ライフサイエンスコーパス: pluripotency

1 tion and a unique chromatin state for primed pluripotency.

2 ting a cascade of molecular events affecting pluripotency.

3 es the gene expression program necessary for pluripotency.

4 notypic features characteristic of formative pluripotency.

5 RF2 is dispensable for end protection during pluripotency.

6 stinct from 5hmC in somatic reprogramming to pluripotency.

7 cription elongation in ESCs, which regulates pluripotency.

8 c variation plays in control of ground state pluripotency.

9 isms involved in regulation of ESC exit from pluripotency.

10 a(2+), and conducive for transition to naive pluripotency.

11 staging post on the trajectory of mammalian pluripotency.

12 rogressively accelerates as cells exit naive pluripotency.

13 ecifically activated during reprogramming to pluripotency.

14 evels at the transition from naive to primed pluripotency.

15 ogramming and impedes acquisition of induced pluripotency.

16 l the importance of RNA decay in maintaining pluripotency.

17 ifically activated during reprogramming into pluripotency.

18 nections between extra-telomeric biology and pluripotency.

19 sential for the induction and maintenance of pluripotency.

20 be essential in furthering our knowledge of pluripotency.

21 ting to apoptosis, aberrant cell growth, and pluripotency.

22 network activation during induction of naive pluripotency.

23 itrosylation during nuclear reprogramming to pluripotency.

24 ng that becomes more evident in primed-state pluripotency.

25 itical gene required for the exit from human pluripotency.

26 to govern maintenance and induction of naive pluripotency.

27 oxidative mitochondrial metabolism in naive pluripotency.

28 r intracellular Ca(2+) in safeguarding naive pluripotency.

29 ences between embryo and stem cell models of pluripotency.

30 during the reprogramming of somatic cells to pluripotency.

31 entiation, and somatic cell reprogramming to pluripotency.

32 developmentally advanced state called primed pluripotency.

33 is during the exit out of the naive state of pluripotency.

34 and does not prevent transition to formative pluripotency.

35 e lncRNAs caused the stem cells to exit from pluripotency.

36 our and potency during resetting from primed pluripotency.

37 ling cells on their trajectory toward mature pluripotency.

38 embryonic stem cells while preserving their pluripotency.

39 ors that are required for the maintenance of pluripotency.

40 fiers to facilitate nuclear reprogramming to pluripotency.

41 This turns out to be important for hESC pluripotency.

42 also have a role in nuclear reprogramming to pluripotency.

43 identity in the context of reprogramming to pluripotency.

44 these altered properties specifically impact pluripotency.

45 inhibiting BCSC self-renewal and associated pluripotency.

46 logically significant for the maintenance of pluripotency.

47 on, a unique functional feature of formative pluripotency.

48 ism that is essential for stem cells to exit pluripotency.

49 a (2i) inhibitors transition to ground state pluripotency.

50 ous histone and DNA demethylases involved in pluripotency.

51 neage commitment, and reprogramming to naive pluripotency.

52 umenogenesis and drive progression to primed pluripotency.

53 Nonetheless, WNT induces reversion to naive pluripotency.

54 ing to activated WNT signaling, required for pluripotency.

55 ance of the epigenetic dynamics of exit from pluripotency.

56 glutarate-dependent proteins is required for pluripotency acquisition and maintenance.

57 tion of actin polymerization promotes mature pluripotency activation.

58 on enables reprogramming of somatic cells to pluripotency, albeit with generally low efficiency.

59 their unique combination of two properties: pluripotency and a high proliferative capacity.

60 to express stemness genes, preserving their pluripotency and ability to generate chimeric mice.

61 downregulation of many genes associated with pluripotency and active cell cycle, including mTor, Hipp

62 tes expression of neuronal genes to maintain pluripotency and also during differentiation.

63 ediated endocytosis (CME), display a loss of pluripotency and an enhanced expression of differentiati

64 regulatory miR290-295 cluster that regulates pluripotency and are controlled by the canonical stem ce

65 Hippo pathway in the establishment of naive pluripotency and cell competition in the epiblast.

66 ins mechanistically link cell proliferation, pluripotency and cell fate specification.

67 Pluripotency and cell fates can be modulated through the

68 tro and in vivo and leads to upregulation of pluripotency and CSC factors.

69 enous lipid availability in regulating human pluripotency and define E8 hPSCs as a stable, naive-to-p

70 kout mouse embryonic stem cells fail to exit pluripotency and differentiate efficiently.

71 hown that the TETs influence 5mC metabolism, pluripotency and differentiation during early embryonic

72 st notably, telomeres have a broad impact on pluripotency and differentiation.

73 a broad network of genes and, therefore, of pluripotency and differentiation.

74 PSCs open new avenues for studying mammalian pluripotency and dissecting the molecular mechanisms gov

75 Sox2, the key regulator of pluripotency and early development was significantly red

76 other RBPs from mRNAs and promote exit from pluripotency and embryonic patterning in the mouse.

77 dothelial cells that both maintain stem cell pluripotency and enable the generation of differentiated

78 cluding ZNF398, a human-specific mediator of pluripotency and epithelial character in hPSCs.

79 inhibition of ZNF398 abolishes activation of pluripotency and epithelial genes and colony formation.

80 ating a subset of genes, including the naive pluripotency and germline marker Dppa3 (Stella, Pgc7).

81 pluripotency state between naive and primed pluripotency and harbor molecular, cellular, and phenoty

82 plex as a regulatory mechanism for m(6)A and pluripotency and highlight the potential of this interac

83 he antiviral response primes iPSCs away from pluripotency and induces numerous aberrant gene products

84 , inextricably linked to the balance between pluripotency and lineage commitment.

85 HD8 is essential for both the maintenance of pluripotency and neural differentiation, providing mecha

86 scription factor critical for maintenance of pluripotency and neurogenesis, has been found associated

87 8:pre-let-7:TUTase ternary complex regulates pluripotency and oncogenesis by controlling processing o

88 8 has important functions in regulating both pluripotency and oncogenesis, and suggest that sGRP78 ma

89 se results indicate that transition to naive pluripotency and oncogenic transformation share common e

90 switch to suppress the antiviral IFN during pluripotency and present genetic approaches to enhance t

91 ne repression, inhibiting the acquisition of pluripotency and preserving cell differentiation.

92 l to study this window: upon exit from naive pluripotency and prior to tissue differentiation, it und

93 ed in the pathways associated with stem cell pluripotency and proliferation.

94 from the naive to the primed states of cell pluripotency and reduces, by orders of magnitude, the co

95 We show that EPHA2 maintains pluripotency and restrains commitment by antagonising ER

96 s work identifies Netrin-1 as a regulator of pluripotency and reveals that it mediates different effe

97 ancers of several stemness genes to regulate pluripotency and self-renewal in pluripotent stem cells.

98 ominent pioneer factor that is essential for pluripotency and self-renewal of embryonic stem cells(3)

99 Maintenance of pluripotency and specification towards a new cell fate a

100 xt of the nonlocal influence of telomeres on pluripotency and stemness, we discuss major opportunitie

101 vern cell identity, are sufficient to induce pluripotency and transdifferentiate cells.

102 global translation rate, spontaneous loss of pluripotency, and compromised differentiation potential.

103 stablishment and maintenance of stemness and pluripotency, and their altered expression plays key rol

104 al hyperactivation of enhancers drives naive pluripotency, and this can be achieved in vitro by inhib

105 The mechanisms that regulate pluripotency are still largely unknown.

106 olite has a role in the maintenance of naive pluripotency as well as in PGC differentiation, likely t

107 Here, we uncover developmental pluripotency associated 2 and 4 (DPPA2/4) as epigenetic

108 the Hox complexes, and the downregulation of pluripotency associated microRNAs.

109 state establishment by core sets of dominant pluripotency associated transcription factor networks, w

110 en, identifying, among others, developmental pluripotency-associated 2 (Dppa2) and Dppa4 as positive

111 ral pluripotent stem cell lines that express pluripotency-associated genes, retain high viability and

112 These include pluripotency-associated transcription factors, repressiv

113 LIF occupy a ground state with highly active pluripotency-associated transcriptional and epigenetic c

114 epiblast (Epi) transits from naive to primed pluripotency, before giving rise to the three germ layer

115 a master regulator and inducer of stem cell pluripotency, binds to DNA in nucleosomes in a sequence-

116 TA6-AS1 did not affect undifferentiated cell pluripotency but inhibited cardiomyocyte differentiation

117 gly, Id1 is not required for naive or primed pluripotency but rather stabilizes epiblast identity dur

118 4, along with Sox2 and Klf4 (SK), can induce pluripotency but structurally similar factors like Oct6

119 cells (mPGCs), epigenetic reprogramming and pluripotency, but its role in the evolutionarily diverge

120 T signals drives the transition into rosette pluripotency by inducing OTX2.

121 TDP-43 also promotes pluripotency by regulating alternative polyadenylation o

122 Acquisition of pluripotency by somatic cells is a striking process that

123 he axon guidance cue Netrin-1 promotes naive pluripotency by triggering profound signalling, transcri

124 In addition, the MKL1-actin imposed block of pluripotency can be bypassed, at least partially, when t

125 Here we show that acquisition of naive pluripotency can follow transcriptionally and mechanisti

126 Nuclear reprogramming to pluripotency can revert both the age and the identity of

127 scription factors are required for stem-cell pluripotency, cell differentiation and cell reprogrammin

128 s endowed with self-renewal, tumorigenicity, pluripotency, chemoresistance, differentiation, invasive

129 The initial exit from pluripotency coincides with the establishment of a globa

130 ell (PSC) states are in vitro adaptations of pluripotency continuum in vivo.

131 methylcytosine (5mC) levels during exit from pluripotency correlated with an upregulation of the de n

132 pression of OCT4A is one of the hallmarks of pluripotency, defined as a stem cell's ability to differ

133 Mechanistically, Nanog, but not other pluripotency-determining factors including Oct4, Sox2, a

134 rate-dependent enzymes in the maintenance of pluripotency during cellular reprogramming to induced pl

135 Moreover, naive pluripotency during embryonic development coincides with

136 pluripotent stem cells and in disruption of pluripotency during in vitro differentiation.

137 What sustains their pluripotency during propagation remains unclear.

138 eraction network that determines the fate of pluripotency during reprogramming.

139 apitulate essential and specific features of pluripotency dynamics during an inaccessible period of h

140 2) resembles Oct4, whilst Oct6 does not bind pluripotency enhancers.

141 and NANOG, that correspond predominantly to pluripotency enhancers.

142 n of Oct4/Sox2 heterodimers is essential for pluripotency establishment; however, reliance on Oct4/So

143 known as Nsd2 and MMSET) has a dual role in pluripotency exit and germ layer specification of embryo

144 d cell-matrix interaction is a key player in pluripotency exit regulation.

145 y, interfering with abscission impairs naive pluripotency exit, and artificially inducing abscission

146 is associated with reversible initiation of pluripotency exit, whereas the latter, a full EMT, is as

147 inery leading to faster abscission regulates pluripotency exit.

148 s at a naive-to-primed intermediate state of pluripotency expressing several naive-like developmental

149 and KDM6A-mediated epigenetic activation of pluripotency factor gene expression in combination with

150 ctor 1 (HIF-1) that epigenetically activates pluripotency factor gene transcription in response to ch

151 nd results in reversible upregulation of the pluripotency factor Klf4.

152 3.41 miRNA cluster (C19MC) and enrichment of pluripotency factor LIN28A.

153 The stem cell pluripotency factor Oct4 serves a critical protective ro

154 , a central stem cell pool maintained by the pluripotency factor SHOOTMERISTEMLESS (STM), is surround

155 recludes the chromatin association of master pluripotency factor, POU5F1, and pluripotent gene activa

156 tem cells (mESCs) via DNA hypomethylation at pluripotency-factor promoters.

157 resses the p53 pathway, induces the Yamanaka pluripotency factors (OCT4, SOX2, KLF4 and MYC) and driv

158 Notably, naive pluripotency factors are exchanged for postimplantation

159 Pluripotency factors maintain uncommitted cells of the b

160 litating transcription of genes encoding the pluripotency factors NANOG, SOX2, and KLF4, which along

161 Here, we show that core pluripotency factors OCT4 and SOX2 suppress chaperone-me

162 suggest that CMA mediates the effect of core pluripotency factors on metabolism, shaping the epigenet

163 that the pioneering activity of the maternal pluripotency factors Pou5f3 and Sox3 determines competen

164 (EpEX) significantly increases the levels of pluripotency factors through a signaling cascade that in

165 wever, a rescue in the expression profile of pluripotency factors was not obtained.

166 y deeply conserved lineage specification and pluripotency factors, and can extend our understanding o

167 pecification through increased expression of pluripotency factors, but how their expression is regula

168 tive polyadenylation of transcripts encoding pluripotency factors, including Sox2, which partially pr

169 s is mediated by male-genome transmission of pluripotency factors.

170 HMGA2), which activates the transcription of pluripotency factors.

171 ream expression of Nanog, which are both key pluripotency factors.

172 led that reprogramming into primed and naive pluripotency follows diverging and distinct trajectories

173 Therefore, the JNK-JUN pathway safeguards pluripotency from precocious DE differentiation.

174 Sox2 is the only pluripotency gene known to be expressed specifically wit

175 nes but can go as far as reactivation of the pluripotency gene OCT4.

176 Here we show that downregulation of the STM pluripotency gene promotes initiation of flowers and unc

177 rbated the impairment in differentiation and pluripotency gene repression in Tert(-/-) mESCs but not

178 asome, which ensures the rapid expression of pluripotency genes in the next cell cycle.

179 Notably, miRNAs act on neighborhoods of pluripotency genes to increase variation of target genes

180 y changes in the regulatory elements of core pluripotency genes, and orchestrated global changes in c

181 Moreover, KDM5B inhibited the expression of pluripotency genes, SOX2 and NANOG, and decreased the st

182 mb and polycomb H3K27me3 repressive marks to pluripotency genes, thereby exerting vast epigenetic cha

183 FAP2C and BLIMP1 to upregulate germ cell and pluripotency genes, while repressing WNT signalling and

184 e and/or activation of germ cell markers and pluripotency genes.

185 tin landscape, with bivalently marked primed pluripotency genes.

186 d the occupancy of KDM5B on the promoters of pluripotency genes.

187 metabolism, cell division, DNA methylation, pluripotency, Glu metabolism, neurogenesis, and cardioge

188 Clutch size correlated with the pluripotency grade of mouse embryonic stem cells and hum

189 wn to regulate cell fate, tissue growth, and pluripotency; however, a unified understanding of its ro

190 lr16 was required for optimal maintenance of pluripotency in embryonic stem cells.

191 haracterising the developmental programme of pluripotency in Homo sapiens Here, we confirm that naive

192 Here, we show that exit from naive pluripotency in mouse ES cells generally occurs after a

193 Nanog supports pluripotency in naive cells, while Nodal supports plurip

194 ic lineages before implantation but sustains pluripotency in primed cells of the post-implantation ep

195 potency in naive cells, while Nodal supports pluripotency in primed cells, but the handover from Nano

196 However, ground state pluripotency in some inbred strain backgrounds is unstab

197 ratoma, a recognized standard for validating pluripotency in stem cells, could be a promising platfor

198 ifestation in the derivation or induction of pluripotency in vitro.

199 NA sequencing revealed pathways activated by pluripotency inducing culture that were shared across al

200 es through a mesodermal state prior to naive pluripotency induction, whereas another transiently rese

201 We postulate that exit from pluripotency involves intermediates that retain pluripot

202 entity transitions and suggesting that naive pluripotency is a multidimensional attractor state.

203 To understand how pluripotency is established, we therefore investigated t

204 ome during the transition of naive-to-primed pluripotency is largely accompanied by transcriptional r

205 Pluripotency is maintained in part by a unique transcrip

206 between epiblast cellular morphology and its pluripotency is not well understood.

207 Progression through states of pluripotency is required for cells in early mammalian em

208 g all amniotic vertebrates and that epiblast pluripotency is restricted to an intermediate cellular s

209 The developmental potential of cells, termed pluripotency, is highly dynamic and progresses through a

210 e in somatic tissues, suggesting a conserved pluripotency-linked mechanism.

211 is associated with complete and irreversible pluripotency loss.

212 ial transition (MET) prior to EMT-associated pluripotency loss.

213 ce on Oct4/Sox2 heterodimers declines during pluripotency maintenance.

214 n ERK-mediated "toggle switch" that promotes pluripotency marker expression and stem-like features in

215 nalling were not strongly coupled to loss of pluripotency marker expression, regardless of the differ

216 that PRDM1 is required for the loss of some pluripotency markers and the onset of neural, neural cre

217 nset of lineage determinants and the loss of pluripotency markers are temporally and spatially coordi

218 tic for dedifferentiation and acquisition of pluripotency markers including Yamanaka factors.

219 iting stem-like properties and expression of pluripotency markers NANOG and OCT4 can arise from origi

220 Expression of these pluripotency markers occurred before the cells re-entere

221 ied novel Notch targets, such as early naive pluripotency markers or transcriptional repressors such

222 rogenitor populations retained expression of pluripotency markers, secreted factors associated with c

223 th all three germ layers despite maintaining pluripotency markers.

224 rofile RNA components that interact with the pluripotency master gene Oct4.

225 se results suggest that the IFN-I system and pluripotency may be incompatible with each other and thu

226 The pluripotency module is governed by dynamic alterations i

227 x that can drive enhancer activation, govern pluripotency network and stemness circuitry.

228 escent ground-state ESCs with an intact core pluripotency network and transcriptome signatures akin t

229 ries, which implicates reprogramming and the pluripotency network as a central hub in cancer formatio

230 sed genes are several core components of the pluripotency network that act to drive their own express

231 hat we recently associated with stability of pluripotency networks, and identified as a genetic vulne

232 gene networks while turning off or rewiring pluripotency networks.

233 Pluripotency of a DNA tetrahedron (DNA(TT)) has made the

234 ends the lifespan of worms and maintains the pluripotency of embryonic stem cells (ESCs).

235 otection of genome integrity, maintenance of pluripotency of embryonic stem cells, antibody-gene dive

236 presence of active CME is essential for the pluripotency of embryonic stem cells.

237 that membrane mechanics gate exit from naive pluripotency of mouse embryonic stem cells.

238 Reprogramming to pluripotency of MSCs reduced circFOXP1 and non-canonical

239 ed "Glioma", "Signalling pathways regulating pluripotency of stem cells" to be the most relevant path

240 actor 1 complex (PAF1C) component, maintains pluripotency of stem cells, by unclear mechanisms, and i

241 " underpins multidimensional access to naive pluripotency, offering a conceptual framework for unders

242 t and in embryonic stem cells by maintaining pluripotency or by regulating differentiation.

243 Cs) respond to environmental cues by exiting pluripotency or entering a quiescent state.

244 rulation EMT coincides with loss of epiblast pluripotency, pluripotent cells in development and in vi

245 As and protein coding genes, associated with pluripotency, primitive streak, limb development and ext

246 that - as in animals- downregulation of the pluripotency program is important for organogenesis in p

247 expression of Sox2, thereby restricting the pluripotency program to the stage when inside cells are

248 d the precise timing from naive to formative pluripotency progression and enabled the spatiotemporal

249 How pluripotency progression and morphogenesis are linked an

250 otent intermediate whereby control over both pluripotency progression and morphogenesis pivots from W

251 Pluripotency progression of mouse embryonic stem cells (

252 dynamic transcriptional networks underlying pluripotency progression.

253 is found to reduce the stability of crucial pluripotency-promoting transcripts.

254 g early embryonic development, cells exiting pluripotency rapidly switch to TRF2-dependent end protec

255 zation and transcriptional output of the key pluripotency regulator Sox2 and its essential enhancer S

256 a genome-wide CRISPR screen to identify ESC pluripotency regulators, which generated insights into h

257 er activity required to maintain the dynamic pluripotency regulatory landscape in an accessible state

258 a indicate that Whsc1 links silencing of the pluripotency regulatory network with activation of mesen

259 of transcripts, including many encoding key pluripotency-related factors (such as Eed and Jarid2), s

260 We show that Sall4, a pluripotency-related transcription factor gene, has mult

261 factors regulating human naive versus primed pluripotency remain incompletely defined.

262 the initial naive and final primed phases of pluripotency, respectively.

263 ow that resetting from primed to naive human pluripotency results in acquisition of a DNA methylation

264 nto a stem-like state, expressing markers of pluripotency.See related commentary by Koncar and Agniho

265 Formation of a pluripotency-specific chromatin network is a critical ev

266 uit the chromatin factor SMC1 to orchestrate pluripotency-specific intrachromosomal looping.

267 Using gene-specific gRNAs, we describe a pluripotency-specific lncRNA interacting network in the

268 ription network that maintains expression of pluripotency-specific transcription factors and represse

269 XPSCs represent a pluripotency state between naive and primed pluripotency

270 tissue lineages and defines the continuum of pluripotency states in time and space.

271 entifies key genes associated with different pluripotency states.

272 Here, using chicken epiblast and mammalian pluripotency stem cell (PSC) models, we show that PSCs u

273 Core pluripotency stem cell master regulators (OCT4, SOX2 and

274 binding factors and the role of telomeres in pluripotency/stemness.

275 ndent H3K27ac maintenance and recruitment of pluripotency TFs and Brg1.

276 nal programmes are important for maintaining pluripotency, the requirement for cell adhesion to the e

277 roblasts could be reprogrammed to a state of pluripotency, this was inhibited in the absence of Cltc.

278 into a stem-like state expressing markers of pluripotency through an EGFR-ERK-EGR1-dependent axis.

279 ar basis for an irreversible transition from pluripotency to differentiation.

280 IST requires the natural context surrounding pluripotency to initiate chromosome silencing.

281 to N-cadherin regulates the transition from pluripotency to neural identity, but the mechanism by wh

282 arly mouse embryonic development: from naive pluripotency to the specification of primordial germ cel

283 lecular map of cellular differentiation from pluripotency towards all major embryonic lineages, and e

284 eity, whereby cells reversibly progress from pluripotency towards primitive endoderm while retaining

285 TET1 interacts with the pluripotency transcription factor NANOG which may contri

286 weakens during somatic cell reprogramming by pluripotency transcription factors.

287 rylation, whilst FGF4-ERK1/2 disrupts a core pluripotency transcriptional circuit required for Epha2

288 g, and offers a mechanism by which the naive pluripotency transcriptional programme can be partially

289 es m(6)A abundance transcriptome-wide and in pluripotency transcripts, resulting in increased cell st

290 tion of Zmym2 compromises the totipotency-to-pluripotency transition during early development.

291 ed for expression prior to the initiation of pluripotency transition to the formative state.

292 deling, we find that hESCs commit to exiting pluripotency unexpectedly early.

293 of WNT signalling while preventing exit from pluripotency using lysophosphatidic acid, we 'trap' and

294 To reveal how cells exit human pluripotency, we designed a CRISPR-Cas9 screen exploitin

295 ing the antiviral response in the context of pluripotency, we engineered a system to engage these def

296 reference to ex vivo-cultured cell models of pluripotency when appropriate.

297 ripotency involves intermediates that retain pluripotency while simultaneously exhibiting lineage-bia

298 not serum/LIF alone, rapidly revert cells to pluripotency with near 100% efficiency.

299 dentified gene networks regulating stem cell pluripotency, Wnt signaling, melanocyte development, pig

300 of H/ACA snoRNA levels in stem cells impairs pluripotency, yet it remains unclear how H/ACA snoRNAs c