ライフサイエンスコーパス: mESC

1 Reverting serum mESCs to ground-state 2i mESCs removes these promoter-promoter interactions in a

2 ent at bivalent promoters in ground-state 2i mESCs, is necessary, but not sufficient, to establish th

3 PII, enhancing RA signaling and accelerating mESC differentiation in response to RA.

4 d the gene expression profile of embryo- and mESC-derived CPCs and CMs at different developmental sta

5 ), endothelial cells (EDCs), fibroblasts and mESCs.

6 ed pervasive transcription in both yeast and mESCs.

7 mechanisms may not yet be fully developed as mESCs express lower levels of IFN-stimulated genes and d

8 pluripotency-associated genes and attenuates mESC self-renewal without inducing differentiation.

9 compared control and ERbeta knockout (BERKO) mESCs at defined stages of neural development and examin

10 scripts are differentially expressed between mESCs and mEpiSCs and that these genes show expected cha

11 embryonic stem cell-derived cardiomyocytes (mESC-CMs).

12 on of extracellular matrix remodeling causes mESCs to differentiate.

13 at perturbing cell-secreted signaling causes mESCs to exit their stable self-renewing state in define

14 fferentiation competency of the Cdk2ap1(-/-) mESCs was restored upon the ectopic expression of Cdk2ap

15 ing and modulates mouse embryonic stem cell (mESC) differentiation in part through deacetylation of c

16 the analysis of murine embryonic stem cell (mESC) differentiation in vitro in response to inducers o

17 is study, we used mouse embryonic stem cell (mESC) differentiation to uncover a new mechanism for PI3

18 n three syngeneic mouse embryonic stem cell (mESC) lines: htt(-/-), extended poly-Q (Htt-Q140/7), and

19 kout (H1DeltaTKO) mouse embryonic stem cell (mESC) model system.

20 is essential for mouse embryonic stem cell (mESC) pluripotency and early development.

21 anisms regulating mouse embryonic stem cell (mESC) self-renewal and lineage differentiation, we have

22 ar foundations of mouse embryonic stem cell (mESC) self-renewal by applying a proven Bayesian network

23 Mouse embryonic stem cell (mESC) self-renewal can be maintained by activation of th

24 edium-throughput murine embryonic stem cell (mESC)-based high-content screening of 17000 small molecu

25 atin modifiers in mouse embryonic stem cell (mESC).

26 xa6 and Hoxa7 in mouse embryonic stem cells (mESC) by recruiting MLL1 to chromatin.

27 fferentiation of mouse embryonic stem cells (mESC) into neural lineages, we compared control and ERbe

28 Murine embryonic stem cells (mESC) were fused with human endothelial cells in stable,

29 gulating 5hmC in mouse embryonic stem cells (mESC).

30 T3) signaling in mouse embryonic stem cells (mESC).

31 in demethylated mouse embryonic stem cells (mESCs) and epiblast-derived stem cells.

32 tly expressed in mouse embryonic stem cells (mESCs) and has been implicated in mESC maintenance.

33 unction study in mouse embryonic stem cells (mESCs) and identified 20 lincRNAs involved in the mainte

34 Naive mouse embryonic stem cells (mESCs) and primed epiblast stem cells (mEpiSCs) represen

35 g maintenance of mouse embryonic stem cells (mESCs) and subsequent embryogenesis.

36 Mouse embryonic stem cells (mESCs) are clonal populations derived from preimplantati

37 ly reported that mouse embryonic stem cells (mESCs) are deficient in expressing type I interferons (I

38 Mouse embryonic stem cells (mESCs) are key tools for genetic engineering, developmen

39 opmental stages, mouse embryonic stem cells (mESCs) are resistant to cell fate conversion induced by

40 We have measured mouse embryonic stem cells (mESCs) at different states during differentiation (t=0h,

41 ipotent state of mouse embryonic stem cells (mESCs) by enabling LIF-dependent STAT3 phosphorylation,

42 ve reported that mouse embryonic stem cells (mESCs) can be selectively induced in vitro to differenti

43 ion of Nup153 in mouse embryonic stem cells (mESCs) causes the derepression of developmental genes an

44 Female mouse embryonic stem cells (mESCs) contain two active X chromosomes, with one underg

45 Mouse embryonic stem cells (mESCs) cultured under serum/LIF conditions exhibit heter

46 Mouse embryonic stem cells (mESCs) deficient for DGCR8, a key component of the micro

47 Studies with mouse embryonic stem cells (mESCs) demonstrated an increase in overall beta(1,3)gala

48 ripotency, while mouse embryonic stem cells (mESCs) display a naive or primed pluripotent state.

49 MLL3 and MLL4 in mouse embryonic stem cells (mESCs) does not disrupt self-renewal.

50 fferentiation of mouse embryonic stem cells (mESCs) generates a population with many of the propertie

51 ipotent state of mouse embryonic stem cells (mESCs) has been increasingly well-characterized.

52 embryos and from mouse embryonic stem cells (mESCs) have primarily been studied within a cell populat

53 e we "stressed" murine embryonic stem cells (mESCs) in vitro with epinephrine (EPI) during their adip

54 cient to convert mouse embryonic stem cells (mESCs) into 2-cell-embryo-like ('2C-like') cells, measur

55 terconversion of mouse embryonic stem cells (mESCs) is a valuable in vitro model for early embryonic

56 fferentiation of mouse embryonic stem cells (mESCs) is accompanied by changes in replication timing.

57 A methylation in mouse embryonic stem cells (mESCs) lacking the de novo DNA methyltransferases (Dnmts

58 Mouse embryonic stem cells (mESCs) maintain pluripotency and indefinite self-renewal

59 t3/4 (Pou5f1) in mouse embryonic stem cells (mESCs) maintained under standard culture conditions to g

60 pluripotency in mouse embryonic stem cells (mESCs) relies on the activity of a transcriptional netwo

61 ion of Cited2 in mouse embryonic stem cells (mESCs) remains elusive.

62 Mouse embryonic stem cells (mESCs) represent a valuable research tool to conduct in

63 e maintenance of mouse embryonic stem cells (mESCs) requires LIF and serum.

64 apping of 5fC in mouse embryonic stem cells (mESCs) reveals that 5fC preferentially occurs at poised

65 gene editing in mouse embryonic stem cells (mESCs) to produce mice with targeted gene disruptions an

66 The ability of mouse embryonic stem cells (mESCs) to self-renew or differentiate into various cell

67 be generated in mouse embryonic stem cells (mESCs) via CRISPR/Cas9.

68 pluripotency of mouse embryonic stem cells (mESCs) was extracted from several ChIP-Seq and knockdown

69 fferentiation of mouse embryonic stem cells (mESCs), and is particularly high in the promoter regions

70 II) promoters in mouse embryonic stem cells (mESCs), and this activity correlates with CpG islands.

71 OG expression in mouse embryonic stem cells (mESCs), and to dissect the lineage potential of mESCs at

72 pluripotency of mouse embryonic stem cells (mESCs), but the detailed mechanism remains unclear.

73 of Brca2(cko/ko) mouse embryonic stem cells (mESCs), carrying a null (ko) and a conditional (cko) all

74 d PRC2-deficient mouse embryonic stem cells (mESCs), demonstrating an H3K27me3-independent pathway fo

75 re, we show that mouse embryonic stem cells (mESCs), either lacking Tet3 alone or with triple deficie

76 In murine embryonic stem cells (mESCs), Gsk3beta is inhibited by multiple mechanisms, in

77 ansduce, such as mouse embryonic stem cells (mESCs), human ESCs (hESCs), and induced pluripotent stem

78 3) substrates in mouse embryonic stem cells (mESCs), providing a broad profile of GSK-3 activity and

79 In mouse embryonic stem cells (mESCs), the transcriptional network can be divided into

80 on self-renewing mouse embryonic stem cells (mESCs), where shear stresses varying by >1000 times (0.0

81 In mouse embryonic stem cells (mESCs), Wnt proteins stimulate mESC self-renewal and sup

82 nal regulator of mouse embryonic stem cells (mESCs), Yin-yang 2 (YY2), that is controlled by the tran

83 A transcripts in mouse embryonic stem cells (mESCs).

84 RNAs (sgRNAs) in mouse embryonic stem cells (mESCs).

85 cision making in mouse embryonic stem cells (mESCs).

86 translation in murine embryonic stem cells (mESCs).

87 cerevisiae and murine embryonic stem cells (mESCs).

88 nd 5mC levels in mouse embryonic stem cells (mESCs).

89 cell mass stage murine embryonic stem cells (mESCs).

90 sphate groups in mouse embryonic stem cells (mESCs).

91 maintenance of murine embryonic stem cells (mESCs).

92 fferentiation of mouse embryonic stem cells (mESCs).

93 self-renewal of mouse embryonic stem cells (mESCs).

94 dies (nEBs) from mouse embryonic stem cells (mESCs).

95 cells (FSCs) and mouse embryonic stem cells (mESCs).

96 -purple (P), in mouse embryonic stem cells (mESCs).

97 e fabricated by encapsulating pure mESC-CMs, mESC-CMs + adult CFs, or mESC-CMs + fetal CFs in fibrin-

98 r efficient derivation of germline-competent mESCs from any mouse strain, including strains previousl

99 nhancing Brf1 expression does not compromise mESC pluripotency but does preferentially regulate mesen

100 then integrated these data into a consensus mESC functional relationship network focused on biologic

101 rated that STAT3 activation and consequently mESC fate were manipulable by flow rate, position in the

102 ing of the regulatory topology that controls mESC fate decisions as well as to develop robust directe

103 itors (2i), and LIF, similar to conventional mESCs.

104 e have developed a novel approach to convert mESCs to XEN cells (cXEN) using growth factors.

105 We demonstrate that SIRT1-deficient mESCs are hypersensitive to methionine restriction/deple

106 We demonstrate mESC culture for several days under continuous microflui

107 Our results demonstrated mESCs were susceptible to viral infection, but they were

108 scription is up-regulated in differentiating mESCs and that chemical inhibition of beta-catenin/TCF1

109 idelity, particularly in the differentiating mESCs.

110 expression dynamics of retinoic acid driven mESC differentiation from pluripotency to lineage commit

111 involved in germ layer specification during mESC differentiation in a cooperative and redundant fash

112 ce of a saturated soluble environment (i.e., mESC-conditioned medium), we ascertained that flow-induc

113 elopmental pluripotency state to the earlier mESC-like pluripotency state, providing new insights int

114 e endoderm cells of which cognate embryonic (mESCs) or extra-embryonic (XEN) stem cell lines can be d

115 Then, a genetically-engineered mESC line with the stable integration of this vector was

116 The results suggest that Icaritin enhances mESCs self-renewal by regulating cell cycle machinery an

117 ole of Myc in the maintenance of murine ESC (mESC) pluripotency through the regulation of a set of mi

118 (BMP4) is sufficient to maintain mouse ESCs (mESCs) in a self-renewing state, this does not preclude

119 We report that, in naive mouse ESCs (mESCs), p53 restricts the expression of the de novo DNA

120 mined the potential of EXT1(-/-) mouse ESCs (mESCs), that are deficient in HS, to differentiate into

121 endogenous Fgf4, which is necessary to exit mESC self-renewal, but not for XEN cell maintenance.

122 P4 is more prone to degradation in EXT1(-/-) mESCs culture medium compared with that of wild type cel

123 We observed that EXT1(-/-) mESCs lost their differentiation competence and failed t

124 NANOG fluctuations provide opportunities for mESCs to explore multiple lineage options, modulating th

125 somatic cell type cell cycle regulation for mESCs to enter into the differentiation process.

126 (CPCs) and cardiomyocytes (CMs) derived from mESCs and mouse embryos.

127 cXEN cells can be derived from mESCs cultured with Erk and Gsk3 inhibitors (2i), and LI

128 represent a pluripotent state distinct from mESCs.

129 ingle cell gene expression measurements from mESCs cultured in serum/LIF or serum-free 2i/LIF conditi

130 medium or threonine dehydrogenase (Tdh) from mESCs decreased accumulation of SAM and decreased trimet

131 Here, we use gastruloids, mESC-based organoids, as a model system with which to st

132 Finally, we generated mESC-like hESCs by culturing them in mESC conditions.

133 els were significantly altered in H1DeltaTKO mESC.

134 fluorescence microscopy of intact H1DeltaTKO mESC demonstrated both a loss of nucleolar RNA content a

135 stituted immune system was tolerant to host, mESC, and BM transplant donor antigens.

136 extensive metabolic aberrations in htt(-/-) mESCs, including (i) complete failure of ATP production

137 In mESC-CM monolayers, CF-conditioned media did not alter C

138 Gli2 protein was heterogeneously detected in mESC nuclei by immunofluorescence microscopy and this re

139 sociation and disrupted Prdm14's function in mESC gene expression and PGC formation in vitro.

140 tem cells (mESCs) and has been implicated in mESC maintenance.

141 The functional improvements in mESC-CM + fetal CF patches were associated with differen

142 y, the functions of the affected proteins in mESC closely overlapped with those of the human T cell n

143 ng that it was mediated by the NPY system in mESC's.

144 a complex interplay between Tet1 and Tet2 in mESC, and to distinct roles for these two proteins in re

145 nerated mESC-like hESCs by culturing them in mESC conditions.

146 In mESCs, the proteins bind to active and poised TBP-bound

147 In mESCs, these genes are associated with dominant proximal

148 endent on miRNAs that are highly abundant in mESCs.

149 r II (TGFBR2) and for biological activity in mESCs.

150 erting methionine to S-adenosylmethionine in mESCs, methionine adenosyltransferase 2a (MAT2a), is und

151 erarchical signalling pathway alterations in mESCs.

152 on following the loss of miRNA biogenesis in mESCs.

153 Targeted disruption of Cdk2ap1 in mESCs resulted in abrogation of leukemia inhibitory fact

154 the presence of two active X chromosomes in mESCs prevents exit from pluripotency by blocking MAPK s

155 Taken together, a deletion of Cited2 in mESCs results in abnormal mitochondrial morphology and i

156 ey directly and/or functionally crosstalk in mESCs.

157 diate type I IFN expression are deficient in mESCs.

158 criminates apoptosis from differentiation in mESCs.

159 eliminated by siRNA knockdown of ERalpha in mESCs.

160 mponents in the IFN pathway are expressed in mESCs.

161 ranscriptional control of gene expression in mESCs.

162 d Nanog transcript and protein expression in mESCs.

163 scriptional activity of Oct3/4 fluctuates in mESCs and that Oct3/4 plays an essential role in sustain

164 nisms associated with E-cadherin function in mESCs is compounded by the difficulty in delineating the

165 the effects of type I IFNs are functional in mESCs; however, these mechanisms may not yet be fully de

166 regulate specific sets of expressed genes in mESCs and during differentiation.

167 8) overrepresented in p53-regulated genes in mESCs.

168 expand the catalog of p53 regulated genes in mESCs.

169 Finally, forced activation of Gli2 in mESCs increased their proliferation rate.

170 ngly, these loci are enriched for H3K9me3 in mESCs, implicating this mark in DNA methylation homeosta

171 MSL is the main HAT acetylating H4K16 in mESCs, is enriched at many mESC-specific and bivalent ge

172 e active (retinoic acid-inducible gene I) in mESCs.

173 lf2 expression can replace Mek inhibition in mESCs, allowing the culture of Klf2-null mESCs under Gsk

174 he metabolism of glucose was investigated in mESCs, which contained a deletion in the gene for Cited2

175 can induce dsRNA-activated protein kinase in mESCs, and this activation resulted in a strong inhibiti

176 Deletion of B-type lamins in mESCs caused a reduced interaction between regions of Hi

177 ts that functionally regulate mRNA levels in mESCs, including one in the Dgcr8 mRNA.

178 RYBP-PRC1 is recruited to target loci in mESCs and is also involved in Xist RNA-mediated silencin

179 omotes the persistence of DNA methylation in mESCs, likely reflecting one mechanism by which DNA meth

180 iated crosstalk between lncRNAs and mRNA, in mESCs, is thus surprisingly prevalent, conserved in mamm

181 huttles between the cytoplasm and nucleus in mESCs but accumulates in the cytoplasm in an inactive fo

182 to promote self-renewal and pluripotency in mESCs partly by opposing MAPK/ERK-mediated differentiati

183 SP7 to modulate transcriptional processes in mESCs similar to MYC.

184 pathway showed unique expression profiles in mESCs and validated this observation by RT-PCR analysis.

185 ntiation and antidifferentiation programs in mESCs.

186 f MSL and NSL to transcription regulation in mESCs is not well understood.

187 in a better understanding of self-renewal in mESCs.

188 C, or NC2 by anchor away in yeast or RNAi in mESCs leads to near-identical transcriptome phenotypes,

189 Hoxa6 and Hoxa7, transcriptionally silent in mESCs, and activated by retinoic acid.

190 to keep a subset of bivalent genes silent in mESCs, while developmental genes require MSL for express

191 ted sequencing of 295 dCas9 binding sites in mESCs transfected with catalytically active Cas9 identif

192 transition from Lewis(x)-type structures in mESCs to sialylated Galbeta1,3GalNAc-type glycans on dif

193 ) and Rbl2/p130 are remarkably suppressed in mESCs treated with Icaritin.

194 deletion, RNAi-mediated depletion of Tet1 in mESCs led to a significant reduction in 5hmC and loss of

195 ating a transgenic system we exhibit that in mESCs, the pluripotency master regulator Oct4, counterac

196 Here, we show that, in mESCs, the Polycomb repressive complex 2 (PRC2)-associat

197 Epiblast-state transition in mESCs involves heparan sulfate proteoglycans (HSPGs), wh

198 ) and activates its nuclear translocation in mESCs.

199 chastic NANOG fluctuations are widespread in mESCs, with essentially all expressing cells showing flu

200 Icaritin increases mESCs proliferation while maintains their self-renewal c

201 anscriptional activator with TCF1 influences mESC fate.

202 itor cells, suggesting that the induction is mESC specific.

203 f serum factors and feeder cells to maintain mESCs in culture.

204 f MAPK/ERK signaling, both known to maintain mESCs in the absence of LIF, rescued Tet1 depletion, fur

205 tylating H4K16 in mESCs, is enriched at many mESC-specific and bivalent genes.

206 e of methionine metabolism in SIRT1-mediated mESC maintenance and embryonic development.

207 The analysis of newly generated mutant mESCs revealed that DGCR8 is essential for the exit from

208 n-regulated gene in Zbtb24 homozygous mutant mESCs, which can be restored by ectopic ZBTB24 expressio

209 nctions of DGCR8, we complemented the mutant mESCs with a phosphomutant DGCR8, which restored microRN

210 mental potential of low-NANOG and high-NANOG mESCs, grown in different conditions, and confirm that m

211 These experiments utilized novel mESC lines in which Ptch1, Ptch2, Smo, Shh and 7dhcr wer

212 STAT3 phosphorylation, with E-cadherin null mESCs exhibiting over 3000 gene transcript alterations a

213 Indeed, while Klf2-null mESCs can survive under LIF/Serum, they are not viable u

214 in mESCs, allowing the culture of Klf2-null mESCs under Gsk3 inhibition alone.

215 Application to Tdg null mESCs further suggests that 5fC production coordinates w

216 udy, we assembled an extensive compendium of mESC data: approximately 2.2 million data points, collec

217 vely, our studies show that 3D co-culture of mESC-CMs with embryonic CFs is superior to co-culture wi

218 g NKG2D in vitro resulted in less killing of mESC by allogeneic NK cells, indicating NKG2D is a likel

219 likely mechanism for NK-mediated killing of mESC.

220 revealing a previously undescribed level of mESC regulation through the use of microfluidic perfusio

221 a significant reduction in 5hmC and loss of mESC identity.

222 we conclude that YY2 is a major regulator of mESC self-renewal and lineage commitment and document a

223 thway converges on c-myc, a key regulator of mESC self-renewal.

224 Here, we show that transplantation of mESC-derived TEPs results in the efficient establishment

225 Here, we report that small aggregates of mESCs, of about 300 cells, self-organise into polarised

226 triggered in three-dimensional aggregates of mESCs, the population self-organizes macroscopically and

227 data support the conclusion that analysis of mESCs in the hours/days immediately following efficient

228 h adherent and three-dimensional cultures of mESCs to probe the establishment and maintenance of NMps

229 ency factor in the proper differentiation of mESCs by modulating the phosphorylation level of pRb.

230 gulatory mechanism during differentiation of mESCs into cardiomyocytes.

231 ession of YY2 directs the differentiation of mESCs into cardiovascular lineages.

232 cell energy level during differentiation of mESCs into the cardiomyocytes and their apoptosis.

233 that the CDK2AP1-mediated differentiation of mESCs was elicited through the regulation of pRb.

234 ual RBPs inhibited neural differentiation of mESCs.

235 ithdrawal of LIF leads to differentiation of mESCs.

236 n event necessary for the differentiation of mESCs.

237 for the CDK2AP1-mediated differentiation of mESCs.

238 ling pathway inhibits the differentiation of mESCs.

239 oliferation and colony forming efficiency of mESCs.

240 The enhancement of mESCs self-renewal is characterized by increased populat

241 The failure of mESCs to express IFNalpha/beta was further demonstrated

242 es proliferation and cellular homeostasis of mESCs.

243 Isotope labeling of mESCs revealed that threonine provides a substantial fra

244 employed dictates the cellular phenotype of mESCs.

245 symmetrical self-renewal and pluripotency of mESCs in culture.

246 Cs), and to dissect the lineage potential of mESCs at different NANOG states.

247 these findings suggest that the potential of mESCs includes the capacity to give rise to both extra-e

248 ent unique and uncharacterized properties of mESCs and are important for understanding innate immunit

249 ere, we report single cell RNA-sequencing of mESCs cultured in three different conditions: serum, 2i,

250 I IFNs do not affect the stem cell state of mESCs.

251 ed teratomas indistinguishable from those of mESCs, and underwent efficient osteogenic differentiatio

252 Further analysis on mESC maintenance or differentiation-related gene express

253 ed pathways should have functional impact on mESC proliferation and differentiation.

254 ting pure mESC-CMs, mESC-CMs + adult CFs, or mESC-CMs + fetal CFs in fibrin-based hydrogel.

255 he unique behaviors of individual embryo- or mESC-derived cardiac cells.

256 Our mESC network predicts many novel players involved in sel

257 In differentiating p53(-/-) mESCs, elevated methylation persists, albeit more mildly

258 with DNA methylation heterogeneity, p53(-/-) mESCs display increased cellular heterogeneity both in t

259 lation imbalance in p53-deficient (p53(-/-)) mESCs is the result of augmented overall DNA methylation

260 e not present in 2i ground-state pluripotent mESCs but appear upon their further development into pri

261 By using this protocol, mESCs can be derived in 3 weeks and fully characterized

262 ole of paracrine signaling, we cultured pure mESC-CMs within miniature tissue "micro-patches" supplem

263 atches were fabricated by encapsulating pure mESC-CMs, mESC-CMs + adult CFs, or mESC-CMs + fetal CFs

264 to patches containing adult CFs, while pure mESC-CM patches did not form functional syncytium.

265 YY2 plays a critical role in regulating mESC functions through control of key pluripotency facto

266 t that beta-catenin's function in regulating mESCs is highly context specific and that its interactio

267 This study demonstrates that self-renewing mESCs possess the molecular machinery to sense shear str

268 file strikingly reminiscent of self-renewing mESCs with high Nanog expression.

269 confirmed by Capture Hi-C on Eed(-/-) serum mESCs.

270 r further development into primed-like serum mESCs.

271 Reverting serum mESCs to ground-state 2i mESCs removes these promoter-pr

272 c stem cells (mESCs), Wnt proteins stimulate mESC self-renewal and support the naive state.

273 With this approach, we found that mESC-derived Nkx2-5(+) CPCs preferentially become SMCs o

274 fferent developmental stages and showed that mESC-derived CMs are phenotypically similar to embryo-de

275 We conclude that mESCs are deficient in type I IFN expression, but they c

276 wn in different conditions, and confirm that mESCs are more susceptible to enter differentiation at t

277 We further demonstrate that mESCs must be released from Oct4-maintained pluripotency

278 This raises the possibility that mESCs can generate self-renewing XEN cells without the r

279 Here, we report that mESCs are able to respond to type I IFNs, express IFN-st

280 g (with heparin) HSPG function, we show that mESCs also mechanically sense shear stress via HSPGs to

281 Here we show that mESCs treated with the E-cadherin neutralising antibody

282 These data suggest that mESCs are a unique stem cell type possessing a DNA methy

283 We suggest that mESCs possess a unique DNA methylation-independent mecha

284 erstanding the impact of UPF1 and NMD on the mESC transcriptome.

285 However, full conversion of EpiSCs to the mESC-like state with chimerism competence could be readi

286 y maintenance in the epiblast from which the mESCs are derived.

287 When placed in vivo, these mESC-derived TEPs differentiate into cortical and medull

288 ric mice can be generated by injecting these mESCs into host blastocysts.

289 at Tet1 targets, ultimately contributing to mESC differentiation and the onset of embryonic developm

290 matic morphological changes in EpiSCs toward mESC phenotypes with simultaneous activation of inner ce

291 d medium (CM) collected from UV (UV)-treated mESCs.

292 or the reduction of p53 levels in UV-treated mESCs.

293 Proteomic profiling of purified wild-type mESC nucleoli identified a total of 613 proteins, only ~

294 extended poly-Q (Htt-Q140/7), and wild-type mESCs (Htt-Q7/7) using untargeted metabolite profiling.

295 rk of pluripotency-associated factors, using mESCs as a model.

296 that fluctuations have similar kinetics when mESCs are cultured in standard conditions (serum plus le

297 Increased pHi also occurs with mESC differentiation and, when prevented, attenuates spo

298 represented in the probe set associated with mESCs maintained in the absence of puromycin.

299 represented in the probe set associated with mESCs maintained in the presence of puromycin.

300 emonstrated that XEN-like cells arise within mESC cultures.