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1 act myocardium, interventricular septum, and endocardial cushion.
2 esicle, prevertebral bodies (notochord), and endocardial cushion.
3 s aberrant Wnt/beta-catenin signaling in the endocardial cushions.
4 llular matrix, called cardiac jelly, to form endocardial cushions.
5  delay in the formation of the outflow tract endocardial cushions.
6 lure of fusion" between the atrioventricular endocardial cushions.
7 minantly the product of the atrioventricular endocardial cushions.
8 nchyme that characterizes development of the endocardial cushions.
9 t (OFT) but not atrioventricular canal (AVC) endocardial cushions.
10 s develop from rudimentary structures termed endocardial cushions.
11 n amorphic cellular nodules within their OFT endocardial cushions.
12 of mutant Shp2 (Q79R-Shp2) in the developing endocardial cushions.
13 s of invagination, rather than first forming endocardial cushions.
14  that relies on the successful remodeling of endocardial cushions.
15 ressing GATA4 activity within the developing endocardial cushions.
16 nt embryos are thicker myocardium and larger endocardial cushions.
17 xpressing cells in the cardiac outflow tract endocardial cushions.
18 rder to elucidate its function in developing endocardial cushions.
19 erate the progenitor cells that populate the endocardial cushions.
20 sence of hyaluronan (HA), cardiac jelly, and endocardial cushions, a loss of vascular integrity, and
21 nt endocardium was associated with acellular endocardial cushions, absent epithelial-to-mesenchymal t
22 sia of the right ventricle, (3) overabundant endocardial cushions accompanied by ventricular septal d
23 ematopoietic progenitors are enriched in the endocardial cushion and contribute, in a Nkx2-5-dependen
24  morphogenesis by enhancing apoptosis in the endocardial cushions and (2) promote aortic sac malforma
25 ression of Wnt-9a in ovo results in enlarged endocardial cushions and AV inlet obstruction.
26 of the rock gene were used to treat cultured endocardial cushions and cells.
27 e cardiovascular abnormalities involving the endocardial cushions and myocardium.
28  and Tbx5 are co-expressed in the developing endocardial cushions and myocardium.
29 ble heterozygous embryos having hypocellular endocardial cushions and perimembranous and muscular VSD
30 endoderm, outflow tract and atrioventricular endocardial cushions and post-migratory neural crest der
31 chymal transition that supplies cells to the endocardial cushions and repositions cardiac neural cres
32 ricular septum is equated with fusion of the endocardial cushions and that failure of fusion can expl
33  is essential for proper formation of the AV endocardial cushions and the cardiac outflow tract.
34 P expression is specific for the myocardium; endocardial cushions and valves exhibit only background
35  factor Tbx20 is expressed in the developing endocardial cushions and valves throughout heart develop
36 e specialized cells, unlike that of adjacent endocardial cushions and valves, is not dependent on blo
37  displayed defects in the left ventricle and endocardial cushions, and exhibited dysregulated ventric
38 ural crest, intestine, pancreas, testis, and endocardial cushions, and plays a crucial role in cell p
39 ing, absence of mesenchymal cells within the endocardial cushions, and selective hypoplasia of the RV
40  primary atrial septum, the atrioventricular endocardial cushions, and the cap of mesenchyme on the s
41 he endocardium also resulted in hypocellular endocardial cushions, and we observed VSDs in rare E15.5
42                                              Endocardial cushions are critical to maintain unidirecti
43                        In Sox9-null mutants, endocardial cushions are markedly hypoplastic.
44                                              Endocardial cushions are precursors of mature atrioventr
45                                              Endocardial cushions are the precursors of the cardiac v
46 n the endocardium and its derivatives in the endocardial cushions are unknown.
47  of TGFbeta2, but not TGFbeta3, within mouse endocardial cushions at a time coincident with transform
48    In multiple assays of cells from prefused endocardial cushions, BMP2 is sufficient to activate Sma
49 fail to express ErbB3, which is required for endocardial cushion cell differentiation and proliferati
50 ushion cell proliferation as well as promote endocardial cushion cell migration.
51     Previously, Tbx20 has been implicated in endocardial cushion cell proliferation and differentiati
52 hese studies indicate that Twist1 can induce endocardial cushion cell proliferation as well as promot
53 a2 is expressed and obligatory for mammalian endocardial cushion cell transformation.
54  migration and repressing differentiation in endocardial cushion cells during embryonic development.
55 xperiments were performed in primary chicken endocardial cushion cells in order to elucidate its role
56 esenchymal cell types, the role of Twist1 in endocardial cushion cells is unknown.
57 t provide a suitable migratory substrate for endocardial cushion cells unless MMP-2 and MT-MMP are ac
58 nt resulted in increased Tbx20 expression in endocardial cushion cells, and loss of Tbx20 led to incr
59 ibited with Tbx20-specific siRNA in cultured endocardial cushion cells.
60 sly reported associations: phenylephrine and endocardial cushion defect (odds ratio = 8.0; 95% confid
61  interval): cyanotic CHD (6.44, 3.95-10.50), endocardial cushion defects (5.47, 2.89-10.36), and left
62                                              Endocardial cushion defects were found in 3 out of 39 he
63 truncus arteriosus, transposition complexes, endocardial cushion defects, and univentricular hearts.
64 eptal defects, and left-sided malformations (endocardial cushion defects, hypoplastic left heart, and
65 uble-outlet right ventricle (DORV), TOF, and endocardial cushion defects.
66 cteristic heart valve lesions resulting from endocardial cushion defects.
67  cardiovascular lineages and is required for endocardial cushion development and embryonic viability,
68 elates second heart field, neural crest, and endocardial cushion development and suggests that pertur
69 ination of the diverse signals that regulate endocardial cushion development and valve elongation.
70   A collagen gel assay, long used to examine endocardial cushion development in avian models, is now
71  this defect, we examined the later steps in endocardial cushion development including mesenchymal ce
72 nt of VSDs through their additive effects on endocardial cushion development with Sox7+/-;Wnt4+/- dou
73 trioventricular septal defects have abnormal endocardial cushion development with the delayed appeara
74 by beta-catenin has been implicated in early endocardial cushion development, but its roles in later
75 ole Rho GTPase-associated kinases (ROCKs) in endocardial cushion development.
76 cession of molecular steps in the pathway of endocardial cushion development.
77 al cell differentiation and migration during endocardial cushion development.
78 cts on GATA4/SMAD4 interactions required for endocardial cushion development.
79 y disrupting a signaling cascade involved in endocardial cushion development.
80 hion cells in order to elucidate its role in endocardial cushion development.
81 EKK3 as a critical signaling molecule during endocardial cushion development.
82 l appropriately, suggesting a defect late in endocardial cushion development.
83 e effects of wild-type Shp2 and Q79R-Shp2 on endocardial cushion development.
84 iginate from errors in atrioventricular (AV) endocardial cushion development.
85 in, mouse embryo hearts develop overabundant endocardial cushions due to hyperproliferation and lack
86 f the rock1 and rock2 genes was found in the endocardial cushions during development.
87 n mesenchymal valve precursor populations in endocardial cushions during embryonic development.
88  (AV) septal defects resulting from aberrant endocardial cushion (EC) formation are observed at incre
89 d regurgitation in a dilated heart and lacks endocardial cushion (EC) formation.
90                Cardiac valves originate from endocardial cushions (EC) formed by endothelial-to-mesen
91  abutting myocardium and endocardium to form endocardial cushions (EC) in a process known as epitheli
92 es develop from undifferentiated mesenchymal endocardial cushions (EC), and activated interstitial ce
93 ctures derived from mesenchymal cells of the endocardial cushions (ECs) are composed of highly organi
94  proceeds through coordinated steps by which endocardial cushions (ECs) form thin, elongated and stra
95              During valvulogenesis, globular endocardial cushions elongate and remodel into highly or
96 KK3 integrates signaling cascades activating endocardial cushion EMT.
97 cies variations for avian and mouse cultured endocardial cushion explants.
98 in protein, which marks mesenchymal cells in endocardial cushions following epithelial-mesenchymal tr
99 -mesenchymal transition in explant assays of endocardial cushions following Notch inhibition within s
100  opportunity to identify a gene required for endocardial cushion formation and for specification or m
101 valuate the molecular requirements of normal endocardial cushion formation and the segmental interact
102 tation, cardiac myocyte differentiation, and endocardial cushion formation are preprogrammed in the p
103 itical non-redundant role in early phases of endocardial cushion formation during cardiac morphogenes
104 3 in vessel remodeling, vessel integrity and endocardial cushion formation during the development of
105 ayed defects in atrioventricular canal (AVC) endocardial cushion formation in the heart.
106 secting regulatory pathways are required for endocardial cushion formation, valve progenitor cell pro
107 cardial projections accompanied by defective endocardial cushion formation.
108  heart is consistent with a role for Slug in endocardial cushion formation.
109 endothelial-to-mesenchymal transition during endocardial cushion formation.
110               Developmental abnormalities in endocardial cushions frequently contribute to congenital
111  dextrodorsal outflow ridge and the superior endocardial cushion, fusion with the inferior margins of
112 , secretory and transcriptional events drive endocardial cushion growth and remodeling into thin fibr
113 protein at comparable levels did not enhance endocardial cushion growth or alter the morphology of th
114                                        Their endocardial cushions have increased Erk activation, but
115 heart tube fails to develop normally and the endocardial cushions in both the conus and the atriovent
116            We have previously shown that the endocardial cushions in FOG-2 deficient mice are hyperpl
117              The dramatic enlargement of the endocardial cushions in the absence of Hhex is due to de
118                             The formation of endocardial cushions in the atrioventricular (AV) canal
119 ation (EMT) occurs during the development of endocardial cushions in the atrioventricular (AV) canal
120 rmation occurs during the development of the endocardial cushions in the atrioventricular (AV) canal
121 f the single heart tube fail to form and the endocardial cushions in the atrioventricular and conus/t
122 mutant embryos showed significantly enlarged endocardial cushions in the atrioventricular canal and i
123  throughout the fibrous cardiac skeleton and endocardial cushions in the developing heart but is abse
124                           Development of the endocardial cushions in the heart involves cell migratio
125 arise from improper growth and remodeling of endocardial cushions into leaflets.
126           NFATc1 is necessary for remodeling endocardial cushions into mature heart valve leaflets an
127 lopment of the cardiac atrioventricular (AV) endocardial cushions is essential for proper ventricular
128                    Fusion of the sternum and endocardial cushions is impaired in the mutant mice asso
129 teoglycan-rich extracellular matrix (ECM) of endocardial cushions is replaced by a specialized and st
130 ch Tbx20 regulates the Wnt pathway to direct endocardial cushion maturation and valve elongation, and
131 evidence for Wnt signaling as a regulator of endocardial cushion maturation as well as valve leaflet
132 nt for myocardial segmental regulation of AV endocardial cushion mesenchymal cell formation in mice.
133 ively affect RV development or generation of endocardial cushion mesenchyme but did result in marked
134  mouse heart, ECE-2 mRNA is expressed in the endocardial cushion mesenchyme from embyronic day (E) 12
135 ute at least in part to the formation of the endocardial cushion mesenchyme.
136 ments for TGFbeta2 and TGFbeta3 during mouse endocardial cushion morphogenesis.
137 ar septal defects can result from incomplete endocardial cushion morphogenesis.
138 an is particularly strongly expressed in the endocardial cushions of the atrioventricular and outflow
139 ) and the secreted Wnt antagonist Frzb in AV endocardial cushions of the developing chicken heart.
140 ly expressed in myocardial cells, and not in endocardial cushion or outflow tract tissues.
141 d dominant negative MEK-1 prevented enhanced endocardial cushion outgrowth, whereas expression of con
142      Deletion of ERK1 completely rescued the endocardial cushion phenotype, whereas ERK2 protein redu
143                                 Formation of endocardial cushions, primordia of valves and septa, is
144 to the proximal aspects of the outflow tract endocardial cushions, resulting in the failure of membra
145 hereas ERK2 protein reduction did not affect endocardial cushion size.
146                    Cardiac valves arise from endocardial cushions, specialized regions of the develop
147 ic forces, but the interrelationship between endocardial cushion structure and the mechanics of atrio
148  highly expressed in the conotruncus and the endocardial cushion, structures that give rise to the af
149 quired for the successful development of the endocardial cushion swellings and the embryonic heart se
150 ith ECs undergoing EndMT to give rise to the endocardial cushions that ultimately develop into the ca
151 hat neural crest contribution to the outflow endocardial cushions (the precursors of the semilunar va
152  de novo source of tissue macrophages in the endocardial cushion, the primordium of the cardiac valve
153 al, and thus play a key role in formation of endocardial cushions, the detailed signaling mechanisms
154 ellings of extracellular matrix known as the endocardial cushions, the endothelial lining of the hear
155      These cardiac structures arise from the endocardial cushions through dynamic interactions betwee
156  embryonic day 12.5, when fusion between the endocardial cushion tissue and the atrial and ventricula
157 rimarily in the myocardium, endocardium, and endocardial cushion tissue.
158 ur-chambered organ requires the formation of endocardial cushion tissue.
159 ell proliferation and differentiation in the endocardial cushion tissue.
160 l cells into the extracellular matrix of the endocardial cushion tissues.
161 We found no difference in the ability of the endocardial cushions to undergo myocardialization or in
162 te a function for Smad6 in the regulation of endocardial cushion transformation.
163           Atrioventricular and outflow tract endocardial cushions were excised from chick embryos, in
164 enchymal transition within the outflow tract endocardial cushions were observed.
165 ells undergoes EMT to form the mesenchyme of endocardial cushions, which function as primordia for de
166 nstrate that these embryos have hypocellular endocardial cushions with severely reduced numbers of me
167 sequent malalignment of the atrioventricular endocardial cushions with the proximal outflow cushions.
168              These structures arise from the endocardial cushions within the atrioventricular canal (

 
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