ライフサイエンスコーパス: mESC

1 mESCs can self-renew indefinitely in vitro.

2 mESCs were differentiated into mature Tbr1 or Ctip2-posi

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

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

5 ow the utility of ASTAR-seq, we profiled 384 mESCs under naive and primed pluripotent states as well

6 pe mTert protein, was fully functional, as a mESC line with homozygous hmTert alleles proliferated fo

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

8 tial role in early embryonic development and mESC homeostasis, and offers insights into the functiona

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

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

11 ed pervasive transcription in both yeast and mESCs.

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

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

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

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

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

17 222 insulated neighborhoods without causing mESC differentiation.

18 ' RNA analyses, a mouse embryonic stem cell (mESC) complementation assay and retrieval of patient-rel

19 ChR2) transfected mouse embryonic stem cell (mESC) derived motor neurons to explore short and long-te

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

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

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

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

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

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

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

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

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

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

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

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

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

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

34 on approaches in mouse embryonic stem cells (mESCs) and deep sequencing of rRNA intermediates, we inv

35 linked RNAs from mouse embryonic stem cells (mESCs) and found a high enrichment for tRNAs.

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

37 ldehyde prefixed mouse embryonic stem cells (mESCs) and investigated loop domains (median size of 200

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

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

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

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

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

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

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

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

46 re, we show that mouse embryonic stem cells (mESCs) can be coaxed to robustly undergo fundamental ste

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

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

49 Mouse embryonic stem cells (mESCs) cultured in the presence of LIF occupy a ground s

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

51 Mouse embryonic stem cells (mESCs) cultured with MEK/ERK and GSK3beta (2i) inhibitor

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

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

54 cid (RA)-induced mouse embryonic stem cells (mESCs) differentiation experiment.

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

56 Mouse embryonic stem cells (mESCs) display unique mechanical properties, including l

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

58 DNMT3L-deficient mouse embryonic stem cells (mESCs) exhibit downregulation of DNMT3A, especially DNMT

59 that pluripotent mouse embryonic stem cells (mESCs) form aggregates that upon embedding in an extrace

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

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

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

63 eased in Tet2 KO mouse embryonic stem cells (mESCs) in comparison with wild-type mESCs.

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

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

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

67 differentiating mouse embryonic stem cells (mESCs) leads to a surprisingly restricted defect in cran

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

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

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

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

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

73 nce of Mettl5 in mouse embryonic stem cells (mESCs) results in a decrease in global translation rate,

74 e-knockout (TKO) mouse embryonic stem cells (mESCs) reveal that Dnmt3b3 prefers Dnmt3b2 over Dnmt3a2

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

76 d datasets from murine embryonic stem cells (mESCs) to identify insulated neighborhoods that confine

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

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

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

80 instability in murine embryonic stem cells (mESCs) via DNA hypomethylation at pluripotency-factor pr

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

82 etroelements, in mouse embryonic stem cells (mESCs)(1-3).

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

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

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

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

87 In mouse embryonic stem cells (mESCs), chemical blockade of Gsk3alpha/beta and Mek1/2 (

88 In mouse embryonic stem cells (mESCs), CpG-rich developmental regulator genes are repre

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

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

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

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

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

94 plantation embryos and embryonic stem cells (mESCs), where loss of PRDM10 results in severe cell grow

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

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

97 cerevisiae and murine embryonic stem cells (mESCs).

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

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

100 e transitions of mouse embryonic stem cells (mESCs).

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

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

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

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

105 translation in murine embryonic stem cells (mESCs).

106 transduction in mouse embryonic stem cells (mESCs).

107 organization in mouse embryonic stem cells (mESCs).

108 rsensitivity) in mouse embryonic stem cells (mESCs).

109 e mTert locus in mouse embryonic stem cells (mESCs).

110 nd 127 miRNAs in mouse embryonic stem cells (mESCs).

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

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

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

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

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

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

117 In contrast, mESCs producing lower relative amounts of FL BRCA2 exhib

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

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

120 the DNMT3A protein level in DNMT3L-deficient mESCs partially recovers DNA methylation.

121 DNA methylation analysis of DNMT3L-deficient mESCs reveals hypomethylation at many DNMT3A target regi

122 e neuronal differentiation of Nono-deficient mESCs.

123 e that growth inhibition in PRDM10-deficient mESCs is in part mediated through EIF3B-dependent effect

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

125 Epistasis experiments with Tdg-deficient mESCs show no involvement of epigenetic DNA demethylatio

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

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

128 idelity, particularly in the differentiating mESCs.

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

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

131 Like human ESCs, the engineered mESCs contained high telomerase activity, which was repr

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

133 of the GNAT-HAT complexes for the mouse ESC (mESC) state.

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

135 deep layer cortical neurons from mouse ESCs (mESCs).

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

137 Depletion of H3.3 from mESCs reduces acetylation on histone H3 at lysine 27 (H3

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

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

140 Moreover, data obtained from mESCs suggest that variants causing a decline in FL BRCA

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

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

143 els were significantly altered in H1DeltaTKO mESC.

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

145 cessibility in 170 genetically heterogeneous mESCs.

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

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

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

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

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

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

152 ssive epigenetic systems play minor roles in mESC self-renewal and naive ground state establishment b

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

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

155 In mESCs, these genes are associated with dominant proximal

156 endent on miRNAs that are highly abundant in mESCs.

157 is, did not affect Wnt pathway activation in mESCs.

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

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

160 erarchical signalling pathway alterations in mESCs.

161 on following the loss of miRNA biogenesis in mESCs.

162 ng, transcriptomic and epigenetic changes in mESCs.

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

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

165 diate type I IFN expression are deficient in mESCs.

166 criminates apoptosis from differentiation in mESCs.

167 eveals that it mediates different effects in mESCs depending on its receptor dosage, opening perspect

168 eliminated by siRNA knockdown of ERalpha in mESCs.

169 ng factor PPIE, which is highly expressed in mESCs but not hESCs.

170 mponents in the IFN pathway are expressed in mESCs.

171 d Nanog transcript and protein expression in mESCs.

172 ranscriptional control of gene expression in mESCs.

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

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

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

176 s as novel candidate REs of the Oct4 gene in mESCs.

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

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

179 ith median values ranging from 11 to 34 h in mESCs and contact-inhibited MEFs, respectively.

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

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

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

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

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

185 y DNMT3A2, the predominant DNMT3A isoform in mESCs.

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

187 Tet2 knockout in mESCs affected the levels of several small noncoding RNA

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

189 impairs about half of all chromatin loops in mESCs and causes deregulation of gene expression.

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

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

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

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

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

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

196 In contrast, mFast is nuclear retained in mESCs, and its processing is suppressed by the splicing

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

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

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

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

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

202 Thus, telomerase in mESCs with the hmTert alleles was subjected to human-lik

203 localized in the cytoplasm of hESCs than in mESCs.

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

205 tion, contrary to a previous report that, in mESCs, DNMT3L regulates DNA methylation positively or ne

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

207 ) and activates its nuclear translocation in mESCs.

208 e 2,613 high-confidence trans-REs (TREs), in mESCs.

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

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

211 mouse embryonic stem cell cultures (InDelphi-mESC) is able to accurately predict CRISPR/Cas9 gene edi

212 anscriptional activator with TCF1 influences mESC fate.

213 Treatment of Cltc knockdown mESCs with actin polymerization inhibitors resulted in a

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

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

216 the monolayer-based differentiation method, mESCs can be directed to generate specific deep-layer co

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

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

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

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

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

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

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

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

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

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

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

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

229 likely mechanism for NK-mediated killing of mESC.

230 control self-renewal for the maintenance of mESC state.

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

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

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

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

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

236 gulatory mechanism during differentiation of mESCs into cardiomyocytes.

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

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

239 n event necessary for the differentiation of mESCs.

240 ual RBPs inhibited neural differentiation of mESCs.

241 key role during neuronal differentiation of mESCs.

242 oliferation and colony forming efficiency of mESCs.

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

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

245 es proliferation and cellular homeostasis of mESCs.

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

247 employed dictates the cellular phenotype of mESCs.

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

249 il the surprising morphogenetic potential of mESCs to execute key aspects of organogenesis through th

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

251 a/beta and Mek1/2 to sustain self-renewal of mESCs in combination with leukaemia inhibitory factor an

252 e MYC regulatory network for self-renewal of mESCs.

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

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

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

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

257 Our mESC network predicts many novel players involved in sel

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

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

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

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

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

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

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

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

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

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

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 nd pluripotency gene repression in Tert(-/-) mESCs but not wild-type mESCs, whereas inhibition of H3K

274 erase reverse transcriptase null (Tert(-/-)) mESCs exhibit genome-wide alterations in chromatin acces

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

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

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

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

279 force microscopy (AFM), we demonstrate that mESCs lacking Cltc display higher Young's modulus, indic

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

281 of wild-type are not pathogenic, given that mESCs are fully viable and resistant to DNA-damaging age

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

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

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

285 We have previously shown that mESCs lacking the clathrin heavy chain (Cltc), an essent

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

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

288 roblast-like cells differentiated from these mESCs contained little telomerase activity.

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

290 ization signal, has very low activity in TKO mESCs, indicating that an accessory protein is absolutel

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

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

293 ression in Tert(-/-) mESCs but not wild-type mESCs, whereas inhibition of H3K27me3 demethylation led

294 m cells (mESCs) in comparison with wild-type mESCs.

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

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

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

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

299 greater cellular stiffness, compared with WT mESCs.

300 to values similar to those obtained with WT mESCs.