ライフサイエンスコーパス: hESC

1 hESC-derived mDA neurons display A9 characteristics and

2 hESCs can spontaneously diploidize and can be maintained

3 hESCs limit the mutagenic potential of Lig3-mediated EJ

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

5 n of perfusable grafts containing additional hESC-derived cardiomyocytes show higher cardiomyocyte an

6 ual colonies varied significantly within all hESC lines.

7 nd LUXendin651, we describe islet, brain and hESC-derived beta-like cell GLP1R expression patterns, r

8 accessibility were similar across hiPSC and hESC cell lines.

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 s, cardiac differentiation from ARID1A (-/-) hESCs is prominently suppressed, whereas neural differen

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) contain nodal-like cardiomyocytes that spontan

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

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

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

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

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

23 Using a human embryonic stem cell (hESC)-based pancreatic differentiation system, we show t

24 ration markers in human embryonic stem cell (hESC)-derived beta-cells and human islets.

25 ce ACE2 levels in human embryonic stem cell (hESC)-derived cardiac cells and lung organoids.

26 ed the ability of human embryonic stem cell (hESC)-derived epicardium to augment the structure and fu

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

28 bryonic stem cell-derived endothelial cells (hESC-ECs) are seeded both into patterned microchannels a

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

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

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

32 py drugs against human embryonic stem cells (hESC) in which we engineered TP53 deletion by genome edi

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

34 eq experiment in human embryonic stem cells (hESC) revealed that DNMT3B, mCA and H3K36me3 share the s

35 l organoids from human embryonic stem cells (hESC) to investigate the effect of PCE on early human br

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

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

38 toid bodies from human embryonic stem cells (hESCs) and (PBMC)-originated, iPSCs employing the "fried

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

40 use Neurog2/1 in human embryonic stem cells (hESCs) and human induced pluripotent stem cells (hiPSCs)

41 Human embryonic stem cells (hESCs) and induced pluripotent stem cells (iPSCs) have p

42 Human embryonic stem cells (hESCs) and induced pluripotent stem cells (iPSCs) have t

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

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

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

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

47 ells (GPCs) from human embryonic stem cells (hESCs) derived from mutant Huntingtin (mHTT) embryos or

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

49 Human embryonic stem cells (hESCs) exhibit an intrinsic capacity for self-organizati

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

51 tion in mice and human embryonic stem cells (hESCs) expressing mutant fatty acid synthase (FASN; R181

52 fferentiation of human embryonic stem cells (hESCs) from endoderm toward terminally differentiated he

53 ation of mouse haploid embryonic stem cells (hESCs) from female gametes that also outlines how to mai

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

55 enerate isogenic human embryonic stem cells (hESCs) harboring clinically relevant mutations in telome

56 C phenotypes and human embryonic stem cells (hESCs) harbouring the same disease mutation are also lac

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

58 ound that single human embryonic stem cells (hESCs) have different and biased differentiation potenti

59 rofiles in naive human embryonic stem cells (hESCs) have not been systematically characterized.

60 lls derived from human embryonic stem cells (hESCs) have recently been investigated clinically as a f

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

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

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

64 ons derived from human embryonic stem cells (hESCs) into the striatum and assessed their survival, gr

65 When and how human embryonic stem cells (hESCs) irreversibly commit to differentiation is a funda

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

67 ntiated state in human embryonic stem cells (hESCs) is critical for further application in regenerati

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

69 lls derived from human embryonic stem cells (hESCs) may reveal why certain constellations of genetic

70 Os) derived from human embryonic stem cells (hESCs) or human induced pluripotent stem cells (hiPSCs)

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

72 enerate isogenic human embryonic stem cells (hESCs) that lack the individual protein isoforms.

73 rdiogenesis from human embryonic stem cells (hESCs) through distinct mechanisms.

74 Here, we use human embryonic stem cells (hESCs) to address how changing morphogen levels influenc

75 We engineered human embryonic stem cells (hESCs) to carry NCBRS-associated heterozygous SMARCA2 K7

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

77 to differentiate human embryonic stem cells (hESCs) to thalamic organoids (hThOs) that specifically r

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

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

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

81 We used human embryonic stem cells (hESCs) with a common dyskerin mutation (DKC1_A353V), whi

82 Maintenance of human embryonic stem cells (hESCs) with stable genome is important for their future

83 ing behaviors of human embryonic stem cells (hESCs), affecting their proliferation and differentiatio

84 pluripotency in human embryonic stem cells (hESCs), and individual subunits have varied and specific

85 s), derived from human embryonic stem cells (hESCs), provide a platform to study human brain developm

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

87 hancers in naive human embryonic stem cells (hESCs).

88 ls (RPCs) and in human embryonic stem cells (hESCs).

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

90 TET1 gene in H9 human embryonic stem cells (hESCs).

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

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

93 erentiation from human embryonic stem cells (hESCs).

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

95 types including human embryonic stem cells (hESCs).

96 ed in vitro from human embryonic stem cells (hESCs).

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

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

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

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

101 ion of "gastrulation-like" nodes in cultured hESCs.

102 the TET1 catalytic domain in TET1-deficient hESCs significantly increased 5hmC levels and elevated P

103 reased in teratomas formed by TET1-deficient hESCs.

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

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

106 w post-transcriptional modulations determine hESC function.

107 tional metabolic zonation in differentiating hESCs.

108 ygen gradient was applied to differentiating hESCs at the pre-hepatoblast stage.

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

110 e splicing patterns and their changes during hESC differentiation.

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

112 miRomes and transcriptomes generated during hESC-directed chondrogenesis identified key functionally

113 ghts extensive translation of lncRNAs during hESC pancreatic differentiation and provides a blueprint

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

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

116 We engineered hESCs to ectopically express human ETS variant 2 (ETV2).

117 RNA-sequencing of engrafted hESC-CMs confirmed the increased expression of matured v

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

119 effect of antiarrhythmic drugs on human ESC (hESC) und human induced pluripotent stem cell (hiPSC) de

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

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

122 In addition, the bars for hESC, Y-hiPSC, AG4-ZCNAN10, AG4 and LS in Supplementary

123 we demonstrate that SMARCB1 is essential for hESC super-enhancer silencing in neural differentiation

124 This turns out to be important for hESC pluripotency.

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

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

127 aneously beating cardiomyocytes derived from hESC and hiPSC was generally consistent with clinical ex

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

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

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

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

132 aneously beating cardiomyocytes derived from hESCs and hiPSCs were made using Microelectrode Arrays (

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

134 human retinal organoids differentiated from hESCs using an improved retinal differentiation system.

135 te innate lymphoid cell differentiation from hESCs.

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

137 n of AGM-derived hematopoietic lineages from hESCs.

138 of transplantable dopamine progenitors from hESCs.

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

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

141 Mutant H9 hESCs remained pluripotent, even though the level of hyd

142 xpression profiles of undifferentiated hESC, hESC-, fetal- and adult-ventricular(V) CM, two candidate

143 ongruent patient-specific cell types-hiPSCs, hESCs and direct-lineage-converted cells-derived from cu

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

145 of chondrogenesis will enable us to improve hESC chondrogenic differentiation protocols.

146 MitoIK, ATP was absent in hESC-VCMs.

147 ellular dye transfer and Ca(2+) diffusion in hESC colonies.

148 amic visualization/quantification of GJIC in hESC colonies.

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

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

151 ddition, the inhibition of the RA pathway in hESC-derived pancreatic progenitors downstream of NEUROG

152 ntified key regulatory networks prominent in hESC chondrogenesis.

153 D1 overexpression and SMARCD1 suppression in hESC-VCMs synergistically interacted to increase the con

154 acteristics of intercellular Ca(2+) waves in hESC colonies induced by sonoporation of single cells.

155 In hESCs, cytoplasm-localized hFAST binds to the WD40 domai

156 man NEUROG2 together with human NEUROG2/1 in hESCs using molecular, cellular, and electrophysiologica

157 DSBs in hESCs are also repaired via homologous recombination (HR

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

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

160 that while telomerase is highly expressed in hESCs, it is quickly silenced, specifically due to telom

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

162 ediated repair and a low mutant frequency in hESCs.

163 systems, SMARCB1 represses bivalent genes in hESCs and antagonizes chromatin accessibility at super-e

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

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

166 -interacting domain (PWWP) demolished mCA in hESCs, suggesting that PWWP domain of DNMT3B directs the

167 we show the DNA damage response mechanism in hESCs is composed of known, yet unlikely components.

168 carry out site-specific gene modification in hESCs.

169 ng the fidelity of the bivalent promoters in hESCs.

170 ccounts for the majority of UBE3A protein in hESCs and neurons.

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

172 ial in triggering the checkpoint response in hESCs.

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

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

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

178 Treatment of FLCN KO hESC with a Wnt inhibitor, but not ESRRB/FLCN double mut

179 CRISPR/Cas9-generated B3GALT5-knockout (KO) hESCs displayed an altered GSL profile, increased clonin

180 Here we show that FLCN Knock-out (KO) hESCs maintain the naive pluripotent state but cannot ex

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

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

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

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

185 In human GPCs (hGPCs) derived from 3 mHTT hESC lines, transcription factors associated with glial

186 bank, a biobank of >100,000 individual mouse hESC lines with targeted mutations in 16,970 genes.

187 Mouse hESCs are genomically and karyotypically stable, are inn

188 ion of EXOSC3 or PAPD5 levels in DKC1 mutant hESCs led to functional improvements in TERC levels and

189 While SMARCA2 mutant hESCs were phenotypically normal, differentiation to neu

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

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

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

193 re in-depth understanding of different naive hESCs.

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

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

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

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

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

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

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

201 ere sharply downregulated relative to normal hESC GPCs; NKX2.2, OLIG2, SOX10, MYRF, and their downstr

202 , which is highly expressed in mESCs but not hESCs.

203 es, either somatic cell nuclear transfer (NT-hESCs) or with defined factors (iPSCs).

204 at targeting ZNF207/BuGZ sensitizes p53-null hESC to cisplatin.

205 CRISPR/Cas9 knockout screen in the TP53-null hESC in the presence and absence of sublethal concentrat

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

207 t-time comparative transcriptome analysis of hESC- and iPSC-derived lentoid bodies at differentiation

208 The ultrastructure analysis of hESC- and iPSC-derived lentoid bodies identified closely

209 Comparative transcriptome analysis of hESC- and iPSC-derived lentoid bodies revealed 13,563 (>

210 This genomic assessment of hESC chromatin regulation by SMARCB1 reveals a novel pos

211 d remarkable similarities between the BRV of hESC and hiPSC derived cardiomyocytes in vitro and the H

212 Cotransplantation of hESC-derived epicardial cells and cardiomyocytes doubled

213 ssing other cytotoxic insults on cultures of hESC.

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

215 e demethylase LSD1 during differentiation of hESC-gut tube intermediates into pancreatic endocrine ce

216 t tissue in vitro and to improve efficacy of hESC-cardiomyocyte grafts in infarcted athymic rat heart

217 Herein, we examine the long-term efficacy of hESC-derived pancreatic endoderm cells (PECs) to maintai

218 del by applying it to our own experiments of hESC colony growth; while this is based on a particular

219 apparently as a means of priming the fate of hESC populations once they undergo differentiation.

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

221 tative framework for modelling the growth of hESC colonies from a given seeding density based on stoc

222 modelling and optimisation of the growth of hESC colonies.

223 se properties using phase-contrast images of hESC colonies of different sizes (0.1-1.1 [Formula: see

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

225 indings suggest that genetic manipulation of hESC-derived pulmonary cells will enable studies of this

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

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

228 our study points out the great potential of hESC and hiPSC derived tissue to be used routinely for m

229 g (RNA-Seq) based transcriptome profiling of hESC- and iPSC-derived lentoid bodies at differentiation

230 evant to efforts to determine the quality of hESC colonies and establish colony characteristics datab

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

232 Analysis identified regulators of hESC-directed chondrogenesis such as miR-29c-3p with 10

233 Next-generation RNA sequencing (RNA-Seq) of hESC- and iPSC-derived lentoid bodies detected expressio

234 mechanisms maintaining genomic stability of hESC and our ability to modulate them is essential in pr

235 quencing was performed on distinct stages of hESC-directed chondrogenesis.

236 e-dependent nature of ZIKV susceptibility of hESC-derived trophectoderm cells.

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

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

239 deficiency impairs the intrinsic ability of hESCs to differentiate to neuroectoderm, presumably by d

240 duced by extracellular matrix, aggregates of hESCs formed single-lumen cysts composed of epithelial c

241 hancing mesoderm differentiation capacity of hESCs.

242 of lncRNAs is localized in the cytoplasm of hESCs than in mESCs.

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

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

245 ink G1 length to differentiation outcomes of hESCs.

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

247 probability distribution for a population of hESCs and predicts differentiation outcome toward neuroe

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

249 newal and initial cell fate specification of hESCs.

250 ss of B3GALT5 induces a distinctive state of hESCs displaying unique GSL profiling with expression of

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

252 ontaneous differentiation similar to that of hESCs.

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

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

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

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

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

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

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

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

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

262 uclear N-MYC localization relative to primed hESCs.

263 om being induced by Activin in proliferating hESCs.

264 drugs reduced ACE2 expression and protected hESC-derived lung organoids against SARS-CoV-2 infection

265 Homozygous FASN R1819W hESC-derived NSPCs show reduced rates of proliferation i

266 resence of Cell Tracer significantly reduces hESC mobility.

267 a unique lineage-specific role in regulating hESC differentiation.

268 In addition, B3GALT5-KO rendered hESCs more resistant to calcium chelator in blocking ent

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

270 ual readout of the decidualization response (hESC-PRLY cells).

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

272 ssed and suppressed, respectively, in single hESC-VCMs as well as the 3D constructs Cardiac Micro Tis

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

274 e molecules and influx of Ca(2+) into single hESCs.

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

276 hes, and mathematical modeling, we find that hESCs commit to exiting pluripotency unexpectedly early.

277 The hESC-derived perivascular progenitors described here hav

278 6j did not include all n = 6 samples for the hESC, Y-hiPSC and AG4-ZSCAN10 groups as was stated in th

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

280 ntly necessary to genetically manipulate the hESC genome.

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

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

283 In vitro, the hESC-ECs lining the luminal walls readily sprout and ana

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

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

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

287 e mechanism linking histone modifications to hESC fate decision.

288 We transplanted hESC-derived midbrain dopamine (mDA) or cortical glutama

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

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

291 1(+) hematoendothelial cells in SR-1-treated hESCs, as well as a twofold expansion of CD34(+)CD45(+)

292 oietic differentiation relative to wild-type hESCs.

293 gene expression profiles of undifferentiated hESC, hESC-, fetal- and adult-ventricular(V) CM, two can

294 sion of neurogenic genes in undifferentiated hESCs.

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

296 s via stepwise retinal differentiation using hESCs.

297 pithelial and fiber cell transcriptomes with hESC- and iPSC-derived lentoid bodies transcriptomes and

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

299 Additionally, when compared with WT hESCs, cardiac differentiation from ARID1A (-/-) hESCs i

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