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1  is unique to eutheria, suggesting a role in placental development.
2 GFBP-1 overexpression has a marked effect on placental development.
3 ized by shallow uterine invasion and altered placental development.
4 r fusion of the chorion and allantois during placental development.
5 yonic lethality because of severe defects in placental development.
6  complexes, contributes to the regulation of placental development.
7 t Rtl1 is the main target gene of miR-127 in placental development.
8 rine growth restriction (IUGR), and impaired placental development.
9 on-surgical embryo transfer alone can impact placental development.
10 e embryo and can substantially contribute to placental development.
11 viral antibodies in protecting and restoring placental development.
12  play a central role in our understanding of placental development.
13  of a key growth factor regulating fetal and placental development.
14 epare the uterus for embryo implantation and placental development.
15 the paternal genome has a major influence on placental development.
16 he extensive evolutionary diversification of placental development.
17 , a factor associated with CS regulation and placental development.
18 through early gestation (to E8.5) to support placental development.
19 st stem cells (TSCs) are used to study mouse placental development.
20  receptor gamma (PPARgamma) is essential for placental development.
21 ch is exacerbated in diabetes and may affect placental development.
22 ed for proper branching morphogenesis during placental development.
23 l and previously undefined role for FoxO1 in placental development.
24 ose the ectoplacental cavity, and incomplete placental development.
25  Thus, Rb and E2f4 play cooperative roles in placental development.
26 to endothelial cell activation and impairing placental development.
27  may play important roles in early stages of placental development.
28 f the angiogenic factors required for normal placental development.
29  extracellular proteolytic activities during placental development.
30 tenance of proliferating trophoblasts during placental development.
31 e villous trophoblast differentiation during placental development.
32 ent anti-angiogenic molecule), and defective placental development.
33 9/MKP4 performs an essential function during placental development.
34 ed that ARNT function is required for murine placental development.
35 elopment and chorion-allantois fusion during placental development.
36 nstead plays a physiological role related to placental development.
37  receptor gamma (PPARgamma) is essential for placental development.
38 have reached the embryos because of abnormal placental development; abnormal placentas were observed
39 approach, demonstrating an essential role in placental development and a non-essential role in embryo
40 e serine proteases and is required for mouse placental development and embryo survival.
41  by unregulated matriptase activity, as both placental development and embryonic survival in HAI2-def
42 placentas, which encoded known regulators of placental development and epithelial morphogenesis.
43 tivation of Rb and E2f3 in TS cells restored placental development and extended the life of embryos t
44 le sFlt-1 in monocytes that causes defective placental development and fetal death in DBA/2-mated CBA
45 Flt-1 release in monocytes causing defective placental development and fetal death.
46 derstand the role of placental imprinting in placental development and fetal growth, we examined conc
47 sed in the placenta, is essential for normal placental development and fetal growth.
48 he parental chromosomes, and are crucial for placental development and fetal growth.
49 herefore potentially important in regulating placental development and fetal growth.
50 t AIB3 is required for PPARgamma function in placental development and for normal heart development.
51 stem cells (TSCs) are key factors for proper placental development and function and, in turn, for app
52               Intrauterine infection affects placental development and function, and subsequently may
53 nalling molecules for angiogenesis and hence placental development and function.
54            Congenital HCMV infection impairs placental development and functions and should be consid
55                                              Placental development and genomic imprinting coevolved w
56 (DUSP9/MKP-4) plays an essential role during placental development and is one of a subfamily of three
57 or answering questions of both embryonic and placental development and providing therapeutic proteins
58 pressed PRL family member, leads to impaired placental development and retarded growth at both embryo
59 or associated with human-specific pattern of placental development and should be taken in considerati
60                                      Optimal placental development and the ability of the placenta to
61  retinoic acid-responsive gene implicated in placental development and the progression of human breas
62                      However, restoration of placental development and the rescue of IUGR by tetraplo
63 nic lethality that was secondary to impaired placental development and was associated with very low p
64        Homeobox genes regulate embryonic and placental development, and are widely expressed in the h
65 condition of afibrinogenemia retarded embryo-placental development, and consistently led to abortion
66  by fetal loss, growth restriction, abnormal placental development, and defects in maternal decidual
67 ntial for extraembryonic cell proliferation, placental development, and fetal viability.
68 es in mice, cause defects in trophoblast and placental development, and/or affect conceptus survival
69 ession, we demonstrate that fetal growth and placental development are seriously compromised by this
70                       Studies of early human placental development are severely hampered by the lack
71 essed in the spongiotrophoblast, late in rat placental development bear Asn-linked oligosaccharides t
72 egulation by PPARgamma contributes to normal placental development but also that the essential functi
73 our data show that pRB and E2F4 cooperate in placental development, but play largely non-overlapping
74 and efficient branching morphogenesis during placental development, but, unlike its Drosophila orthol
75 c cues from within the TSC niche to regulate placental development by modulating the cellular cytoske
76                                        Human placental development combines elements of tumorigenesis
77                Reduced MMP activity early in placental development could impair cytotrophoblast remod
78 clampsia, deficient HB-EGF signalling during placental development could impair trophoblast survival,
79                                 During human placental development, cytotrophoblast stem cells differ
80                                     Although placental development depends on careful coordination of
81 vides a unique opportunity to examine normal placental development directly, and should provide the b
82  Perturbed trophoblast function and impaired placental development early in pregnancy are key feature
83 est that hPSCs are a valuable model of human placental development, enabling us to recapitulate proce
84 on of the fetus (IUGR) results from impaired placental development, frequently associated with matern
85 ltiple occasions during evolution to improve placental development in a process of convergent evoluti
86 d has been shown to have roles in foetal and placental development in animal models.
87 s markedly enhanced angiogenic responses and placental development in DC expanded IL-10(-/-) dams.
88  signaling is central to the early stages of placental development in mammals.
89 ing transcription factor required for normal placental development in mice.
90 t with a requirement for HIF activity during placental development in utero, TSCs derived from HIF-nu
91 gest that LIMK1 activity helps promote human placental development in utero.
92                     The 'insults' that alter placental development include hypoxia and abnormal mater
93 f Rb null mice despite persistent defects in placental development, indicating that deregulated E2f-2
94 s embryonic development disrupted, but mouse placental development is also grossly altered with the l
95                                      Healthy placental development is essential for reproductive succ
96 d that the essential function of ESX1 during placental development is mediated by its ability to coup
97                                              Placental development is profoundly influenced by oxygen
98 rdingly, Arid3a(-/-) mouse post-implantation placental development is severely impaired, resulting in
99 vator MED1, which plays an important role in placental development, is a target for miR-205.
100 nd DHA proportions in cord blood; therefore, placental development may be an important variable in de
101            The influence of these factors on placental development needs further investigation.
102                                        Early placental development occurs in a predominantly low oxyg
103 itative RT-PCR analysis of genes involved in placental development revealed significant attenuation o
104 egulation of a network of genes required for placental development, suggesting a central role for the
105 or (EGFR) exhibit strain-specific defects in placental development that can result in mid-gestational
106 ssential X-chromosome-imprinted regulator of placental development that influences fetal growth, and
107                           During early human placental development, the conceptus attaches itself to
108 ify Arid3a as a critical regulator of TE and placental development through execution of the commitmen
109 hat treatment of the mother with LMWH allows placental development to proceed and affords significant
110 gration in tumor progression (in addition to placental development), we examined the affect of cultur
111  level of EGFR signaling required for normal placental development, we characterized congenic strains
112                    To understand its role in placental development, we established a novel Egfl7 knoc
113 r reversal can be induced at other stages of placental development, we examined earlier placental spe
114  role of bHLH transcription factors in human placental development, we first characterized Id express
115 ning cell columns during the early stages of placental development, when the architecture of the basa
116            Such fusion is essential to human placental development, where interactions between tropho
117             In this review, we will overview placental development with a focus on how villous struct
118 ase kinase kinase MEKK4 exhibit dysregulated placental development with increased trophoblast invasio
119        These results make PLAC1 a marker for placental development, with a possible role in the estab
120 of implantation and leading to retarded feto-placental development without apparent defects in decidu

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