ライフサイエンスコーパス: yolk sac

1 Predominant histology was yolk sac.

2 m which is derived the embryo proper and the yolk sac.

3 n both the labyrinth of the placenta and the yolk sac.

4 isceral endoderm defects observed in the cKO yolk sac.

5 important role in the proper development of yolk sac.

6 especially apparent in small vessels of the yolk sac.

7 n vessel remodeling in the developing murine yolk sac.

8 to induce vessel remodeling in the mammalian yolk sac.

9 s and emerge within the blood islands of the yolk sac.

10 and vasculogenesis were normal in embryo and yolk sac.

11 r and innate lymphoid cell precursors in the yolk sac.

12 oid progenitors (EMPs) present in the murine yolk sac.

13 y in trophoblast giant cells in the parietal yolk sac.

14 omic data for the coelomic fluid bathing the yolk sac.

15 he placenta, and the epithelial cells of the yolk sac.

16 lood vessel formation in the embryo body and yolk sac.

17 om Mesp1-Cre(+) cells in both the embryo and yolk sac.

18 ickettsiae isolated from embryonated hen egg yolk sacs.

19 Indian Hedgehog are reduced in chato mutant yolk sacs.

20 endothelial Rac1-deficient embryos and their yolk sacs.

21 cripts, whereas there were few changes in KO yolk sacs.

22 ses precursor cells of the embryo proper and yolk sac(1).

23 hen the blastoderm begins to spread over the yolk sac, a process involving coordinated epithelial sur

24 it is physiologically expressed in the fetal yolk sac, a tissue derived from the extraembryonic endod

25 In embryos, all blood cells within the yolk sac and aorta were of Flk-1(+) origin.

26 of specific myeloid cell progenitors of both yolk sac and bone marrow origin.

27 rom erythromyeloid progenitors (EMPs) in the yolk sac and develop in the forming CNS.

28 eover, those cells are not released from the yolk sac and disseminated into embryonic tissues.

29 of several embryonic regions, including the yolk sac and dorsal aorta, that undergoes vasculogenesis

30 cted proliferative capacity persist in E10.5 yolk sac and E11.5 liver.

31 microscopy has advanced our understanding of yolk sac and early embryonic vascularization.

32 In null mice, vessels throughout the yolk sac and embryo form and recruit smooth muscle in a

33 ulatory differences in Epo/EpoR signaling in yolk sac and embryonic erythropoiesis.

34 ing development, MCs enter the skin from the yolk sac and embryonic liver and are later mixed with ce

35 CNS, originate during embryogenesis from the yolk sac and enter the CNS quite early (embryonic day 9.

36 ion of cancer cells after injection into the yolk sac and extravasation of cancer cells into tissues

37 hematopoietic progenitors located within the yolk sac and fetal liver as well as definitive hematopoi

38 mouse macrophages derived from the embryonic yolk sac and from fetal liver.

39 ilarities with microglial progenitors in the yolk sac and immature microglia in early embryos.

40 ell type was present abundantly in the early yolk sac and in fewer numbers (approximately 5% of that

41 sful establishment of nascent vasculature in yolk sac and in the developing embryos.

42 VE-PTP-null mice were most pronounced in the yolk sac and include a complete failure to elaborate the

43 yonic (E9) B-cell progenitors located in the yolk sac and intraembryonic hemogenic endothelium before

44 auses midgestation lethality, with defective yolk sac and intraembryonic vasculature.

45 Parietal endoderm (PE) contributes to the yolk sac and is the first migratory cell type in the mam

46 mergence of definitive erythropoiesis in the yolk sac and its transition to the fetal liver.

47 d extraembryonic ectoderm, as well as in the yolk sac and labyrinth tissues that form later.

48 types in normal embryos, as well as in E13.5 yolk sac and labyrinth.

49 ineage tracing revealed that the majority of yolk sac and many adult hematopoietic cells derive from

50 rated through primitive hematopoiesis in the yolk sac and migrate into the brain rudiment after estab

51 ively from precursors originating within the yolk sac and migrate to the CNS under development, witho

52 nd visualized at embryonic day (E)9.0 in the yolk sac and neuroectoderm; 2) at E10.5, CX3CR1 single-p

53 ainly from progenitor cells generated in the yolk sac and of 'passenger' or 'transitory' myeloid cell

54 rrent with reduced erythrocyte velocity, and yolk sac and pericardium oedema.

55 Yolk sac and placenta are required to sustain embryonic

56 s and is expressed in the visceral endoderm, yolk sac and placenta.

57 the aorta, vitelline and umbilical arteries, yolk sac and placenta.

58 ession of one or more imprinted genes in the yolk sac and placenta.

59 rom primitive hematopoiesis in the embryonic yolk sac and self-renew throughout life.

60 delete YY1 from the visceral endoderm of the yolk sac and the definitive endoderm of the embryo.

61 extensive arterial morphogenesis both in the yolk sac and the embryo proper and disrupted arterial-ve

62 ath had markedly deformed vasculature of the yolk sac and the embryo, as well as poorly looped hearts

63 revealed abnormalities in both the visceral yolk sac and the embryo, including stunted extraembryoni

64 that the brain vasculature, like that of the yolk sac and the eye choriocapillaris and hyaloid vascul

65 The function of the primary yolk sac and the origin of extraembryonic mesoderm remai

66 scuss the intricate relationship between the yolk sac and the primate embryo and highlight the pivota

67 We demonstrate that DPFCs originate in the yolk sac and then rapidly migrate to other extra- and in

68 genitor cells (HSCs/Ps) originating from the yolk sac and/or para-aorta-splanchno-pleura/aorta-gonad-

69 cing (RNA-seq) data for the human and murine yolk sacs and compare those data with data for the chick

70 Further analysis of yolk sacs and embryos revealed a significant reduction o

71 The defects in Osr1-null yolk sacs and embryos were virtually identical to those

72 Aggf1+/- KO caused defective angiogenesis in yolk sacs and embryos.

73 nt, have aberrant vasculogenesis in embryos, yolk sacs and placentas, and die between embryonic day 1

74 It is found in yolk sacs and the outer cells of pre-implantation mouse

75 Genetic fate mapping revealed that yolk-sac and fetal monocyte progenitors gave rise to the

76 r developing structures, such as the kidney, yolk sac, and choroid plexus, suggests a possible genera

77 n leads to vascular defects in the placenta, yolk sac, and embryo proper, as well as abnormal neural

78 o found in other embryonic niches (placenta, yolk sac, and extraembryonic vessels), attempts to detec

79 etal liver, dorsal aorta, vitelline vessels, yolk sac, and heart.

80 ood islands, the equivalent of the mammalian yolk sac, and migrate out to colonize the embryo.

81 lex homolog), transfers IgY across the avian yolk sac, and represents a new class of Fc receptor rela

82 ascular abnormalities in the lung, placenta, yolk sac, and retina.

83 ion of target transcripts in placenta and/or yolk sac, and that some of these would be important for

84 roscopic analyses of E9.5 EKLF(-/-)KLF2(-/-) yolk sacs, and cytospins, indicate that erythroid and en

85 ected in R. prowazekii purified from hen egg yolk sacs, and G3PDH activity was assayable in R. prowaz

86 uclear envelope protein in the regulation of yolk-sac angiogenesis by TGFbeta signaling and reveal th

87 evelop adjacent to blood vessel walls in the yolk sac, aorta-gonad-mesonephros region, embryonic live

88 bryo and fetus: para-aortic splanchnopleura, yolk sac, aorta-gonad-mesonephros, liver, and bone marro

89 hematopoietic repopulating cells from murine yolk sac, aorta-gonad-mesonephros, placenta, fetal liver

90 at targets of miRNAs highly expressed in the yolk sac are significantly derepressed in GW182(gt/gt) m

91 embryo and highlight the pivotal role of the yolk sac as a multifunctional hub for haematopoiesis, ge

92 Our results support the contribution of the yolk sac as a source of microglial precursors.

93 EMPs develop in the yolk sac at embryonic day (E) 8.5, migrate and colonize

94 erythroid colonies from HIF-1alpha-deficient yolk sacs at E9.5.

95 otential in vitro have been described in the yolk sac before emergence of HSCs, and fetal macrophages

96 d/myeloid progenitors [EMPs]) emerges in the yolk sac beginning at embryonic day 8.25 (E8.25) and col

97 the hemangioblast as the cell of origin for yolk sac blood and endothelium.

98 f-renewal in adults and also participates in yolk sac blood island formation.

99 In most vertebrates, yolk sac blood islands are the initial sites of appearan

100 Primitive hematopoiesis occurs in the yolk sac blood islands during vertebrate embryogenesis,

101 there is a marked absence of erythrocytes in yolk sac blood islands.

102 transgenic mouse line led to a disruption in yolk sac blood vessel development.

103 ascular deletion of Brg1 results in aberrant yolk sac blood vessel morphology, which is rescued by ph

104 tic activity in mammalian development is the yolk-sac blood island, which originates from the hemangi

105 which will form the endoderm of the visceral yolk sac, BMP4-treated XEN cells regulated hematopoiesis

106 xposed animals (whole larvae, as well as the yolk sac, brain, and heart).

107 ut the same in both WT and KO mouse visceral yolk sac, brain, and spinal column.

108 or erythro-myeloid progenitors (EMPs) in the yolk sac, but it decreased the expression of alpha4-inte

109 mma-globin was co-expressed in the embryonic yolk sac, but not in the fetal liver; and wild-type beta

110 They appear in the yolk sac by embryonic day 7.5, begin to enter the embryo

111 sites of embryonic hematopoiesis such as the yolk sac by way of blood flow.

112 istration of synthetic TB4 partially rescues yolk sac capillary plexus formation in Hand1-null embryo

113 tion, bilaminar disc formation, amniotic and yolk sac cavitation, and primordial germ cell-like cell

114 ion, bi-laminar disc formation, amniotic and yolk sac cavitation, and trophoblast diversification.

115 asts, LIM-3 was expressed neither in primary yolk sac cells transformed by unfused v-Myb nor in BM2 c

116 d Gpx3 in the same vesicles of d-13 visceral yolk sac cells, suggesting uptake by pinocytosis.

117 ly 140,000 liver and 74,000 skin, kidney and yolk sac cells, we identify the repertoire of human bloo

118 This study demonstrates that later yolk-sac Chinook larvae (before exogenous feeding) are e

119 heir mutagenesis in mice impaired neural and yolk sac ciliogenesis, leading to morphogenetic anomalie

120 In differentiating mouse ES cells and mouse yolk sac cultures, addition of Indian Hh ligand increase

121 1-knock-out mice: no mature large vessels in yolk sacs, defective angiogenesis in the brain and inter

122 cKO embryos display profound yolk sac defects at 9.5 days post coitum (dpc), includin

123 ood of embryonic day (E) 10.5 embryos, while yolk sac definitive hematopoiesis was quantitatively nor

124 ts; for example, most tissue macrophages are yolk sac derived, monocytes and macrophages follow a mul

125 loblastic nucleated erythroblasts resembling yolk sac-derived cells.

126 Functionally, yolk sac-derived chemokine (C-C motif) receptor 2(-) mac

127 Significantly, E9.5 yolk sac-derived EMPs cultured in vitro have similar mur

128 We conclude that yolk sac-derived EMPs, the first of 2 origins of definit

129 in vitro but were rather supported on mouse yolk sac-derived endothelial cell (C166) feeder layers.

130 ctor Runx1 is essential for the formation of yolk sac-derived erythroid/myeloid progenitors (EMPs) an

131 with different ontogenetic origins: prenatal yolk sac-derived Kupffer cells and peripheral blood mono

132 , red pulp macrophages, a discrete subset of yolk sac-derived macrophages, were found to be altered i

133 irculating adult monocytes or from primitive yolk sac-derived macrophages.

134 Whereas yolk sac-derived microglia reside in the brain, blood-de

135 Previously, we determined that yolk sac-derived primitive erythroblasts mature in the b

136 The recent paradigm shift that microglia are yolk sac-derived, not hematopoietic-derived, is reshapin

137 embryogenesis is hallmarked by two phases of yolk sac development.

138 However F4/80(HI) macrophages from the yolk sac did not respond to LPS treatment.

139 e products of transient hematopoiesis in the yolk sac, dorsal aorta, and developing heart tube functi

140 y in multiple anatomical sites including the yolk sac, dorsal aorta, and heart tube.

141 roglia in the brain that originates from the yolk sac during early development.

142 , which is rapidly superseded by a secondary yolk sac during gastrulation.

143 increase in the incidence of pericardial and yolk sac edema relative to controls.

144 n dilbit WAF-exposed embryonic zebrafish but yolk sac edema was similar in all exposures.

145 of toxicity included pericardial, ocular and yolk sac edema, nondepleted yolk, spinal curvature, tail

146 erm cell tumor predominantly consisting of a yolk sac element (Fig 1).

147 Embryonic large molecule derived from yolk sac (ELYS) is a constituent protein of nuclear pore

148 Required histology included yolk sac, embryonal carcinoma, or choriocarcinoma.

149 identify, in the fetal liver, a sequence of yolk sac EMP-derived and HSC-derived haematopoiesis, and

150 and HSC-derived haematopoiesis, and identify yolk sac EMPs as a common origin for tissue macrophages.

151 wn as GW182, is selectively expressed in the yolk sac endoderm and that gene trap disruption of GW182

152 Moreover, the Snx13-null visceral yolk sac endoderm cells showed dramatic changes in the o

153 in trophoblast lineages of the placenta and yolk sac endoderm, which occurs only from the maternally

154 iR-17/20/93/106 clusters highly expressed in yolk sac endoderm.

155 erize an ontogenic process of blood cell and yolk sac endothelial maturation that is required to disp

156 tivated a cardiac transcriptional program in yolk sac endothelium, leading to the emergence of CD31+P

157 After exiting the yolk sac, EryP begin to express cell adhesion proteins,

158 Yolk sac erythro-myeloid progenitors (EMP) contribute su

159 cells that develop during organogenesis from yolk-sac erythro-myeloid progenitors (EMPs) distinct fro

160 tissue-resident macrophages are derived from yolk sac erythromyeloid progenitors and fetal liver prog

161 ne-restricted potential originating from the yolk sac even before the emergence of the first hematopo

162 ved during primitive hematopoiesis in murine yolk sac explant cultures and embryonic stem cell assays

163 xtensively self-renew and can be seeded from yolk sac/foetal liver progenitors with little input from

164 Yolk sacs from embryonic day 11.5 (E11.5) Zfp36l2 KO mic

165 i, the exocoelomic cavity, and the secondary yolk sac function together as a physiological equivalent

166 OX7 is broadly expressed across the RUNX1(+) yolk sac HE population compared with SOX17.

167 ly well studied, the molecular regulation of yolk sac HE remains poorly understood.

168 Embryonic SSMs originated from yolk sac hematopoiesis and were replaced by a postnatal

169 We modeled T21 yolk sac hematopoiesis using human induced pluripotent s

170 specification in the dorsal aorta, enhanced yolk sac hematopoiesis, and exuberant cardiac blood isla

171 We show that the previously reported lack of yolk-sac hematopoiesis and vascular development in Ldb1(

172 nadal macrophages are derived from primitive yolk-sac hematopoietic progenitors and exhibit hallmarks

173 We found that the formation of yolk sac hemogenic endothelium and its hematopoietic pot

174 onal states characteristic of the definitive yolk sac, HSCs undergoing specification, and definitive

175 The chicken yolk sac IgY receptor (FcRY) is the ortholog of the mamm

176 ted remarkable proliferative capacity in the yolk sac immediately before the onset of circulation, wh

177 wer numbers (approximately 5% of that in the yolk sac) in the caudal half of the developing embryos.

178 In the absence of Eng, yolk sacs inappropriately express the cardiac marker, Nk

179 topoietic ontogeny reminiscent of the murine yolk sac, including overlapping waves of hemangioblast,

180 ere present in RapGEF2(+/+) and RapGEF2(-/-) yolk sacs indicating that the bipotential early progenit

181 We detected a capD transcript in yolk sacs infected with R. prowazekii at ten days post-i

182 nt of the primitive erythroid lineage in the yolk sac is a temporally and spatially restricted progra

183 y, vascular remodeling of the extraembryonic yolk sac is abnormal in Brg1(fl/fl):Tie2-Cre(+) embryos.

184 show that TRPM6 activity in the placenta and yolk sac is essential for embryonic development.

185 The yolk sac is phylogenetically the oldest of the extraembr

186 as shown that vessel remodeling in the mouse yolk sac is secondarily effected when cardiac function i

187 primitive endoderm (PE), which will form the yolk sac, is a crucial developmental decision.

188 ve erythropoiesis, beginning at E8.25 in the yolk sac, is completely c-myb-dependent.

189 in European sea bass (Dicentrarchus labrax) yolk-sac larvae was explored.

190 obin switches are recapitulated, and because yolk sac-like and fetal liver-like cells are sequentiall

191 e species indicates that the human secondary yolk sac likely performs key functions early in developm

192 e dorsal aorta, and only later appear in the yolk sac, liver, and placenta.

193 Cx3cr1(+) yolk-sac macrophage descendants resided in the adult spl

194 Yolk-sac macrophages of EMP origin produced neonatal ost

195 ty of organs in which substantial numbers of yolk-sac macrophages persisted in adulthood.

196 SIRT1(-/-) yolk sacs manifested fewer primitive erythroid precursor

197 In a chicken yolk sac membrane model, under the same ultrasound param

198 nic malformations, including ruffling of the yolk sac membrane, defective extraembryonic mesoderm mor

199 feration were confined to the YY1-expressing yolk sac mesoderm indicating that loss of YY1 in the vis

200 escued angiogenesis and apoptosis in the cKO yolk sac mesoderm, but also restored the epithelial defe

201 ponsive paracrine signal, originating in the yolk sac mesoderm, is required to promote normal viscera

202 eral endoderm causes defects in the adjacent yolk sac mesoderm.

203 responsible for this vascular defect was the yolk sac mesothelial cells, not the cardiomyocytes or th

204 nstrate that PDGF receptors cooperate in the yolk sac mesothelium to direct blood vessel maturation a

205 ibed roles of the extraembryonic mesoderm in yolk sac morphogenesis and in the closure of the ectopla

206 ve yolk sac vasculogenesis, both cardiac and yolk sac morphology of Tmod1(-/-Tg(alphaMHC-Tmod1)) embr

207 Blood vessels were absent in the yolk sac of DGCR8 KOs after E12.5.

208 The vascular structure was absent in the yolk sac of Drosha homozygotes at E14.5.

209 and TC-(57)CoB12 accumulated in the visceral yolk sac of KO mice where megalin is expressed and provi

210 Hematopoiesis initiates within the yolk sac of mammalian embryos in overlapping primitive a

211 ein expression disappeared from the visceral yolk sac of RFC1-/- embryos, while cubilin protein was w

212 progenitors (EMPs) that first appear in the yolk sac of the early developing embryo.

213 (2)(1)(0)Po also accumulates in the yolk sac of the embryo and in the fetal and placental ti

214 st compounds into the embryonic body and the yolk sac of the zebrafish embryo using TK experiments, a

215 (0)-resins can be carefully implanted in the yolk sac of zebrafish embryos and display excellent bioc

216 leaved caspase-3 were abnormally abundant in yolk sacs of Ripk1(D325A/D325A) embryos.

217 on of the allantois that are unavailable for yolk sac or dorsal aorta, and review how this system has

218 hat FcRn is expressed in the endoderm of the yolk sac placenta but not in other cells of the yolk sac

219 placenta, we have studied FcRn in the mouse yolk sac placenta in detail.

220 k sac placenta but not in other cells of the yolk sac placenta or in the chorioallantoic placenta.

221 tic cues that drive the morphogenesis of the yolk sac placenta.

222 lial cells termed haemogenic, present in the yolk sac, placenta and aorta, through an endothelial-to-

223 ls, termed hemogenic endothelium, within the yolk sac, placenta, and aorta.

224 y give rise to chorio-allantoic and visceral yolk sac placentae, respectively.

225 the endoderm of both FcRn(+/+) and FcRn(-/-) yolk sac placentas and in the mesenchyme of FcRn(+/+) bu

226 was missing from the mesenchyme of FcRn(-/-) yolk sac placentas, indicating that IgG enters the endod

227 Resident macrophages are derived from yolk sac precursors and seed the liver during embryogene

228 In contrast, microglia and their yolk sac precursors develop independently of IL-34 but r

229 resident macrophages originally derived from yolk sac precursors.

230 od vessel formation as determined by lack of yolk sac primary capillary plexus formation and disorgan

231 tiple progenitor pools, microglia arise from yolk sac progenitors and are widely considered to be equ

232 ng early embryogenesis, microglia arise from yolk sac progenitors that populate the developing centra

233 ptor 2(+) macrophages derived from primitive yolk sac, recombination activating gene 1(+) lymphomyelo

234 with dilated pericardial sacs and failure of yolk sac remodeling suggestive of cardiovascular failure

235 pothesise that the hypoblast-derived primary yolk sac serves as a source for early extraembryonic mes

236 e made earlier, that displayed labyrinth and yolk sac-specific defects, but our findings extend those

237 protein is a rodent-specific, placenta- and yolk sac-specific member of the tristetraprolin (TTP) fa

238 uced levels of VEGFA are observed in the cKO yolk sac, suggesting a cause for the angiogenesis defect

239 ells, identifying the earliest stages in the yolk sac, throughout embryonic development and in all ad

240 bryonic vascular development, was reduced in yolk sac tissues of zimp10 null embryos.

241 endoderm (PrE), which forms extra-embryonic yolk sac tissues.

242 al IgY in egg yolk is transferred across the yolk sac to passively immunize chicks during gestation a

243 d vascular abnormalities seen in Brg1 mutant yolk sacs to the same extent as LiCl treatment.

244 monitoring for early detection of malignant yolk sac tumor (YST) recurrence, were recommended.

245 associated with worse outcome, whereas pure yolk sac tumor (YST) was associated with better outcome,

246 s differentiated derivatives, teratoma (TE), yolk sac tumor (YST), and choriocarcinoma.

247 malignant histologic types of pediatric GCT, yolk sac tumor (YST; n = 18), and seminoma (n = 9).

248 my, which revealed a 5-cm tumor that was 95% yolk sac tumor and 5% embryonal carcinoma, and retroperi

249 ixed germ cell tumor with 85% embryonal, 10% yolk sac tumor, and 5% mature teratoma histologies.

250 of Mexican-born mothers had a higher risk of yolk sac tumors (HR, 1.46; 95% CI, 0.99-2.17), while chi

251 d major dysplasia and malignant tumors, with yolk sac tumors and embryonal carcinomas positive for al

252 ial lipodystrophy and a history of childhood yolk sac tumour.

253 nign teratoma, epidermoid cyst and malignant yolk-sac tumours) and stromal tumours (such as juvenile

254 tic progenitor that gives rise to primitive (yolk sac-type) erythrocytes and megakaryocytes.

255 into the extra-embryonic region to form the yolk sac, umbilical cord and placenta.

256 Several of these mutants also display yolk sac vascular defects, suggesting a role for thrombi

257 embryonic lethality at ~ E11.5 due to severe yolk sac vascular defects.

258 Brg1 mutants, Chd4 mutant embryos had normal yolk sac vascular morphology.

259 severe defects in the reorganization of the yolk sac vascular plexus.

260 Brg1 from embryonic blood vessels results in yolk sac vascular remodeling defects.

261 at PITX2 helps to mediate the restoration of yolk sac vascular remodeling under both conditions.

262 oid rescue experiments reveals that abnormal yolk-sac vascularization is the probable cause of lethal

263 ts in angiogenic remodeling of embryonic and yolk sac vasculature, cardiac development, smooth muscle

264 orrhage, failure of remodeling embryonic and yolk sac vasculature, defective placental angiogenesis a

265 ial for normal growth and development of the yolk sac vasculature.

266 Wnt signaling was upregulated in Chd4 mutant yolk sac vasculature.

267 lethality may be attributable to defects in yolk sac vasculogenesis and angiogenesis.

268 diated activation of Tbeta4 is essential for yolk sac vasculogenesis and embryonic survival, and admi

269 wnstream target of Hand1 and reveal impaired yolk sac vasculogenesis as a primary cause of early embr

270 o undergo cardiac looping and have defective yolk sac vasculogenesis, both cardiac and yolk sac morph

271 primitive erythroid cells, and an absence of yolk sac vasculogenesis, followed by embryonic lethality

272 erythroid cells affect cardiac development, yolk sac vasculogenesis, or viability in the mouse.

273 oid cell fragility and subsequent defects in yolk sac vasculogenesis, we expressed Tmod1 specifically

274 For in utero gene delivery, we did yolk sac vessel injection at midgestation of mouse embry

275 N629D/N629D yolk sac vessels and aorta consist of sinusoids without

276 e the ability to roll and adhere on inflamed yolk sac vessels during late fetal development, whereas

277 Yolk sac vessels in the E10.5 null mutant fail to remode

278 g, adhesion, and extravasation from inflamed yolk sac vessels is apparent late in development, but th

279 tically modulate Wnt signaling in developing yolk sac vessels to mediate normal vascular remodeling.

280 As previously reported for INS in the yolk sac, we demonstrate complex, tissue-specific imprin

281 Capillaries of the yolk sacs were disorganized, and the endothelium of majo

282 The human embryo retains a yolk sac, which goes through primary and secondary phase

283 hypoblast gives rise to a transient primary yolk sac, which is rapidly superseded by a secondary yol

284 Subsequently, definitive MEPs expand in the yolk sac with Meg-CFCs and definitive erythroid progenit

285 While yolk sac (YS) also contained lymphopoietic cells after E

286 denocarcinoma (PDAC) originate from both the yolk sac (YS) and bone marrow.

287 ro MF-depletion strategy and fate-mapping of yolk sac (YS) and fetal liver (FL) hematopoiesis.

288 lack systemic blood circulation, that the E9 yolk sac (YS) and the intra-embryonic para-aortic splanc

289 ly validate the use of gestational sac (GS), yolk sac (YS) diameter, crown-rump length (CRL), and emb

290 The putative progenitors of trMacs, yolk sac (YS) erythromyeloid progenitors, did not expres

291 During chicken yolk sac (YS) growth, mesodermal cells in the area vascu

292 The extra-embryonic yolk sac (YS) is the first hematopoietic site in the mou

293 tes and macrophages, but was dispensable for yolk sac (YS) macrophages and for the development of YS-

294 evidence that support either extra-embryonic yolk sac (YS) macrophages or hematopoietic stem cells (H

295 enitor/colony-forming cells of the embryonic yolk sac (YS), which are endowed with megakaryocytic pot

296 The relative contribution of yolk sac (YS)-derived cells to the circulating definitiv

297 lineage tracing, we identify a first wave of yolk sac (YS)-derived primitive myeloid progenitors that

298 t ACE+CD45-CD34+/- hemangioblasts are common yolk sac (YS)-like progenitors for not only endothelium

299 lose association in the blood islands of the yolk sac (YS).

300 cluding impaired vascular development in the yolk sac (YS).