ライフサイエンスコーパス: blastocyst

1 ays were inhibited (from 3.1 to 1.6 pmol/100 blastocysts).

2 regulates lineage specification of the mouse blastocyst.

3 ed in the inner cell mass (ICM) of the mouse blastocyst.

4 ophectoderm lineage required for producing a blastocyst.

5 ue to a decrease in Igf2 and H19 mRNA in ZDD blastocyst.

6 quired for the formation of EPI cells in the blastocyst.

7 of epiblast and PrE progenitors in the mouse blastocyst.

8 d maternal endometrium and the free-floating blastocyst.

9 tive centrosomes was established only in the blastocyst.

10 tion human embryos from the zygote until the blastocyst.

11 n accurately organizing the developing mouse blastocyst.

12 ining cellular plasticity and organizing the blastocyst.

13 ithin the inner cell mass (ICM) of the mouse blastocyst.

14 rimitive endoderm upon reintroduction to the blastocyst.

15 on in the inner cell mass (ICM) of the mouse blastocyst.

16 generated by injecting these mESCs into host blastocysts.

17 iated trophoblast stem cells derived from KO blastocysts.

18 les to determine their receptive function to blastocysts.

19 ric contribution of these cells to non-human blastocysts.

20 onic stem cells (FX-hESCs), derived from FXS blastocysts.

21 nges in up to 33% (ZFNs) and 46% (TALENs) of blastocysts.

22 PSCs and the inner cell mass (ICM) of human blastocysts.

23 yonic stem cell lines generated from Emb-LPD blastocysts.

24 nserved and better resemble their respective blastocysts.

25 important for the expression of NANOG in the blastocysts.

26 into Dark Agouti (DA) X Sprague Dawley (SD) blastocysts.

27 eriod can modulate gene expression in bovine blastocysts.

28 em cells can be derived from parthenogenetic blastocysts.

29 tein was present at the 4-cell stage and the blastocysts.

30 gnificantly decreased the apoptosis index of blastocysts.

31 ffected the level of NANOG expression in the blastocysts.

32 n and methylation patterns closer to in vivo blastocysts.

33 ikely a significant pool of methyl groups in blastocysts.

34 ion are suppressed in Cnr1(-/-) or Faah(-/-) blastocysts.

35 es derived from the inner cell mass of human blastocysts.

36 s hatched blastocysts, but not as morulae or blastocysts.

37 knockdown reduces Sox2/FGF4/ERK signaling in blastocysts.

38 reduction in inner cell mass cell number in blastocysts.

39 nt role during the progression of embryos to blastocysts.

40 ophectoderm proliferation in Suds3 knockdown blastocysts.

41 ted arrested embryos and excluded cells from blastocysts.

42 ssed in the trophectoderm of human and mouse blastocysts.

43 the skewed lineage specification of Klf5 KO blastocysts.

44 reduced to <2% in the majority (79%) of PNT blastocysts.

45 to the inner cell mass (ICM) in 128-256 cell blastocysts (6dpf), approximately 2 days later than the

46 trophectoderm (TE) in preimplantation monkey blastocysts also expressed X-linked genes from both alle

47 Likewise, fewer blastocyst and expanded blastocyst were collected from t

48 We apply SCALE to mouse blastocyst and human fibroblast cells and find that cis

49 rresponding to the epiblast of the diapaused blastocyst and indicate that mTOR regulates developmenta

50 e derive from the polar trophectoderm of the blastocyst and persist through early gestation (to E8.5)

51 and internal primitive endoderm (PE) in the blastocyst and subsequently give rise to chorio-allantoi

52 onic and abembryonic hemispheres of the late blastocyst and their allocation to the TE and ICM, sugge

53 17(+) endoderm progenitors to integrate into blastocysts and contribute to chimeric embryos.

54 found to be differentially expressed between blastocysts and degenerates.

55 ertible within the inner cell mass of murine blastocysts and embryonic stem (ES) cells.

56 he reconstructed SCNT embryos developed into blastocysts and ES cells capable of contributing to trad

57 tal failure in implanted beta1 integrin-null blastocysts and found that primitive endoderm cells are

58 state of the inactive X, occurring in mouse blastocysts and germ cells.

59 ent of both embryonic stem cells (ESCs) from blastocysts and iPSCs from somatic cells [10, 12].

60 typic and molecular outcomes in Rab11a(null) blastocysts and mouse embryonic fibroblasts.

61 aining embryos were capable of developing to blastocysts and producing embryonic stem cells similar t

62 ain a gene expression signature of diapaused blastocysts and remain pluripotent.

63 y detected at levels below 1%, decreasing in blastocysts and stem-cell lines to undetectable levels,

64 The abundance of TET1 mRNA was high in the blastocysts and TET1 protein was present at the 4-cell s

65 t, germline DNA methylation is erased in the blastocyst, and a bimodal pattern is established anew at

66 vitro fertilization, resulting in transgenic blastocysts, and by mating, resulting in healthy transge

67 ergence of epiblast cells in preimplantation blastocysts, and ceasing during human embryonic stem cel

68 methylation in cultured ES cells compared to blastocysts, and in vivo are methylated only after impla

69 Indeed, c-Myc is depleted in diapaused blastocysts, and the differential expression signatures

70 rief phase of endometrial receptivity to the blastocyst--and were released into the endometrial fluid

71 as when injected into pre-implantation-stage blastocysts, apparently because the injected cells under

72 echanisms involved in Cdx2 expression in the blastocyst are also utilized in the postimplantation emb

73 However, male and female blastocysts are similarly hypomethylated, indicating tha

74 d that TE-deprived ICMs derived from 32-cell blastocysts are still able to reconstruct TE during in v

75 Thus, mouse blastocysts are unusual in being able to generate AdoMet

76 re to attain uterine receptivity will impede blastocyst attachment and result in a compromised pregna

77 luminal epithelium and stroma at the site of blastocyst attachment, but luminal epithelial COX2 expre

78 evaginations, defective crypt formation, and blastocyst attachment, leading to severely compromised p

79 1A), a BMP type 1 receptor, is necessary for blastocyst attachment.

80 Upon injection into blastocyst, BCL2-expressing EpiSCs contributed to all bo

81 l) embryos were able to properly form normal blastocysts but died at peri-implantation stages.

82 XY(d-1) females produced substantially more blastocysts but fewer than XO controls.

83 raft in both pig and cattle pre-implantation blastocysts but show limited contribution to post-implan

84 CHD4 can form a morphologically normal early blastocyst, but are unable to successfully complete the

85 lation and second as a major methyl donor in blastocysts, but its origin is unknown.

86 ndergo caspase-mediated apoptosis as hatched blastocysts, but not as morulae or blastocysts.

87 e derived from primed hESCs or directly from blastocysts, but their X chromosome state has remained u

88 Here we show that blastocysts can form without TEAD4 but that TEAD4 is req

89 ation in PrE cells only after they reach the blastocyst cavity and form a mature epithelium, in a pro

90 Positional cues provided by the blastocyst cavity are thought to be instrumental for cel

91 distinct, with 2i being the most similar to blastocyst cells and including a subpopulation resemblin

92 Blastocysts collected from Emb-LPD mothers within standa

93 embryos cultured in vitro formed fewer (38%) blastocysts compared to control embryos (74%).

94 Interspecies blastocyst complementation enables organ-specific enrich

95 potential of PSC-derived islets generated by blastocyst complementation in a xenogeneic host.

96 bryogenesis, and human disease, interspecies blastocyst complementation might allow human organ gener

97 Here, we establish a versatile blastocyst complementation platform based on CRISPR-Cas9

98 ditional cell ablation approach with a novel blastocyst complementation strategy, we generated murine

99 erived iPS cells to reform hematopoiesis via blastocyst complementation.

100 rowing human organs through the technique of blastocyst complementation.

101 em cells (PSCs) in mice through interspecies blastocyst complementation.

102 nner cell mass of the mouse pre-implantation blastocyst comprises epiblast progenitor and primitive e

103 se development leads to the formation of the blastocyst consisting of the inner cell mass (ICM) and t

104 be propagated in vitro and, when placed into blastocysts, contribute to all tissues of the embryo and

105 inner cell mass (ICM) lineages in the mouse blastocyst correlates with cell position, as TE derives

106 Here, blastocysts could be recovered from progesterone-induced

107 Total SAM levels in mouse blastocysts decreased significantly only when both pathw

108 been transferred into Mstn(tm1Sjl/+) dams as blastocysts demonstrated that the effects of maternal my

109 Blastocyst-derived embryonic stem cells (ESCs) and gonad

110 nal properties of iPS-derived and endogenous blastocyst-derived HSCs, despite the extensive chronolog

111 s transcriptional profiles highly similar to blastocyst-derived TSCs, with comparable methylation and

112 profiles, and DNA methylation patterns with blastocyst-derived TSCs.

113 Among normally fertilized ST zygotes, blastocyst development (62%) and embryonic stem cell iso

114 h significant decline in oocyte cleavage and blastocyst development after in-vitro fertilization.

115 growth, induces reversible pausing of mouse blastocyst development and allows their prolonged cultur

116 uggest that Rab11a critically controls mouse blastocyst development and soluble matrix metalloprotein

117 gated the parameters affecting efficiency of blastocyst development and stem-cell derivation.

118 tochondrial distribution, euploidy rate, and blastocyst development following fertilization in vitro,

119 calcium-dependence to hyper-adhesiveness as blastocyst development proceeds from E3 to E4.5.

120 5F1) in diploid human zygotes and found that blastocyst development was compromised.

121 ned the expression of orthologous genes, and blastocyst development was established, but maintenance

122 ygotes resulted in a substantial increase in blastocyst development, whereas injection of CDKN1C-spec

123 commit to either fate asynchronously during blastocyst development.

124 elf-renewal, somatic cell reprogramming, and blastocyst development.

125 resulted in a 45% reduction (P = 0.0006) in blastocyst development.

126 tion inhibits somatic cell reprogramming and blastocyst development.

127 the morula stage and cell sub-populations in blastocysts, differential histone modification expressio

128 ls of the inner cell mass (ICM) of the mouse blastocyst differentiate into the pluripotent epiblast o

129 the absence of a functional TE, Chd4 mutant blastocysts do not implant and are hence not viable.

130 ells within the inner cell mass (ICM) of the blastocyst does not respond to differentiation signals a

131 here it blocks the transition from morula to blastocyst during embryonic development.

132 h all somatic H1 subtypes are present in the blastocyst, each stage of preimplantation development is

133 aintenance of inner cell mass cells of mouse blastocysts, embryonic fibroblasts, and myoblasts, but i

134 Rates were higher with blastocyst embryos (day of transfer, 5 or 6) than with c

135 embryos and 52.4% and 80.7% for transfer of blastocyst embryos when fresh autologous oocytes were us

136 was detected in oocytes and in IVO produced blastocyst embryos.

137 Following Myc inhibition, pre-implantation blastocysts enter biosynthetic dormancy but can progress

138 lly diapaused blastocysts in vivo and paused blastocysts ex vivo display pronounced reductions in mTO

139 Suds3 knockdown blastocysts exhibit a failure of both trophectoderm prol

140 Fgf4 heterozygous blastocysts exhibited increased numbers of NANOG-positiv

141 isolated from treated ovaries, and isolated blastocysts exhibited reduced cell densities.

142 Blastocysts exhibited transcriptome profiles more closel

143 Here, we further explore the role of Oct4 in blastocyst formation and specification of epiblast versu

144 Blastocyst formation from human SCNT embryos occurs at a

145 t zygote viscoelastic properties can predict blastocyst formation in humans and mice within hours aft

146 r AP-2gamma (Tcfap2c) is a core regulator of blastocyst formation in mice.

147 pression of KDM4A significantly improves the blastocyst formation rate in human SCNT embryos by facil

148 Blastocyst formation requires the proper expression and

149 ch Tcfap2c acts in a hierarchy to facilitate blastocyst formation through transcriptional regulation

150 bryos with Tcfap2c knockdown embryos rescued blastocyst formation via direct contribution to the trop

151 During blastocyst formation, the relative levels of EED and KDM

152 their embryos are less likely to survive to blastocyst formation.

153 hese genes can be used as markers for normal blastocyst formation.

154 s segregation of the TE and ICM lineages and blastocyst formation.

155 es a diverse group of genes expressed during blastocyst formation.

156 stabilizes earlier than the ICM and prior to blastocyst formation.

157 Mouse embryonic stem cells (ESCs), like the blastocyst from which they are derived, contain precurso

158 me profiles more closely resembling those of blastocysts from developmentally competent oocytes.

159 metabolic disorders that were identified in blastocysts from mitochondrial DNA deficient oocytes.

160 differentiation but blocked hatching of the blastocysts from the zona pellucida.

161 ith such increased potency into a tetraploid blastocyst gives rise to an entire embryo with a higher

162 The inner cell mass of the mouse blastocyst gives rise to the pluripotent epiblast (EPI),

163 as well as generation of forces required for blastocyst hatching.

164 and BHMT activity is similarly detectable in blastocyst homogenates but not those of two-cell or moru

165 son to inner cell masses of marmoset primate blastocysts identifies a similar complement of pluripote

166 ce, their secretions play important roles in blastocyst implantation and stromal cell decidualization

167 e completely infertile because of defects in blastocyst implantation and stromal cell decidualization

168 defects in pregnancy are evident as reduced blastocyst implantation and subsequent defects in stroma

169 uterus to influence uterine receptivity and blastocyst implantation for the establishment of pregnan

170 triguingly, i.p. injections of LIF initiated blastocyst implantation in the uteri of both gland-conta

171 Blastocyst implantation is a complex process requiring c

172 In mice, the uterus becomes receptive to blastocyst implantation on day 4, but is refractory by d

173 tances that regulate uterine receptivity for blastocyst implantation.

174 in vivo, lasting 2-3 days around the time of blastocyst implantation.

175 ls into a cup-shaped epithelium as the mouse blastocyst implants is a poorly understood and yet key d

176 ed in the inner cell mass (ICM) of the early blastocyst in a 'salt and pepper' manner, and are subseq

177 beyond cleavage and morula stages to form a blastocyst in vitro.

178 We show that both naturally diapaused blastocysts in vivo and paused blastocysts ex vivo displ

179 ral-like particles and Gag proteins in human blastocysts, indicating that early human development pro

180 d a functional assay utilizing interspecific blastocyst injection and in vitro culture (interspecies

181 mbryonic and placental tissues, as seen in a blastocyst injection assay.

182 Blastocyst injection showed that STAP cells efficiently

183 mmed to pluripotency or near-pluripotency by blastocyst injection, by somatic cell nuclear transfer a

184 romosome and contribute to embryos following blastocyst injection, generating germline-competent chim

185 ages, and chimerize host placentas following blastocyst injection.

186 matrix allows hES cell line derivation from blastocyst inner cell mass and single blastomere cells w

187 During embryo implantation, the blastocyst interacts with and regulates the endometrium,

188 The implanting mouse blastocyst invades the uterine stroma and undergoes a dr

189 ithin the inner cell mass (ICM) of the mouse blastocyst involves initial co-expression of lineage-ass

190 Implantation of the blastocyst is a developmental milestone in mammalian emb

191 from the inner cell mass (ICM) in the mouse blastocyst is determined by position-dependent Hippo sig

192 mass (ICM) and the trophoblast layer of the blastocyst is known to occur, but its functional consequ

193 show that OCT4's major early activity in the blastocyst is to support primitive endoderm differentiat

194 luripotency factor in the inner cell mass of blastocysts, is also expressed in unipotent primordial g

195 le such cells are readily derived from mouse blastocysts it has not been possible to isolate human eq

196 While PBNT zygotes developed to blastocysts less frequently (42%) than controls (75%), g

197 polyploid blastomere, compaction, morula and blastocyst-like stages by light, scanning electron or th

198 The lymphovascular tumor embolus is a blastocyst-like structure resistant to chemotherapy, eff

199 Moreover, blastocyst microinjection showed that the iMuSCs contrib

200 ICMs isolated from more advanced blastocysts no longer retain totipotency, failing to for

201 cted from WT, Cnr1(-/-), and Faah(-/-) mouse blastocysts on day 4 of pregnancy.

202 ng human embryonic stem cell derivation from blastocyst outgrowths.

203 to demonstrate that the bias observed in the blastocyst persists into postimplantation stages and the

204 tal cell number in the resulting morulae and blastocysts positively correlated with the zinc spark am

205 plantation in the maternal uterus, the mouse blastocyst possesses an inner cell mass comprising two l

206 during mammalian embryogenesis arise in the blastocyst, producing the inner cell mass and the trophe

207 ides a twofold increase in the efficiency of blastocyst production after in vitro fertilization.

208 ocyte microinjection reduced lysis, improved blastocyst rate, increased the number of targeted bi-all

209 Sperm motility, viability, fertilization and blastocyst rates were lower in Prdx6 (-/-) spermatozoa t

210 parthenotes and zygotes that developed into blastocysts released more zinc than those that failed to

211 Paused blastocysts remain pluripotent and competent-able to giv

212 ed that derivation from plating intact human blastocysts resulted predominantly in the outgrowth of T

213 re reproducibly down-regulated in Tet1/3 DKO blastocysts, resulting in a characteristic phenotype of

214 at injecting MVs isolated from ES cells into blastocysts results in an increase in their implantation

215 Klf5 Furthermore, Klf5 KO and overexpressing blastocysts showed skewed lineage specification phenotyp

216 ell embryos and individual embryonic day 3.5 blastocysts showed unexpectedly variable gene expression

217 ome DNA methylation datasets from single pig blastocysts showing differences between in vivo and in v

218 ) were compared between embryos reaching the blastocyst stage and growth-arrested embryos (degenerate

219 he oocyte, these aneuploidies persist at the blastocyst stage and the reasons for the high incidence

220 er insemination decreased development to the blastocyst stage at day 7 and reduced numbers of trophec

221 yos failed to proceed from the morula to the blastocyst stage because of defects in the molecular arc

222 at the morula stage; BHMT is abundant at the blastocyst stage but not other preimplantation stages, a

223 is increased in 16-cell embryos, and by the blastocyst stage cells fail to properly adopt a TE gene

224 of embryonic and extra-embryonic lineages in blastocyst stage embryos, the formation of the three ger

225 d in decreased development of embryos to the blastocyst stage in vitro and a reduction in inner cell

226 e development of the mouse embryo beyond the blastocyst stage in vitro.

227 tion of Cdx2 develop normally until the late blastocyst stage leading to the conclusion that Cdx2 is

228 We show that inhibition of aPKC from the mid blastocyst stage not only prevents sorting of PrE precur

229 oid cells is progressively depleted from the blastocyst stage onwards.

230 opment of these fertilized oocytes up to the blastocyst stage was also similar to that registered in

231 This promotes efficient development to the blastocyst stage with no detectable effect on aneuploidy

232 d not reduce developmental efficiency to the blastocyst stage, and genome integrity was maintained pr

233 mpetent to become fertilized, advance to the blastocyst stage, and give rise to live young than their

234 nt of mouse embryos from the morula to early blastocyst stage, based on 4D confocal image volumes.

235 o development and reduces progression to the blastocyst stage.

236 but only if the host embryos are at the pre-blastocyst stage.

237 NANOG and reduced expression of CDX2 at the blastocyst stage.

238 ylase inhibitors, promote development to the blastocyst stage.

239 es to be activated from the four-cell to the blastocyst stage.

240 tic null embryos that develop until the late blastocyst stage.

241 ge, and becomes spatially restricted by late blastocyst stage.

242 ts in defects in TE specification before the blastocyst stage.

243 ks such as H3K27me3 is achieved by the early blastocyst stage.

244 3.3 KD embryos and allows development to the blastocyst stage.

245 os fail to correctly specify lineages at the blastocyst stage.

246 the ability to regenerate TE up to the early blastocyst stage.

247 ergenic and become hypermethylated after the blastocyst stage.

248 y passive loss that reaches a minimum at the blastocyst stage.

249 o arrest of embryonic development around the blastocyst stage.

250 n living mouse oocytes and embryos up to the blastocyst stage.

251 loped slower and largely failed to reach the blastocyst stage.

252 early human embryonic development beyond the blastocyst stage.

253 d the percentage of embryos that reached the blastocyst stage.

254 Embryonic stem (ES) cells are derived from blastocyst-stage embryos and are thought to be functiona

255 include the establishment of XEN cells from blastocyst-stage embryos in either standard embryonic or

256 toderm and primitive endoderm cells of human blastocyst-stage embryos.

257 med on three 5- to 10-cell biopsies from two blastocyst-stage embryos.

258 s at the four-cell, eight-cell, 16-cell, and blastocyst stages.

259 y of cis-regulatory elements employed in the blastocyst, stem cell populations and the postimplantati

260 oalesce as the egg cylinder emerges from the blastocyst structure.

261 Quantitative RT-PCR was conducted on blastocyst tcRNA isolated from individual IVO and IVF pr

262 t alleviate oxidative stress, and Tead4(-/-) blastocysts that formed under these conditions expressed

263 s after 5 d, and the second starts with late blastocysts that upon dissection of the mural trophectod

264 protocol: the first starts with intact early blastocysts that upon zona removal can attach to the sub

265 Supplementation increased development to blastocyst, the final stage of preimplantation developme

266 Like cells of the blastocyst, the resulting naive cells contained two acti

267 mpared with numerous conventional lines from blastocysts, they had unique gene expression and DNA met

268 HHP promotes competence of vitrified bovine blastocysts through modest transcriptional changes.

269 operates on the hypomethylated genome of the blastocyst to achieve tissue-specific patterns of gene e

270 gh-resolution imaging of the transition from blastocyst to egg cylinder.

271 lls communicate with trophoblasts within the blastocyst to increase their ability to migrate into the

272 1 individual cells from early and late human blastocysts to delineate dynamic gene-expression changes

273 Transfer of such blastocysts to recipient females doubles mean litter siz

274 bryos to DKK1 during the period of morula to blastocyst transition (between d 5 and 8 of development)

275 nduced deletion of Oct4 during the morula to blastocyst transition disrupts the ability of inner cell

276 on of p21 transcription during the morula-to-blastocyst transition.

277 xpression blocking development at the morula-blastocyst transition.

278 is regulated through Hippo and Notch in the blastocyst trophectoderm, unexpectedly finding that it i

279 establishment of three cell lineages in the blastocyst: trophectoderm, primitive endoderm, and epibl

280 can contribute to all three lineages of the blastocyst until peri-implantation.

281 following embryo transfer of BHMT knockdown blastocysts versus control.

282 A physiological role for betaine and BHMT in blastocyst viability was further indicated by increased

283 njecting mouse PSCs into Pdx-1-deficient rat blastocysts, we generated rat-sized pancreata composed o

284 Likewise, fewer blastocyst and expanded blastocyst were collected from the reproductive tract of

285 Blastocysts were produced in vitro either without (C-IVF

286 mbryos arrested with 2-4 cells and almost no blastocysts were produced; by contrast, XY(d-1) females

287 eight-cell Tead4(-/-) embryos developed into blastocysts when cultured under conditions that alleviat

288 ower percentage of oocytes cleaved or formed blastocysts when STIM1 was downregulated prior to fertil

289 consistent with the inner cell mass of human blastocysts, where MYC transcriptional activity is highe

290 KN1C gene showed the highest upregulation in blastocysts whereas PHLDA2 was highly expressed in degen

291 ing cancer cell lines into early-stage mouse blastocysts, which induces central immune tolerance.

292 Fertilized eggs develop poorly into blastocysts, which results in significantly decreased fe

293 is expressed in all cell populations of the blastocyst, while Fgfr2 expression becomes restricted to

294 A blastocyst will implant only when the uterus becomes rec

295 lasmy in a stem cell line derived from a PNT blastocyst with 4% mtDNA carryover.

296 producing embryos ranging from four-cell to blastocyst with donor paternal origin confirmed in 7/81

297 e first generated genetic mosaic ovaries and blastocysts with stochastic expression of wild-type or m

298 We treated bovine blastocysts with three different HHP (40, 60 and 80 MPa)

299 controls, and this variability correlated in blastocysts with variably increased 5mC/5hmC in gene bod

300 In blastocysts, XCR is perturbed by mutation of either Tsix