ライフサイエンスコーパス: hESC

1 hESC/iPSC-derived ventricular (v) CMs and their engineer

2 hESCs cultured at low oxygen tensions are more pluripote

3 hESCs with stable knockdown of JMJD1C remain pluripotent

4 erentiation derived from 2 hiPSC lines and 2 hESC lines at 4 stages: pluripotent stem cells, mesoderm

5 ual colonies varied significantly within all hESC lines.

6 ockade prevented the rejection of allogeneic hESC-PE by human PBMCs in a humanized model in vivo.

7 accessibility were similar across hiPSC and hESC cell lines.

8 at hESCs that endogenously express CD30v and hESCs that artificially overexpress CD30v exhibit increa

9 hiPSCs and hESCs form interspecies chimeras with high efficiency, c

10 Both hiPSCs and hESCs share similar transcriptional regulatory mechanism

11 on were highly concordant between hiPSCs and hESCs, and clustering of 4 cell lines within each time p

12 ardiomyocyte differentiation from hiPSCs and hESCs.

13 Because hESC seeding density influences the subsequent pancreati

14 differentially expressed candidates between hESCs and hiPSCs, we identified a mitochondrial protein,

15 of ventricular (V) cardiomyocytes (CMs), but hESC-VCMs and their engineered tissues display immature

16 embryonic stem cell-derived cardiomyocytes (hESC-CMs) and HepG2 cells were treated with glucose, and

17 embryonic stem cell-derived cardiomyocytes (hESC-CMs) are similar to those seen in in vivo-derived m

18 used to establish human embryonic stem cell (hESC) and induced pluripotent stem cell (iPSC) lines wit

19 the formation of human embryonic stem cell (hESC) colonies.

20 low efficiency of human embryonic stem cell (hESC) derivation using somatic cell nuclear transfer (SC

21 he application of human embryonic stem cell (hESC) derivatives to regenerative medicine is now becomi

22 de, DeepCode, for human embryonic stem cell (hESC) differentiation by integrating heterogeneous featu

23 stem cell lines: human embryonic stem cell (hESC) line carrying the common T158M mutation (MECP2(T15

24 nal comparison of human embryonic stem cell (hESC) lines and hiPSC lines and have shown that hiPSCs a

25 report engineered human embryonic stem cell (hESC) lines for modeling these two disorders using locus

26 tly, we generated human embryonic stem cell (hESC) lines where both alleles of NEUROG3 were disrupted

27 stems, as well as human embryonic stem cell (hESC) lines.

28 genitors from the human embryonic stem cell (hESC), line ESI-017.

29 mic annotation in human embryonic stem cell (hESC)-derived pancreatic progenitor cells to guide the i

30 atches of grafted human embryonic stem cell (hESC)-derived progenitors.

31 n cell types, including embryonic stem cell (hESC)-derived, primary cells and established cell lines

32 bryonic stem cell-derived endothelial cells (hESC-ECs) were suspended in PBS or Matrigel and kept at

33 ons derived from human embryonic stem cells (hESC) and cell-free wild-type (WT) VZV, we demonstrated

34 ferentiated hes2 human embryonic stem cells (hESC) and Macaca nemestrina-induced PSC (iPSC) line-7 wi

35 the survival of human embryonic stem cells (hESC) constitutively expressing GFP (H9 Cre-LoxP) in dea

36 Differentiated human embryonic stem cells (hESC) continue to provide a model for studying early tro

37 els derived from human embryonic stem cells (hESC) provide an excellent tool for neurotoxicity screen

38 lls derived from human embryonic stem cells (hESC) transplanted into patients.

39 y mAb-A4 against human embryonic stem cells (hESC), which also bound specifically to N-glycans presen

40 erentiation from human embryonic stem cells (hESC).

41 lls derived from human embryonic stem cells (hESC-MGEs) can mitigate the pathological effects of spin

42 stem cell phenotype by both human ES cells (hESCs) and induced pluripotent stem cells (iPSCs) in res

43 generate nontransgenic naive human ES cells (hESCs).

44 was expressed in human embryonic stem cells (hESCs) and human dermal fibroblasts (hDFs) derived hiPSC

45 tal neurons from human embryonic stem cells (hESCs) and induced pluripotent stem cells (hiPSCs) is fu

46 n order to apply human embryonic stem cells (hESCs) and induced pluripotent stem cells (hiPSCs) to re

47 erived from both human embryonic stem cells (hESCs) and induced pluripotent stem cells (hiPSCs).

48 and behavior of human embryonic stem cells (hESCs) and induced pluripotent stem cells.

49 fferentiate both human embryonic stem cells (hESCs) and patient-derived induced pluripotent stem cell

50 fferentiation of human embryonic stem cells (hESCs) and reprogramming of somatic cells to pluripotenc

51 ors derived from human embryonic stem cells (hESCs) are a potential source of transplantable cells fo

52 Human embryonic stem cells (hESCs) are used as platforms for disease study, drug scr

53 Naive human embryonic stem cells (hESCs) can be derived from primed hESCs or directly from

54 tion conditions, human embryonic stem cells (hESCs) can be directed toward a mesendoderm (ME) or neur

55 Human embryonic stem cells (hESCs) can generate the three germ layers in culture; ho

56 MAD signaling in human embryonic stem cells (hESCs) ensures NANOG expression and stem cell pluripoten

57 e-knockout (TKO) human embryonic stem cells (hESCs) exhibit prominent bivalent promoter hypermethylat

58 used colonies of human embryonic stem cells (hESCs) grown on micropatterned substrate and differentia

59 ced apoptosis of human embryonic stem cells (hESCs) hampers their large-scale culture.

60 ional network of human embryonic stem cells (hESCs) has been extensively studied, relatively little i

61 Human embryonic stem cells (hESCs) have been routinely treated with bone morphogenet

62 Human embryonic stem cells (hESCs) have the capacity to differentiate into all cell

63 lls (hiPSCs) and human embryonic stem cells (hESCs) have the capacity to participate in normal mouse

64 tion outcomes in human embryonic stem cells (hESCs) in vitro Systematic investigation of morphogen si

65 on efficiency of human embryonic stem cells (hESCs) into heart muscle cells (cardiomyocytes) is highl

66 Human embryonic stem cells (hESCs) is a potential unlimited ex vivo source of ventri

67 ies derived from human embryonic stem cells (hESCs) lack HOXA expression compared with repopulation-c

68 d in transformed human embryonic stem cells (hESCs) or hESCs cultured in the presence of ascorbate.

69 m differentiated human embryonic stem cells (hESCs) or induced pluripotent stem cells (iPSCs).

70 lls (hiPSCs) and human embryonic stem cells (hESCs) remains controversial.

71 Human embryonic stem cells (hESCs) represent an unlimited cellular source for genera

72 n epiblast to existing embryonic stem cells (hESCs) reveals conservation of pluripotency but also add

73 s developed from human embryonic stem cells (hESCs) that carry the FMR1 mutation and are grown in cul

74 We used human embryonic stem cells (hESCs) to examine whether mechanical features of the ext

75 fferentiation of human embryonic stem cells (hESCs) to insulin-positive cells.

76 Here, we use human embryonic stem cells (hESCs) to show that the Activin-SMAD2/3 signaling pathwa

77 d p53 binding in human embryonic stem cells (hESCs) undergoing differentiation to define a high-confi

78 l hematopoiesis, human embryonic stem cells (hESCs) were allowed to differentiate in defined conditio

79 Until recently, human embryonic stem cells (hESCs) were shown to exist in a state of primed pluripot

80 In human embryonic stem cells (hESCs), bivalent genes with both activating (H3K4me3) an

81 the proteome of human embryonic stem cells (hESCs), cardiac progenitor cells (CPCs), and cardiomyocy

82 ng mutant FUS in human embryonic stem cells (hESCs), whereas knockdown of endogenous FUS has no effec

83 In human embryonic stem cells (hESCs), Wnt/beta-catenin signaling is active in naive-st

84 types including human embryonic stem cells (hESCs).

85 lls (hiPSCs) and human embryonic stem cells (hESCs).

86 ons derived from human embryonic stem cells (hESCs).

87 rent colonies of human embryonic stem cells (hESCs).

88 self-renewal of human embryonic stem cells (hESCs).

89 and survival of human embryonic stem cells (hESCs).

90 erentiation from human embryonic stem cells (hESCs).

91 POU5F1 locus in human embryonic stem cells (hESCs).

92 ncreased in human endometrial stromal cells (hESCs) during in vitro decidualization.

93 show that a broad repertoire of conventional hESC and transgene-independent human induced pluripotent

94 splantation into injured mouse spinal cords, hESC-MGEs differentiate into GABAergic neuron subtypes a

95 e metabolism of feeder-/feeder-free cultured hESCs.

96 Structurally, high-density hESCs localize their receptors to transforming growth fa

97 lasts and human embryonic stem cell-derived (hESC) neurons.

98 w post-transcriptional modulations determine hESC function.

99 upled to cell-cycle progression that directs hESCs toward NE.

100 During hESC differentiation toward a retinal lineage, a subset

101 e splicing patterns and their changes during hESC differentiation.

102 ctoderm (NE) fate, the first decision during hESC differentiation.

103 ression and upregulate ME genes during early hESC differentiation.

104 al organoids differentiated from gene-edited hESCs lacking RB.

105 yonic-stem-cell-derived pancreatic endoderm (hESC-PE) in mice.

106 RISPR-associated protein 9 (Cas9)-engineered hESC-RUNX1c-tdTomato reporter cell line with AHR deletio

107 The enriched hESC-RGCs possess long axons, functional electrophysiolo

108 after RA + SHH treatment, whereas human ESC (hESC) protocols have been generally less efficient.

109 Here, we created isogenic human ESCs (hESCs) with mutations in GWAS-identified susceptibility

110 se embryonic stem cells (mESCs), human ESCs (hESCs), and induced pluripotent stem cells (hiPSCs).

111 We have examined hESC-derived trophoblasts in the light of stringent crit

112 iously published transcriptomic profiles for hESC differentiated to TB by means of bone morphogenetic

113 Like PHB, HIRA is required for hESC self-renewal.

114 Our data suggest that neurons derived from hESC may have advantages compared to other cells for stu

115 tic behaviour of somatic cells emerging from hESC differentiation and to enable its wide application

116 of definitive in vivo functional HSPCs from hESC.

117 procedure was applied to data obtained from hESC-derived NS grown on MEA chips.

118 ound to be present on multiple proteins from hESC and OC.

119 he generation of insulin-positive cells from hESCs.

120 s in nascent neural progenitors derived from hESCs and hiPSCs in a sonic hedgehog-independent manner.

121 erve that functional MNs can be derived from hESCs at high efficiencies if treated with patterning mo

122 hat axonal infection of neurons derived from hESCs in a microfluidic device with cell-free parental O

123 HLCs differentiated from hESCs and hiPSCs could be engrafted in the liver parench

124 te innate lymphoid cell differentiation from hESCs.

125 ol for generating cortical interneurons from hESCs and analyze the properties and maturation time cou

126 n of AGM-derived hematopoietic lineages from hESCs.

127 these properties can indeed be obtained from hESCs.

128 of transplantable dopamine progenitors from hESCs.

129 enriched population of functional RGCs from hESCs, allowing future studies on disease modeling of op

130 is of human FX neurons derived in vitro from hESCs that provides a convenient tool for studying molec

131 In vitro neural differentiation of FX hESCs can thus serve as a most relevant system for the a

132 tiation of FX human embryonic stem cells (FX-hESCs), derived from FXS blastocysts.

133 onal properties of neurons generated from FX-hESCs.

134 the molecular karyotype of 25 clinical-grade hESC lines by whole-genome single nucleotide polymorphis

135 The large number of available clinical-grade hESC lines with defined molecular karyotypes provides a

136 Here, we grow hESCs in micropatterned colonies of 1-8 cells ('microCol

137 to the H1 human embryonic stem cell line (H1-hESC).

138 hUCMSCs, hESC-MSCs, and hiPSC-MSCs in CPC generated new bone and

139 suitable for delivering cells; (2) hUCMSCs, hESCs, and hiPSCs are promising alternatives to hBMSCs,

140 nitiate the differentiation of the implanted hESCs into new hair cells.

141 as a promising biocompatible tool to improve hESC culture.

142 - and loss-of-function analyses of let-7g in hESC-CMs demonstrate it is both required and sufficient

143 MitoIK, ATP was absent in hESC-VCMs.

144 PLB protein was differentially expressed in hESC (HES2, H9)- and iPSC-derived and adult vCMs.

145 tly present in adult but poorly expressed in hESC/iPSC-vCMs and its defined biological role in beta-a

146 functional consequences of PLB expression in hESC/iPSC-vCMs and hvCMTs.

147 Engineered upregulation of PLB expression in hESC/iPSC-vCMs restores a positive inotropic response to

148 or donor template delivery to mediate HDR in hESC line WA09.

149 Overexpression of let-7 family members in hESC-CMs enhances cell size, sarcomere length, force of

150 al roles and use of sarcKATP and mitoKATP in hESC-VCM.

151 tal ventricular arrhythmias were observed in hESC-CM-engrafted primates.

152 e that pharmacological inhibition of PTEN in hESC-derived neuronal progenitors significantly increase

153 chromatin status and cell fate decisions in hESCs.

154 est TALENs that were used with HDR donors in hESCs to generate an isogenic TS cell line in a scarless

155 egantly combine CRISPR-based gene editing in hESCs with directed beta cell differentiation to investi

156 ut also additional pathways more enriched in hESCs.

157 domain containing E1) is highly expressed in hESCs to maintain their undifferentiated state and preve

158 e 3 lysine 9 (H3K9) demethylase expressed in hESCs, directly interacts with this circuitry.

159 ition of histone H3.3 and gene expression in hESCs.

160 ith WT CD30v but not the T61A-mutant form in hESCs.

161 g RNA (siRNA)-mediated knockdown of GPR64 in hESCs remarkably reduced decidualization.

162 PKM2 expression was increased in hESCs cultured at 5% oxygen compared to 20% oxygen and s

163 ycolysis displayed a nuclear localisation in hESCs and silencing PKM2 did not alter glucose metabolis

164 However, the frequency of HDR remains low in hESCs.

165 gate the regulation of glucose metabolism in hESCs and whether this might impact OCT4 expression.

166 carry out site-specific gene modification in hESCs.

167 hlighting a transcriptional role for PKM2 in hESCs.

168 The maintenance of pluripotency in hESCs is under the control of the TGFbeta pathway.

169 ed in the hypoxic support of pluripotency in hESCs.

170 f the most dynamically expressed proteins in hESCs, CPCs, and cardiomyocytes.

171 nd define stimulus-specific p53 responses in hESCs.

172 s that PHB has an unexpected nuclear role in hESCs that is required for self-renewal and that it acts

173 ctivity, cell cycle changes, and survival in hESCs.

174 at are essential for POU5F1 transcription in hESCs.

175 CRISPR/CAS9 knockout of YAP in hESCs enables Activin to induce Wnt3 expression and stab

176 CD30 and CD30v are believed to increase hESC survival and proliferation through NFkappaB activat

177 rrelation was observed between the increased hESC survival rate and total accumulative displacement o

178 ulatory mechanisms involved, we investigated hESCs grown on three distinct culture platforms: feeder-

179 f-of-principle platform, which uses isogenic hESCs for functional evaluation of GWAS-identified loci

180 All mice received macroencapsulated hESC-derived progenitor cells, and thyroid dysfunction w

181 as a p53-regulated transcript that maintains hESC pluripotency in concert with core pluripotency fact

182 We conclude that YAP maintains hESC pluripotency by preventing WNT3 expression in respo

183 Here we use genetically matched hESC and hiPSC lines to assess the contribution of cellu

184 genes we detect between genetically matched hESCs and hiPSCs neither predict functional outcome nor

185 that, on a hydrogel-based compliant matrix, hESCs accumulate beta-catenin at cell-cell adhesions and

186 By contrast, on a stiff hydrogel matrix, hESCs show elevated integrin-dependent GSK3 and Src acti

187 SCs converted in NCM-MEF, however, all naive hESCs fail to differentiate towards functional cell type

188 However, remaining differences between naive hESCs and embryonic cells related to mono-allelic XIST e

189 f the mTORC2 subunit, in the different naive hESCs.

190 re in-depth understanding of different naive hESCs.

191 artially rescues cell proliferation in naive hESCs caused by inhibition of Wnt secretion.

192 ition of Wnt/beta-catenin signaling in naive hESCs did not cause differentiation.

193 f the stabilization of beta-catenin in naive hESCs reduces cell proliferation and colony formation.

194 role of Wnt/beta-catenin signaling in naive hESCs remains largely unknown.

195 f glycolysis decreases self-renewal of naive hESCs and feeder-free primed hESCs, but not primed hESCs

196 -specific differentiation potential of naive hESCs converted in NCM-MEF, however, all naive hESCs fai

197 Here we show that naive hESCs exhibit increased glycolytic flux, MYC transcripti

198 Thus, our results suggest that naive hESCs secrete Wnts that activate autocrine or paracrine

199 NEUROG3(-/-) hESC lines efficiently formed pancreatic progenitors but

200 Moreover, NEUROG3(-/-) hESC lines were unable to form mature pancreatic endocri

201 ol which enriched for glutamatergic neurons (hESC-neurons).

202 Consequently, YAP-null hESCs exposed to Activin differentiate precisely into be

203 RA affect chromatin state and competency of hESC-derived lineages to adopt specific neuronal fates.

204 ssing other cytotoxic insults on cultures of hESC.

205 thyroid dysregulation on the development of hESC-derived progenitor cells in vivo.

206 results support the clinical development of hESC-derived therapy, combined with tolerogenic treatmen

207 therapy allowed for long-term development of hESC-PE into islet-like structures capable of producing

208 with Matrigel, the long-term engraftment of hESC-ECs was increased through promoting angiogenesis an

209 adhesion and apoptosis genes' expression of hESC-ECs.

210 hypoxia and T3 enhance the functionality of hESC-VCMs and their engineered tissues by selectively ac

211 modelling and optimisation of the growth of hESC colonies.

212 chanistic understanding of the immaturity of hESC/iPSC-vCMs but will also lead to improved disease mo

213 proves long-term survival and integration of hESC-derived donor retinal cells.

214 Although the vast majority of hESC lines have been derived for research purposes only,

215 Promoting maturation of hESC-CMs with let-7 overexpression will be highly signif

216 e components of multiple regulatory nodes of hESC identity, neuroectoderm commitment and neurogenesis

217 gly, resides predominantly in the nucleus of hESC.

218 Since their first isolation the number of hESC lines has steadily increased to over 3000 and new i

219 nsity required to minimise the occurrence of hESC colonies arising from more than one founder cell an

220 a central post-transcriptional regulator of hESC identity and neurogenesis.

221 hiPSC lines analyzed, whereas no staining of hESC-derived hepatocyte-like or cardiomyocyte-like cells

222 olerability of subretinal transplantation of hESC-derived retinal pigment epithelium in nine patients

223 Glucose treatment of hESC-CMs for 6 h and 24 h increased levels of the primar

224 We found that the RCS values of hESC lines correlated directly with their DT, i.e. the f

225 Also, the ability of hESCs to form bona fide trophoblasts has been intensely

226 hancing mesoderm differentiation capacity of hESCs.

227 D2 primes neuroectodermal differentiation of hESCs and hiPSCs by binding and sequestering SMAD4 to th

228 influence tissue-specific differentiation of hESCs by altering the cellular response to morphogens.

229 A9 enhances hematopoietic differentiation of hESCs by specifically promoting the commitment of HEPs i

230 e analysis of early stage differentiation of hESCs with two distinct differentiation cues revealed cl

231 ibutor to early stages of differentiation of hESCs, in which LIN28 plays a central role.

232 the survival rate and cloning efficiency of hESCs by threefold.

233 ts and can be dictated by colony geometry of hESCs.

234 erein we leveraged the mechanosensitivity of hESCs and employed, to our knowledge, a novel technique,

235 nd how the kinematics of single and pairs of hESCs impact colony formation, we study their mobility c

236 t of H3K4me3/H3K27me3 in pure populations of hESCs in G2, mitotic, and G1 phases of the cell cycle, w

237 e system that mounts a vigorous rejection of hESCs and their derivatives.

238 RNA-seq of hESCs depleted of lncPRESS1 revealed that lncPRESS1 cont

239 newal and initial cell fate specification of hESCs.

240 f potassium in the SM facilitate survival of hESCs for at least one week.

241 ontaneous differentiation similar to that of hESCs.

242 Dependence on arginine is maintained once hESCs are differentiated to fibroblasts, neurons, and he

243 formed human embryonic stem cells (hESCs) or hESCs cultured in the presence of ascorbate.

244 assess the contribution of cellular origin (hESC vs. hiPSC), the Sendai virus (SeV) reprogramming me

245 Moreover, we find that LEF-1 and other hESC enhancers recruit RNAPII complexes (eRNAPII) that a

246 Furthermore, GLI3 knock-out hESCs can bypass the requirement for early RA patterning

247 d on lncRNAs highly expressed in pluripotent hESCs and repressed by p53 during differentiation to ide

248 Instead, it induced primed hESC-like proteomic and metabolic profiles.

249 rapid conversion of in-house-derived primed hESCs on mouse embryonic feeder layer (MEF) to a naive s

250 eduction of glycolysis in feeder-free primed hESCs also enhances neural specification.

251 enewal of naive hESCs and feeder-free primed hESCs, but not primed hESCs grown in feeder-supported co

252 tem cells (hESCs) can be derived from primed hESCs or directly from blastocysts, but their X chromoso

253 criptional activity is higher than in primed hESCs and nuclear N-MYC levels are elevated.

254 state resets Xi abnormalities seen in primed hESCs, it may provide cells better suited for downstream

255 and feeder-free primed hESCs, but not primed hESCs grown in feeder-supported conditions.

256 hat the inactive X chromosome (Xi) of primed hESCs was reactivated in naive culture conditions.

257 uclear N-MYC localization relative to primed hESCs.

258 om being induced by Activin in proliferating hESCs.

259 resence of Cell Tracer significantly reduces hESC mobility.

260 at control PI3K/AKT pathway in self-renewing hESCs.

261 Using reporter hESC lines to track the endothelial (SOX17) to hematopoi

262 anti-sialyl-lactotetra staining on all seven hESC lines and three hiPSC lines analyzed, whereas no st

263 radiation (IR) on continuous growth of seven hESC lines.

264 s that the expression of genes, which signed hESC- or HepaRG-cholangiocytes, separates hepatocytic li

265 We showed that SarcIK, ATP in single hESC-VCMs was dormant under baseline conditions, but bec

266 chanical stimulation of disassociated single hESCs to improve their survival.

267 a-catenin signaling is active in naive-state hESCs and is reduced or absent in primed-state hESCs.

268 SCs and is reduced or absent in primed-state hESCs.

269 Using this system, hESCs and hiPSCs can be easily and stably passaged by di

270 common T158M mutation (MECP2(T158M/T158M) ), hESC line expressing no MECP2 (MECP2-KO), congenic pair

271 Our results suggest that hESC-derived cells could provide a potentially safe new

272 4 expression were correlated suggesting that hESC self-renewal is regulated by the rate of glucose up

273 We conclude that hESCs and hiPSCs are molecularly and functionally equiva

274 Here we demonstrate that hESCs that endogenously express CD30v and hESCs that art

275 The hESC-derived perivascular progenitors described here hav

276 TM/ATR signalling activities and further the hESC differentiation.

277 ntly necessary to genetically manipulate the hESC genome.

278 sential to know the genetic stability of the hESC lines before progressing to clinical trials.

279 tome analysis demonstrated similarity of the hESC-derived RGCs to human adult RGCs.

280 ipotency-specific lncRNA that safeguards the hESC state by disrupting SIRT6 activity.

281 ignaling switches the terminal fate of these hESC-derived trophoblasts.

282 nd that the most abundant mRNAs within these hESC-neuron projections were functionally similar to the

283 d genotypic analyses demonstrated that these hESCs/hiPSCs are similar in their osteogenic differentia

284 Thus, hESC-EC are TLR4 deficient but respond to bacteria via N

285 ion and global inactivation of DNMT3B in TKO hESCs partially reverses the hypermethylation at the PAX

286 ted by environmental oxygen and localised to hESC membranes.

287 e mechanism linking histone modifications to hESC fate decision.

288 r in vivo long-term engraftment potential to hESC-hematopoietic derivatives, reinforcing the idea tha

289 Finally, we transplanted hESC-ECs into a mouse myocardial ischemia model.

290 Our results confirm that BAP treated hESC (ESCd) lack a mesoderm signature and are a subtype

291 ng diazoxide protective effect on T3-treated hESC-VCMs.

292 1(+) hematoendothelial cells in SR-1-treated hESCs, as well as a twofold expansion of CD34(+)CD45(+)

293 oietic differentiation relative to wild-type hESCs.

294 (DNMT)3b preferentially in undifferentiated hESCs as compared with CXCR4+ or islets cells.

295 -/-) mice after transplantation, and, unlike hESCs, transplanted hiEndoPCs do not give rise to terato

296 dependently derived, larger set of unmatched hESC and hiPSC lines.

297 ed differences between genetically unmatched hESCs and hiPSCs.

298 s via stepwise retinal differentiation using hESCs.

299 odel organisms, beta-actin and GAP43, within hESC-neuron projections using multiplexed single molecul

300 Interestingly, exposure of YAP(-/-) hESCs to Activin induces cardiac mesoderm markers (BAF60