ライフサイエンスコーパス: placental development

1 to endothelial cell activation and impairing placental development.

2 f the angiogenic factors required for normal placental development.

3 extracellular proteolytic activities during placental development.

4 tenance of proliferating trophoblasts during placental development.

5 ent anti-angiogenic molecule), and defective placental development.

6 9/MKP4 performs an essential function during placental development.

7 ed that ARNT function is required for murine placental development.

8 elopment and chorion-allantois fusion during placental development.

9 nstead plays a physiological role related to placental development.

10 GFBP-1 overexpression has a marked effect on placental development.

11 ized by shallow uterine invasion and altered placental development.

12 r fusion of the chorion and allantois during placental development.

13 yonic lethality because of severe defects in placental development.

14 e been of limited use in understanding human placental development.

15 in vitro models for normal and pathological placental development.

16 isruption of Prl7b1 did not adversely affect placental development.

17 e it is essential for trophoblast fusion and placental development.

18 ast structures that underlie early events in placental development.

19 pproach to modeling viral infection early in placental development.

20 age differentiation, a fundamental aspect of placental development.

21 and exogenous cannabinoids can affect human placental development.

22 ggest that mosaicism is a typical feature of placental development.

23 blast cells into syncytiotrophoblasts during placental development.

24 uccessful implantation of the blastocyst and placental development.

25 llous trophoblast (EVT) cell function during placental development.

26 cRNA-seq) from sheep and cattle during early placental development.

27 hts into evolutionary adaptations underlying placental development.

28 MAP3K4, TRAF4, and HDAC6 associations during placental development.

29 tools to further the understanding of human placental development.

30 ion of the uterine vasculature to facilitate placental development.

31 n, CiPSC reprogramming, spermatogenesis, and placental development.

32 e examined the potential role of renalase in placental development.

33 phoblast function and is required for normal placental development.

34 eticulum (ER) stress, which is necessary for placental development.

35 visualize and study early and late stages of placental development.

36 is unique to eutheria, suggesting a role in placental development.

37 of a key growth factor regulating fetal and placental development.

38 through early gestation (to E8.5) to support placental development.

39 may play important roles in early stages of placental development.

40 on fetal development, neonatal outcomes, and placental development.

41 e villous trophoblast differentiation during placental development.

42 complexes, contributes to the regulation of placental development.

43 t Rtl1 is the main target gene of miR-127 in placental development.

44 rine growth restriction (IUGR), and impaired placental development.

45 on-surgical embryo transfer alone can impact placental development.

46 e embryo and can substantially contribute to placental development.

47 viral antibodies in protecting and restoring placental development.

48 hing is known about NPFF-NPFFR2 functions in placental development.

49 play a central role in our understanding of placental development.

50 epare the uterus for embryo implantation and placental development.

51 the paternal genome has a major influence on placental development.

52 he extensive evolutionary diversification of placental development.

53 , a factor associated with CS regulation and placental development.

54 st stem cells (TSCs) are used to study mouse placental development.

55 receptor gamma (PPARgamma) is essential for placental development.

56 ch is exacerbated in diabetes and may affect placental development.

57 ed for proper branching morphogenesis during placental development.

58 l and previously undefined role for FoxO1 in placental development.

59 ose the ectoplacental cavity, and incomplete placental development.

60 Thus, Rb and E2f4 play cooperative roles in placental development.

61 have reached the embryos because of abnormal placental development; abnormal placentas were observed

62 early gestational diabetes can affect early placental development, affecting maternal metabolism and

63 10alpha resulted in viable fetuses, abnormal placental development and a failure of the placenta to t

64 approach, demonstrating an essential role in placental development and a non-essential role in embryo

65 s that will help deepen our understanding of placental development and associated disorders of pregna

66 ole in cell fate decisions that govern human placental development and disease.

67 dissecting the molecular regulation of human placental development and diseases.

68 e serine proteases and is required for mouse placental development and embryo survival.

69 by unregulated matriptase activity, as both placental development and embryonic survival in HAI2-def

70 placentas, which encoded known regulators of placental development and epithelial morphogenesis.

71 tivation of Rb and E2f3 in TS cells restored placental development and extended the life of embryos t

72 le sFlt-1 in monocytes that causes defective placental development and fetal death in DBA/2-mated CBA

73 Flt-1 release in monocytes causing defective placental development and fetal death.

74 we have conducted a longitudinal analysis of placental development and fetal growth using a mouse mod

75 ficant gene signaling pathways that regulate placental development and fetal growth, including Wnt, H

76 derstand the role of placental imprinting in placental development and fetal growth, we examined conc

77 he parental chromosomes, and are crucial for placental development and fetal growth.

78 herefore potentially important in regulating placental development and fetal growth.

79 sed in the placenta, is essential for normal placental development and fetal growth.

80 t AIB3 is required for PPARgamma function in placental development and for normal heart development.

81 stem cells (TSCs) are key factors for proper placental development and function and, in turn, for app

82 s an experimental model to investigate human placental development and function as well as interactio

83 Opioids affect placental development and function in animal models, but

84 Intrauterine infection affects placental development and function, and subsequently may

85 ingolipids have been implicated in mammalian placental development and function, but their regulation

86 ogenesis is principally required to regulate placental development and function, which in turn is cri

87 s for gaining insights into these aspects of placental development and function, with recent studies

88 n the placenta and how infection compromises placental development and function.

89 aluable in vitro system to investigate human placental development and function.

90 suggesting a potential role for renalase in placental development and function.

91 dels provide limited information about human placental development and function.

92 ight into the regulatory networks that shape placental development and function.

93 d mortality, and may be a result of abnormal placental development and function.

94 regnancy is critically dependent upon proper placental development and function.

95 nalling molecules for angiogenesis and hence placental development and function.

96 Congenital HCMV infection impairs placental development and functions and should be consid

97 Placental development and genomic imprinting coevolved w

98 l growth restriction arise from disorders of placental development and have some shared mechanistic f

99 f-1alpha as a critical molecular mediator of placental development and indicate that prolonged expres

100 (DUSP9/MKP-4) plays an essential role during placental development and is one of a subfamily of three

101 n placental inflammation leads to inadequate placental development and loss of barrier function.

102 Among the molecules supporting placental development and maternal tolerance, the famili

103 ecting placental weight, with connections to placental development and morphology, and transport of a

104 ing of the mechanisms underlying early human placental development and placenta-associated pregnancy

105 d fetal growth restriction, and thus improve placental development and pregnancy outcomes.

106 s as a blueprint for future studies on early placental development and pregnancy.

107 signaling participates in the regulation of placental development and protection against LPS-induced

108 or answering questions of both embryonic and placental development and providing therapeutic proteins

109 ll developmental potential and causes latent placental development and reduced fetal growth.

110 pressed PRL family member, leads to impaired placental development and retarded growth at both embryo

111 or associated with human-specific pattern of placental development and should be taken in considerati

112 specialised functions dedicated to achieving placental development and successful reproduction.

113 role for VE-cadherin in trophoblasts during placental development and suggest that endothelial prote

114 Optimal placental development and the ability of the placenta to

115 retinoic acid-responsive gene implicated in placental development and the progression of human breas

116 However, restoration of placental development and the rescue of IUGR by tetraplo

117 ide an important in vitro tool to understand placental development and the transplacental passage of

118 nic lethality that was secondary to impaired placental development and was associated with very low p

119 e, intrauterine growth restriction, impaired placental development, and a thickened Reichert's membra

120 Homeobox genes regulate embryonic and placental development, and are widely expressed in the h

121 condition of afibrinogenemia retarded embryo-placental development, and consistently led to abortion

122 by fetal loss, growth restriction, abnormal placental development, and defects in maternal decidual

123 ntial for extraembryonic cell proliferation, placental development, and fetal viability.

124 Myc is a key regulator of polyploidy and placental development, and is required for multiple roun

125 es in mice, cause defects in trophoblast and placental development, and/or affect conceptus survival

126 ession, we demonstrate that fetal growth and placental development are seriously compromised by this

127 Studies of early human placental development are severely hampered by the lack

128 These data profile placental development at an unprecedented resolution, pr

129 essed in the spongiotrophoblast, late in rat placental development bear Asn-linked oligosaccharides t

130 egulation by PPARgamma contributes to normal placental development but also that the essential functi

131 tal villi provide a 3D model system of human placental development, but access to first-trimester tis

132 our data show that pRB and E2F4 cooperate in placental development, but play largely non-overlapping

133 es a scalable in vitro model system of human placental development, but the molecular regulators of h

134 and efficient branching morphogenesis during placental development, but, unlike its Drosophila orthol

135 c cues from within the TSC niche to regulate placental development by modulating the cellular cytoske

136 However, the mechanisms by which altered placental development can lead to congenital heart disea

137 s and to understand the relationship between placental development, CHD, and its neurodevelopmental i

138 Human placental development combines elements of tumorigenesis

139 nylation undergoes dynamic regulation during placental development, corresponding to gene expression

140 Reduced MMP activity early in placental development could impair cytotrophoblast remod

141 clampsia, deficient HB-EGF signalling during placental development could impair trophoblast survival,

142 During human placental development, cytotrophoblast stem cells differ

143 Although placental development depends on careful coordination of

144 vides a unique opportunity to examine normal placental development directly, and should provide the b

145 microscopy, we were able to investigate the placental development during the entire mouse pregnancy,

146 Perturbed trophoblast function and impaired placental development early in pregnancy are key feature

147 est that hPSCs are a valuable model of human placental development, enabling us to recapitulate proce

148 face, opening new avenues for discoveries in placental development, evolution, and health across mamm

149 al role in regulating trophoblast fusion and placental development, expanding our understanding of PI

150 on of the fetus (IUGR) results from impaired placental development, frequently associated with matern

151 ve and poised enhancers were associated with placental development genes, though only active enhancer

152 TGF-beta signaling plays a key role in human placental development governing the differentiation prog

153 understanding the mechanisms driving porcine placental development has been limited by the lack of in

154 gulate genes with known importance for human placental development [high-mobility group AT-hook 1 (HM

155 ltiple occasions during evolution to improve placental development in a process of convergent evoluti

156 d has been shown to have roles in foetal and placental development in animal models.

157 s markedly enhanced angiogenic responses and placental development in DC expanded IL-10(-/-) dams.

158 ysiology of the trophoblast cell lineage and placental development in eutherians.

159 signaling is central to the early stages of placental development in mammals.

160 ing transcription factor required for normal placental development in mice.

161 ow that the maternal gut microbiota supports placental development in mice.

162 t with a requirement for HIF activity during placental development in utero, TSCs derived from HIF-nu

163 gest that LIMK1 activity helps promote human placental development in utero.

164 ve emerged as a powerful tool to model early placental development in vitro.

165 lpha, specifically in trophoblasts, on mouse placental development in vivo.

166 The 'insults' that alter placental development include hypoxia and abnormal mater

167 However, new tools for studying human placental development, including 3D organoids, stem cell

168 fferentiation disrupts pathways critical for placental development, including extracellular matrix or

169 f Rb null mice despite persistent defects in placental development, indicating that deregulated E2f-2

170 Placental development involves coordinated expansion and

171 s embryonic development disrupted, but mouse placental development is also grossly altered with the l

172 These findings add to existing evidence that placental development is altered in CHD.

173 is crucial for healthy fetal development and placental development is altered in pregnancy when the f

174 Healthy placental development is essential for reproductive succ

175 ng a cell-type level understanding of normal placental development is essential for uncovering how th

176 reveal that human placental development is itself nutrient-sensitive.

177 d that the essential function of ESX1 during placental development is mediated by its ability to coup

178 Abnormal placental development is one of the main etiological fac

179 Placental development is profoundly influenced by oxygen

180 rdingly, Arid3a(-/-) mouse post-implantation placental development is severely impaired, resulting in

181 A critical step of placental development is the fusion of trophoblast cells

182 vator MED1, which plays an important role in placental development, is a target for miR-205.

183 nd DHA proportions in cord blood; therefore, placental development may be an important variable in de

184 RNAs within a microRNA cluster important for placental development mimic viral molecular patterns to

185 The influence of these factors on placental development needs further investigation.

186 Early placental development occurs in a predominantly low oxyg

187 a quantitative 3D methodology to investigate placental development or pathologies.

188 providing a suite of tools for the study of placental development, our trophoblast models allow the

189 icantly overlap with genes involved in human placental development, pointing to conserved or converge

190 8 in mice impaired trophoblast migration and placental development, resulting in intrauterine growth

191 e level of DEHP display marked impairment in placental development, resulting in poor pregnancy outco

192 itative RT-PCR analysis of genes involved in placental development revealed significant attenuation o

193 egulation of a network of genes required for placental development, suggesting a central role for the

194 perform essential host functions, including placental development, synaptic communication, and trans

195 or (EGFR) exhibit strain-specific defects in placental development that can result in mid-gestational

196 ssential X-chromosome-imprinted regulator of placental development that influences fetal growth, and

197 ed a mechanism regulating cell migration and placental development that underlies the development of

198 During early human placental development, the conceptus attaches itself to

199 s essential for polyploidy to support normal placental development, thereby preventing premature sene

200 ify Arid3a as a critical regulator of TE and placental development through execution of the commitmen

201 on photoacoustic and fluorescence imaging of placental development throughout the pregnancy.

202 or the imprinted Igf2-Igf2r axis on matching placental development to fetal growth and establishes th

203 hat treatment of the mother with LMWH allows placental development to proceed and affords significant

204 oles for AKT1, a serine/threonine kinase, in placental development using a genome-edited/loss-of-func

205 illous trophoblasts (EVT) play a key role in placental development, uterine spiral artery remodeling,

206 sect the role of H19 and Igf2 in cardiac and placental development utilizing multiple mouse models wi

207 gration in tumor progression (in addition to placental development), we examined the affect of cultur

208 level of EGFR signaling required for normal placental development, we characterized congenic strains

209 To understand its role in placental development, we established a novel Egfl7 knoc

210 r reversal can be induced at other stages of placental development, we examined earlier placental spe

211 role of bHLH transcription factors in human placental development, we first characterized Id express

212 ning cell columns during the early stages of placental development, when the architecture of the basa

213 Such fusion is essential to human placental development, where interactions between tropho

214 development as a direct consequence of poor placental development, which has major implications on c

215 In this review, we will overview placental development with a focus on how villous struct

216 ase kinase kinase MEKK4 exhibit dysregulated placental development with increased trophoblast invasio

217 These results make PLAC1 a marker for placental development, with a possible role in the estab

218 of implantation and leading to retarded feto-placental development without apparent defects in decidu