrograde fluid movemen
84 ial interactions coordinate the processes of valve formation with establishment of conduction delay.