ライフサイエンスコーパス: midgestation

1 ient erythropoietin (Epo) production and die midgestation.

2 sed heart failure and embryonic lethality at midgestation.

3 but Gcn5(-/-) p53(-/-) embryos still die in midgestation.

4 lves inhibition of Gli3R and continues after midgestation.

5 Snx13-null mice were embryonic lethal around midgestation.

6 the medial to lateral axis, and only before midgestation.

7 cytokine-dominated mechanism operating after midgestation.

8 bors a large pool of pluripotent HSCs during midgestation.

9 and is fully compatible with development to midgestation.

10 F-3beta) in the pancreatic primordium during midgestation.

11 ch the eccentricity of the optic nerve until midgestation.

12 t, heart, lung, kidney, and limb buds during midgestation.

13 was highly expressed in endothelial cells at midgestation.

14 ion and that tetraploid cells may persist to midgestation.

15 atic precursors from the gut endoderm during midgestation.

16 yield Mrad9(-/-) pups, since embryos died at midgestation.

17 t that deficient embryos do not survive past midgestation.

18 e germ cells were developmentally delayed at midgestation.

19 mice deficient in either Mfn1 or Mfn2 die in midgestation.

20 the development of most mouse embryos beyond midgestation.

21 viable, double knockout embryos died around midgestation.

22 th a transient impairment of fetal growth in midgestation.

23 sis of the inner ear is greatly perturbed by midgestation.

24 embryos deficient in both proteins arrest at midgestation.

25 Most tbp(Delta N/Delta N) fetuses die in midgestation.

26 us progeny of homozygous females died before midgestation.

27 pitulate the tissue architecture in early to midgestation.

28 was markedly elevated in multiple nuclei at midgestation.

29 required for in vivo FAK function until late midgestation.

30 ty of homozygous mutant (Shp-2(-/-)) mice at midgestation.

31 yonic lethality of homozygous mutant mice at midgestation.

32 tribute to the HSC pool increase observed at midgestation.

33 hypertrophy, peak wall stress normalized by midgestation.

34 death of homozygous Fbxl10-mutant embryos at midgestation.

35 2, to control their expression at and beyond midgestation.

36 BV abnormalities as Rasa1-null mice and died midgestation.

37 l embryos lack centrosomes but survive until midgestation.

38 ivors developed eye defects beginning around midgestation.

39 for sustaining proliferation of LaTP during midgestation.

40 n fetal exposure or metabolism of BPA during midgestation.

41 hat functional synaptic contacts are rare at midgestation.

42 Twist1(-/-) embryos die at midgestation.

43 ly positioned metanephric mesenchyme (MM) in midgestation.

44 specific absence of most of the forebrain at midgestation.

45 mately 25 and miR-17 approximately 92 die at midgestation.

46 nts with Diamond-Blackfan anemia, and die in midgestation.

47 ch were merely distorted in Pitx2 mutants at midgestation.

48 ull embryos undergo normal development until midgestation (12.5 to 13.5 days postcoitum), at which ti

49 neous depolarizations in human SP neurons at midgestation (17-23 gestational weeks) were not complete

50 e generated in the human cortical SVZ during midgestation (18-24 gw) under in vitro conditions.

51 In human brain at midgestation (19-21 weeks), huntingtin was detected in a

52 zone of the ganglionic eminences, whereas at midgestation (20 GW), they were also expressed in the te

53 embryonic death, revealing that most act at midgestation (8.5-10.5) or sooner.

54 analysis of human cerebral patterning during midgestation, a critical epoch in cortical regionalizati

55 ic oxide synthase within human myometrium at midgestation, a time when the uterus is normally quiesce

56 In addition, at midgestation, aberrant nerve projection and arborization

57 r2 in the uterine deciduae of mice triggered midgestation abnormalities in decidualization that resul

58 fraction of double-mutant embryos exhibited midgestation abnormalities with perinatal lethality, via

59 gene in mice leads to embryonic lethality in midgestation accompanied by defective erythropoiesis.

60 onservation of enhancers decreases following midgestation across all tissues examined.

61 While Hb Null embryos die in midgestation, adult globin genes are not required for pr

62 In midgestation, after primary neurogenesis in compact vent

63 all regions of the human fetal brainstem at midgestation, an unexpected finding given the trophic ro

64 /- fetuses displayed transient anemia during midgestation and abnormal definitive erythropoiesis.

65 associated with maternal hemoglobin at both midgestation and at delivery (P < 0.01 for both).

66 rnal and cord blood samples were obtained at midgestation and at delivery, respectively.

67 mouse mutation chato, which causes arrest at midgestation and defects characteristic of convergent ex

68 subunit develop intracerebral hemorrhages at midgestation and die shortly after birth.

69 Although NMDA binding increased between midgestation and early infancy to moderately high adult

70 disruption of Raldh2 arrests development at midgestation and eliminates all RA synthesis except that

71 Here, we transiently induced CAErbB2 during midgestation and examined synapse restoration after indu

72 study, we show that Wdr34 mutant mice die in midgestation and exhibit open brain and polydactyly phen

73 ory component of the WAVE complex, arrest at midgestation and have defects in morphogenesis of all th

74 ng measured with 3H-LSD was observed between midgestation and infancy, and between infancy and maturi

75 binding did not change significantly between midgestation and infancy, except for an elevation in the

76 on of distal chromosome 7 (PatDup.d7) die at midgestation and lack placental spongiotrophoblast.

77 Whereas Osr1(-/-) mutant mice died at midgestation and Osr2(-/-) mutant mice had only subtle d

78 omolog1 (Disp1) mutation causes lethality at midgestation and prevents specification of ventral cell

79 per day) can prevent the death of embryos at midgestation and prevents the early embryonic abnormalit

80 sac undergoes cell death and degeneration at midgestation and the fetuses die over a range of several

81 hed the far peripheral edge of the retina by midgestation and the OPL by late gestation.

82 ic valvuloplasty can be performed for severe midgestation aortic stenosis in an attempt to prevent pr

83 erwent fetal aortic valvuloplasty for severe midgestation aortic stenosis with evolving HLHS from Mar

84 ers of vitamin D and iron were determined at midgestation ( approximately 25 wk) and delivery ( appro

85 yvitamin D [1,25(OH)(2)D] were determined at midgestation ( approximately 26 wk) and at delivery in 1

86 on of LKLF by gene targeting die in utero at midgestation around day 12.5 due to severe hemorrhage, m

87 on of Rac1 results in embryonic lethality in midgestation (around E9.5), and defective development of

88 e fetal liver (FL) were also decreased after midgestation because of decreased cell proliferation and

89 These knock-in mice died in midgestation because of hemorrhaging in the central nerv

90 integrin beta8 (itgbeta8) gene die either at midgestation, because of insufficient vascularization of

91 Homozygous mutant mice died at midgestation, before embryonic day 11.5 (E11.5), with va

92 Importantly, in the absence of Etv2 at midgestation, binding of Etv2 at Ets-binding sites in th

93 ) showed normal morphological development to midgestation but died shortly thereafter.

94 Mutant embryos develop normally until midgestation but then exhibit a distinct block in the de

95 Cardiac pathology was not apparent at midgestation but was evident by day 2 of postnatal life,

96 bryos devoid of cytochrome c die in utero by midgestation, but cell lines established from early cyto

97 arly embryo inhibits vascular development at midgestation, but Edn2 overexpression in developing skin

98 l tetraploid embryos develop normally during midgestation, but encounter a secondary developmental bl

99 Mpc1 deletion was homozygous lethal in midgestation, but Mpc1 hypomorphs and tissue-specific de

100 The jaw of Pitx2 mutants was vestigial by midgestation, but significant size reductions were obser

101 We show that human midgestation c-Kit(-) lineage-committed amniotic cells (

102 eir germline Rb(-/-) counterparts, brains of midgestation chimeric embryos exhibited extensive ectopi

103 In addition, using organotypic human midgestation chorionic villous explants, we show that sy

104 sues including testes were miscarried during midgestation, consistent with RTT-linked male embryonic

105 mary human RG that constitute only 1% of the midgestation cortex and classified them as ventricular z

106 o, but, in the mouse model, delivery at late midgestation could not transduce hematopoietic stem cell

107 log-like 2 (Drosophila)], and their death at midgestation could result from two inactive paternal cop

108 assayed replicated efficiently in early and midgestation cultures, and two isolates examined replica

109 n further insight, we examined the causes of midgestation death of embryos with paternal duplication

110 t in aortic arch artery smooth muscle during midgestation, despite intact neural crest cell migration

111 ne in mice results in embryonic lethality at midgestation due to hemorrhaging in the central nervous

112 AML1) gene results in embryonic lethality at midgestation due to hemorrhaging in the central nervous

113 Midgestation (e10.5) Pitx2(-/-) embryos have normally fo

114 By midgestation (e13-e16), PC5 mRNA expression in the devel

115 ., before the onset of corticogenesis, or in midgestation (E70-E81), when superficial cortical layers

116 175-350 cGy) in early gestation (E33-E42) or midgestation (E70-E90); eight nonirradiated macaques wer

117 c and vascular abnormalities, and die during midgestation (E9.5-10).

118 enchymal cells are abundantly distributed in midgestation (E9.5-12.5), and adult derivatives of the t

119 d by modified reverse transcription-PCR from midgestation embryo templates, using a degenerate consen

120 Expression of Brca2 was detected in midgestation embryos and adult testis, thymus, and ovary

121 region is less differentially methylated in midgestation embryos and, like most of the genome, is la

122 al chromosome 7 gene, Mash2, which in normal midgestation embryos exhibits spongiotrophoblast-specifi

123 een for abnormal morphological phenotypes of midgestation embryos identified five mutant lines; the p

124 d from mouse or rat prostatic epithelia from midgestation embryos or adult mice, when combined with t

125 We also observed rare gut bud structures in midgestation embryos that appear to represent murine exa

126 In midgestation embryos, Cbfbeta was expressed in populatio

127 In midgestation embryos, the most extensive expression of P

128 Ctgf is expressed in a variety of tissues in midgestation embryos, with highest levels in vascular ti

129 t is strikingly differentially methylated in midgestation embryos.

130 However, rapid DNA demethylation after midgestation erases these parental imprints, in preparat

131 e Intu null mutants are homozygous lethal at midgestation, exhibiting multiple defects including neur

132 The ALK1 homozygous embryos die at midgestation, exhibiting severe vascular abnormalities c

133 phic features associated with progression of midgestation fetal AS to HLHS.

134 alogously diminished ZIKV infection in human midgestation fetal- and maternal-derived tissue explants

135 Aortic stenosis in the midgestation fetus with a normal-sized or dilated left v

136 In midgestation fetuses with AS and normal LV length, rever

137 Fetal echocardiography can identify midgestation fetuses with AS who are at high risk for de

138 first evidence of detectable BPA sulfate in midgestation fetuses.

139 ples from 32 HLHS and 17 structurally normal midgestation fetuses.

140 st tbp(DeltaN/DeltaN) fetuses (>90%) died in midgestation from an apparent defect in the placenta.

141 Brg1(fl/fl):Tie2-Cre(+) embryos die at midgestation from anemia, as mutant primitive erythrocyt

142 a hypoplastic ventricular chamber and die in midgestation from cardiac insufficiency.

143 , approximately 50% Tgfb1-/- conceptuses die midgestation from defective yolk sac vasculogenesis.

144 owed that >99% of Bright(-/-) embryos die at midgestation from failed hematopoiesis.

145 s for an AML1-ETO allele (AML1-ETO/+) die in midgestation from haemorrhaging in the central nervous s

146 etinoic acid receptor gene RXR(alpha) die in midgestation from hypoplastic development of the myocard

147 als regulate myocardial proliferation during midgestation heart development.

148 sed in the embryonic mouse epicardium during midgestation heart development.

149 MET mRNA expression in the midgestation human fetal cerebral cortex is strikingly r

150 oding the major surfactant protein, SP-A, in midgestation human fetal lung (HFL) is dramatically indu

151 d in the brain and peripheral tissues of the midgestation human fetus.

152 we used Nestin-cre to ablate beta-catenin at midgestation in developing CNS precursors to investigate

153 of Shp-2 leads to an embryonic lethality at midgestation in homozygous mutant mice.

154 ressed abundantly in the proximal CCS during midgestation in mice.

155 hortly after it becomes a distinct tissue at midgestation in the mouse: slowly dividing self-renewing

156 lso associated with impaired fetal growth in midgestation independent of fetal genotype, indicating p

157 children born to GDM mothers and exposed to midgestation infections have an increased vulnerability

158 d forward genetic screen we discovered a new midgestation lethal mouse mutant, called trex, which dis

159 e loss of PKA activity in the mouse leads to midgestation lethality and a completely ventralized neur

160 Complete loss of Gpr161 in mouse causes midgestation lethality and increased Shh signaling in th

161 ng one copy each of Smad2 and Smad3 suffered midgestation lethality due to liver hypoplasia and anemi

162 recessive allele of Axin2, canp, that causes midgestation lethality in homozygotes.

163 N1ICD(+) embryos showed midgestation lethality with defects in angiogenic remode

164 Consistent with a midgestation lethality, UTX-null male and female ES cell

165 entified a mutation in Wdr35 as the cause of midgestation lethality, with abnormalities characteristi

166 However, loss of endogenous TAK1 causes midgestation lethality, with defective yolk sac and intr

167 lts in placental defects and frequent (>90%) midgestation lethality.

168 to an underdeveloped ventricular chamber and midgestation lethality.

169 re, block Sonic hedgehog signaling and cause midgestation lethality.

170 Protein abundance of TfR1 was related to midgestation maternal serum ferritin (SF) (beta = -0.32;

171 of prothrombin-deficient embryos die during midgestation, mice lacking both PAR4 and fibrinogen deve

172 and vitelline and umbilical arteries of the midgestation mouse embryo.

173 ent of a variety of embryonic tissues in the midgestation mouse embryo.

174 loss of CCBE1 also confers severe anemia in midgestation mouse embryos due to defective definitive e

175 viously uncharacterized gene is expressed in midgestation mouse embryos in the branchial arches and l

176 rom aorta/gonad/mesonephros (AGM) regions of midgestation mouse embryos revealed a robust innate immu

177 and in the forebrain, face, and limb buds of midgestation mouse embryos.

178 test these possibilities by producing cloned midgestation mouse fetuses from three different donor so

179 frequency and spectrum of point mutations in midgestation mouse fetuses produced by either natural re

180 elivery, we did yolk sac vessel injection at midgestation of mouse embryos.

181 rsely associated with erythropoietin at both midgestation (P <0.05) and delivery (P <0.001).

182 In contrast, during midgestation perforin was no longer required for pregnan

183 However, c-jun-null mice die at midgestation, precluding critical investigation.

184 mice remained susceptible to alphaGalCer at midgestation, pregnant BALB/cJ mice were resistant to it

185 emonstrate that somatic gene transfer to the midgestation rat placenta may be efficiently accomplishe

186 In contrast, exposure to x-rays at midgestation reduced cortical thickness, mainly due to e

187 Furthermore, disruption of Rasa1 in midgestation resulted in LEC apoptosis in developing LV

188 Surprisingly, mostly during midgestation, SP cells become secondarily displaced and

189 expressed in the mouse placenta beginning at midgestation, specifically in the spongiotrophoblasts.

190 wn-regulated in Gpr48-/- fetal livers during midgestation stage through the cAMP-PKA-CREB pathway, su

191 Homozygous Wnt7b mutant mice die at midgestation stages as a result of placental abnormaliti

192 pha(-/-) embryos to proceed normally through midgestation stages of development.

193 mbers that regulate the postimplantation and midgestation stages of pregnancy.

194 s are colocalized in the cribriform plate at midgestation, suggesting that Ark is expressed in migrat

195 tic females to exogenous testosterone during midgestation, suggesting that early exposure to androgen

196 After midgestation, the highest level of mRNA is in the mammil

197 ies in the Hs2st(-/-) mice occurs only after midgestation, the most dramatic being the complete failu

198 helial expression of the Etv2 gene ceases at midgestation; therefore, vascular development past this

199 bunits in human white matter and cortex from midgestation through early childhood.

200 o their intra- and subcortical targets, from midgestation through infancy.

201 Homozygous mGATA-3 mutant embryos die at midgestation, thus complicating the analysis of its cont

202 creased from 5.19 mm at Fwk 8 to 20.92 mm at midgestation to 32.88 mm just after birth.

203 ith the increase in plasma free choline from midgestation to late gestation (P < 0.001).

204 spiratory function in the human medulla from midgestation to maturity.

205 long-acting anandamide in wild-type mice at midgestation triggered premature decidual senescence uti

206 At midgestation, TWH expression identifies subsets of spina

207 SoxC triple-null embryos die at midgestation unturned and tiny, with normal patterning a

208 In vivo, ZnT1 mRNA was abundant in the midgestation visceral yolk sac and placenta.

209 Higher prenatal PM2.5 exposure at midgestation was associated with asthma development by a

210 Pregnancy loss during midgestation was correlated with dramatically higher ser

211 t with the loss of a perforin requirement at midgestation was the emergence of strain-dependent varia

212 zygous male mice with Nsdhl mutations die by midgestation, we generated a conditional targeted Nsdhl

213 ersely associated with PM2.5 exposure during midgestation (weeks 12-25 for cord blood and weeks 15-27

214 e, nucleated EryPs begin to circulate around midgestation, when connections between yolk sac and embr

215 By midgestation, when invasion is complete, MMP levels are

216 ominant populations in uteri during early to midgestation, whereas T and B cells were constrained.

217 FOG-2(-/-) embryos die at midgestation with a cardiac defect characterized by a th

218 Mutants, however, die at midgestation with cardiovascular and skeletal defects, d

219 ssion is blocked briefly in mouse embryos at midgestation with citral (a general alcohol dehydrogenas

220 Murine embryos nullizygous for Rb die midgestation with defects in cell cycle regulation, cont

221 Rb(-/-) mouse embryos die at midgestation with defects in cell cycle regulation, cont

222 Mice deficient in Shp-2 die at midgestation with defects in mesodermal patterning, and

223 Piezo1-deficient embryos die at midgestation with defects in vascular remodeling, a proc

224 We find that Adm(-/-) embryos die at midgestation with extreme hydrops fetalis and cardiovasc

225 TKO mice died at midgestation with major defects in the circulatory syste

226 d glomeruli fail to form, and animals die at midgestation with neural tube closure and placental defi

227 expressed isoforms (JNK1 and -2) die during midgestation with neural tube closure defects and brain

228 ale embryos for several Nsdhl alleles die in midgestation with placental insufficiency.

229 Strip1-null mutants arrest development at midgestation with profound disruptions in the organizati

230 the O(2)-regulated HIF-1alpha subunit die at midgestation with severe cardiac malformations and vascu

231 T mutant Brachyury mice die in midgestation with severe defects in posterior mesodermal

232 acking protein O-fucosyltransferase 1 die at midgestation with severe defects in somitogenesis, vascu

233 myoglobin-deficient embryos die in utero at midgestation with signs of cardiac failure.

234 ce homozygous for the Shp-2 mutation died at midgestation with similar phenotype to FAK and fibronect

235 l embryonic development, as null mice die in midgestation with widespread unscheduled cell proliferat

236 port here that UBR1-/-UBR2-/- embryos die at midgestation, with defects in neurogenesis and cardiovas

237 t of integrin beta8-deficient embryos die at midgestation, with evidence of insufficient vascularizat

238 Most Dmap1(+/+) progeny died during midgestation, with loss of DNA methylation on imprinted

239 for a null allele at the Hif1a locus die at midgestation, with multiple cardiovascular malformations

240 and Ets2 resulted in embryonic lethality at midgestation, with striking defects in vascular branchin