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1 found entrapped in the cytoplasm of the GDM-trophoblast.
2 ss of cell adhesion in methylation-deficient trophoblast.
3 rentiated along multiple lineages, including trophoblast.
4 ognize the fetal HLA-C molecules on invading trophoblast.
5 pression in the ICM and its silencing in the trophoblast.
6 that recognize allogeneic HLA-C molecules on trophoblast.
7 xpression of HLA-G, a marker of extravillous trophoblast.
8 mediating the down-regulation of SERT in GDM trophoblast.
9 DLX5 is expressed in human but not in murine trophoblast.
10 n of imprinting gene expression in the molar trophoblast.
11 y which CDX2 maintains repression of OCT4 in trophoblast.
12 to HCMV-infected primary fetal extravillous trophoblasts.
13 n primary human placental organ cultures and trophoblasts.
14 ory signature and a disturbed crosstalk with trophoblasts.
15 to bile acid decreased PRDX3 level in human trophoblasts.
16 ches the terminal fate of these hESC-derived trophoblasts.
17 trol or Dex-treated cultured third-trimester trophoblasts.
18 and decreased proliferation of labyrinthine trophoblasts.
19 ar results were obtained with HUVEC and HTR8 trophoblasts.
20 ly target InsRs in fetally derived placental trophoblasts.
23 a paracrine and autocrine manner to protect trophoblast and non-trophoblast cells from ZIKV infectio
25 lethal phenotypes in mice, cause defects in trophoblast and placental development, and/or affect con
27 ional silencing of the CYP27A1 gene in human trophoblast and rat adrenocortical cells reduced the exp
28 eam elements were significantly lower in GDM-trophoblast and showed no response to the insulin stimul
32 fection induced autophagic activity in human trophoblasts and pharmacological inhibition limited ZIKV
33 sence of both FGF2 and BMP4 by conversion to trophoblast, and especially syncytiotrophoblast, whereas
34 y tube formation involving HUVEC and/or HTR8 trophoblasts, and aortic ring endothelial cell outgrowth
35 and BeWo cells and in primary human villous trophoblasts, and this induction was abrogated by CH2231
36 ry effect of MSU crystals was accompanied by trophoblast apoptosis and decreased syncytialization.
40 o secretions from the placenta or from model trophoblast barriers that had been exposed to altered ox
41 trophoblast cells, including basal chorionic trophoblast (BCT) cells located at the chorioallantoic i
42 xtracellular vesicles (EVs), which influence trophoblast behaviour during the implantation process.
44 rved Grhl2-coordinated gene network controls trophoblast branching morphogenesis, thereby facilitatin
47 owever, the regulatory mechanisms that guide trophoblast cell fate decisions during placenta developm
50 human trophoblast cells and an extravillous trophoblast cell line (HTR8), from first and second trim
56 ntinue to provide a model for studying early trophoblast cells (TB), but many questions have been rai
58 In this study, we show that primary human trophoblast cells and an extravillous trophoblast cell l
59 the cell-cell interactome of fetal placental trophoblast cells and maternal endometrial stromal cells
60 d production of progesterone 2-fold in human trophoblast cells and of corticosterone by 90% in rat ad
62 we demonstrate that HCV-RNA sensing by human trophoblast cells elicits a strong antiviral response th
64 Isolation and in vitro culture of Sca-1(+) trophoblast cells from both differentiated TS cell cultu
66 isplayed co-regulation and were expressed in trophoblast cells in a similar domain as in mouse placen
67 ith placebo and n-3 and in vitro in isolated trophoblast cells in response to DHA and EPA treatment.
68 chanisms by which LDA influences PE-affected trophoblast cells in vitro are by modulating cytokine se
74 from pregnant women or conditioned medium of trophoblast cells promoted endometrium receptivity in vi
76 vitro inhibition of 20alpha-HSD activity in trophoblast cells reversed PI-based cART-induced decreas
77 ver, Elf5 is also present in differentiating trophoblast cells that have ceased to express other TSC
78 uterus and interact with invading placental trophoblast cells that transform the maternal arteries t
83 ing implantation defects, disorganization of trophoblast cells, fewer uterine natural killer (uNK) ce
84 ion factor, is highly expressed in chorionic trophoblast cells, including basal chorionic trophoblast
85 human fetal placenta itself, mainly through trophoblast cells, is able to induce homeostatic M2 macr
86 ts and purinergic inflammasome activation in trophoblast cells, uncovering a novel thromboinflammator
87 helial component of the placenta consists of trophoblast cells, which possess the capacity for multil
97 thylated ESCs that are prone to acquire some trophoblast characteristics, Plet1 is required to confer
99 tablish important patterning cues within the trophoblast compartment by promoting differentiation tow
100 anscription factor with pivotal roles in the trophoblast compartment, where it reinforces a trophobla
102 ression restricted to placental extravillous trophoblasts contributes to maternal tolerance to the se
105 based on high throughput analysis of primary trophoblasts, derived from term human placenta and cultu
107 n specific domains of DLX3 and GCM1 in human trophoblast-derived cells by performing immunoprecipitat
108 al compartment, it must evade restriction by trophoblast-derived IFNlambda1 and other trophoblast-spe
111 methylation plays a major role in regulating trophoblast development but that imprinting of the key p
112 We dissected the role of DNA methylation in trophoblast development by performing mRNA and DNA methy
113 ulators in luminal epithelium proliferation, trophoblast development, and uNK maturation during pregn
114 ed, but less is known about its roles during trophoblast development, the extraembryonic lineage that
119 from placental villi at term and colonies of trophoblast differentiated from embryonic stem cells (ES
121 nase 1 (LIMK1) expression regulates invasive trophoblast differentiation by modulating the trophoblas
122 -treated cells, and preventing the premature trophoblast differentiation commonly observed in PE.
123 Feto-placental macrophages regulate villous trophoblast differentiation during placental development
126 methylation-regulated genes associated with trophoblast differentiation that are involved in cell ad
131 us, miR-515-5p may serve a key role in human trophoblast differentiation; its aberrant up-regulation
134 sia, is the failure of invading extravillous trophoblast (EVT) cells to remodel the maternal uterine
135 n leukocyte antigen-G+ (HLA-G+) extravillous trophoblasts (EVT) are rare cells that are believed to p
136 natural killer cells (dNK) and extravillous trophoblasts (EVT) at the maternal-fetal interface was s
137 pregnancy, semiallogeneic fetal extravillous trophoblasts (EVT) invade the uterine mucosa without bei
139 modeling before colonization by extravillous trophoblasts (EVTs); however, the trigger for their infi
141 , we demonstrate that cultured primary human trophoblasts express ACKR2 far more strongly than genes
142 being permissive for ZIKV infection, primary trophoblasts expressed multiple putative ZIKV cell entry
145 study, we show that primary human placental trophoblasts from non-exposed donors (n = 20) can be inf
146 beta3 (from platelets) and alphaVbeta3 (from trophoblasts) from HPA-1a(+) donors was demonstrated by
148 e hypothesized that LDA influences placental trophoblast function and reverses PE-associated abnormal
151 is impaired placentation resulting from poor trophoblast function, which reduces blood flow to the fe
152 In the presence of forskolin, which triggers trophoblast fusion, heme inhibits BeWo cell fusion throu
154 t1 levels favour differentiation towards the trophoblast giant cell lineage, whereas lack of Plet1 pr
155 selective regions of the genome in parietal trophoblast giant cells (p-TGCs) of the mouse placenta.
156 essential for specification of spiral artery trophoblast giant cells (SpA-TGCs) that invade and remod
157 ulted in differentiation of blastomeres into trophoblast giant cells (TGCs), suggesting that geminin
164 sion of miR-515-5p in cultured primary human trophoblasts impaired SynT differentiation and specifica
168 ofiles of term intravillous and extravillous trophoblasts, including the transcriptome of the multinu
170 l macrophages, leading to altered macrophage-trophoblast interaction, is involved in preeclampsia.
171 such critical regulator, programming primary trophoblasts into progenitors of the invasive differenti
172 fetus, progenitors develop into extravillous trophoblasts invading the maternal uterus and its spiral
174 with placental architecture displaying poor trophoblast invasion and spiral artery development in th
175 mentary approaches, including HUVEC-mediated trophoblast invasion in nude mice, in vitro three-dimens
176 been demonstrated to facilitate extravillous trophoblast invasion into maternal decidua during the fi
179 blishment of the correct cellular milieu and trophoblast invasion, all of which involve the action of
180 Chemokines CXCL12 and CXCL16, important for trophoblast invasion, were analysed further and expressi
185 owth factor (PlGF), abundantly produced from trophoblasts is involved in placental angiogenesis.
188 BP51 and decidual cell (DC) and interstitial trophoblast (IT) markers, vimentin and cytokeratin, resp
189 on between the inner cell mass (ICM) and the trophoblast layer of the blastocyst is known to occur, b
191 selectively expressed in the extraembryonic trophoblast lineage and regulates gene expression to pro
192 1 (Plet1), for its function in establishing trophoblast lineage identity and modulating trophoblast
194 y detected in precursors of the extravillous trophoblast lineage, forming cell columns anchored to th
195 n the placenta, expression is limited to the trophoblast lineage, where it remains highly expressed u
199 generation of the inner cell mass (ICM) and trophoblast lineages comprises upregulation of Nanog exp
204 f the defect on insulin receptor (IR) in the trophoblast of the gestational diabetes mellitus (GDM)-a
211 investigate ZIKV infection of primary human trophoblasts (PHTs), which are the barrier cells of the
212 al mTORC1 and mTORC2 signaling and decreased trophoblast plasma membrane System A and L amino acid tr
213 t decreased PRDX3 by excessive bile acids in trophoblasts plays a critical role in the pathogenesis a
215 increase in 1,25(OH)2D3] and the evidence of trophoblast production and secretion of vitamin D metabo
216 mportant function of OVOL1 as a regulator of trophoblast progenitor cell fate during human trophoblas
217 -290 cluster gene (Mirc5) results in reduced trophoblast progenitor cell proliferation and a reduced
218 arlier stages involving development of human trophoblast progenitor cells (TBPCs), which give rise to
221 ic redundancy of Gata3 with paralog Gata2 in trophoblast progenitors ensures the successful progressi
222 onic villi and amniotic epithelial cells and trophoblast progenitors in amniochorionic membranes-that
224 K4me3, H3K27me3, and CpG methylation maps of trophoblast progenitors, purified using the surface mark
231 he HLA-C allotype HLA-C2, expressed by fetal trophoblasts, reduces the risk of developing pregnancy c
233 eginning three weeks after conception, using trophoblast retrieval and isolation from the cervix (TRI
238 by trophoblast-derived IFNlambda1 and other trophoblast-specific antiviral factors and/or use altern
240 provides genetic evidence that impairment of trophoblast-specific GATA2/GATA3 function could lead to
242 aracteristics, Plet1 is required to confer a trophoblast-specific gene expression pattern, including
243 d TFAP2A indicated that they directly couple trophoblast-specific gene induction with suppression of
244 a transgenic animal by exploiting placental trophoblast-specific gene manipulation using lentiviral
245 ring were evaluated for effects of placental trophoblast-specific InsR deficiency on stress sensitivi
246 Male, but not female, mice with placental trophoblast-specific InsR deficiency showed a significan
254 ely hampered by the lack of a representative trophoblast stem cell (TSC) model with the capacity for
255 ophoblast compartment, where it reinforces a trophoblast stem cell (TSC)-specific transcriptional cir
259 ropriate self-renewal and differentiation of trophoblast stem cells (TSCs) are key factors for proper
262 bryonic stem cells (ESCs) and extraembryonic trophoblast stem cells (TSCs) in a three-dimensional sca
264 elete the core PRC2 protein EED in F1 hybrid trophoblast stem cells (TSCs), which undergo imprinted i
265 mutant placenta and in vitro differentiated trophoblast stem cells allow us to identify Blimp1-depen
266 ited decreased decay rates in differentiated trophoblast stem cells derived from KO blastocysts.
267 cience that 3D co-cultures of mouse ESCs and trophoblast stem cells self-organize into embryo-like st
269 cells, facilitated transdifferentiation into trophoblast stem cells, and impaired differentiation of
275 arkers of both junctional zone and labyrinth trophoblast subtypes in a manner comparable to establish
277 he lack of FKBP51 expression in interstitial trophoblasts suggests unopposed constitutive GR action.
280 d layers of protection and relies heavily on trophoblasts, the fetal-derived cells that comprise the
281 pitulate the antiviral properties of primary trophoblasts through the constitutive release of type II
282 s to study susceptibility of human placental trophoblast to ZIKV: cytotrophoblast and syncytiotrophob
283 ong-range chromatin looping mediated by core trophoblast transcription factors as the mechanism contr
284 act with integrins along the surfaces of the trophoblasts, triggering the activation of two signallin
285 c (ESCs) but hypomethylated and expressed in trophoblast (TSCs) stem cells are very rare and may have
286 dditionally expressed in clusters of villous trophoblasts underlying the syncytium, suggesting that t
287 ation-related and physiological processes in trophoblast via both imprinting-dependent and -independe
289 expression in the three germ layers and the trophoblast was abnormal in the EBs of tetraploid ESCs c
290 orted populations of primary first-trimester trophoblasts, we evaluated the first stage of EVT differ
293 n = 6 for each group), and the platelets and trophoblasts were isolated to determine the IR activity,
294 signaling leads to formation of extravillous trophoblast, whereas loss of activin/nodal inhibition le
295 ly, MR766 is highly trophic toward primitive trophoblast, which may put the early conceptus of an inf
296 s are more permissive to ZIKV infection than trophoblasts, which may be refractory to infection.
297 nd that it was also expressed in a subset of trophoblast within the chorion and labyrinth layer of th
298 mechanism by which ES cells communicate with trophoblasts within the blastocyst to increase their abi
300 -FLR strain can replicate in human placental trophoblasts without host cell destruction, thereby serv
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