ライフサイエンスコーパス: pluripotency

1 ssing steps (for example, isolation, induced pluripotency).

2 -specific gene induction with suppression of pluripotency.

3 ortant to the maintenance of, and exit from, pluripotency.

4 c backgrounds in distinct states of cellular pluripotency.

5 pel-like factor 4 (Klf4) expression in naive pluripotency.

6 ng embryonic stem (ES) cell self-renewal and pluripotency.

7 wn about their importance at the exit of ESC pluripotency.

8 of the differentiation capacity that defines pluripotency.

9 diverse phosphorylation systems modulate ESC pluripotency.

10 stem cells as they exit the ground state of pluripotency.

11 anced transcription program underlying naive pluripotency.

12 to all primary embryonic lineages is termed pluripotency.

13 NT and MAPK-ERK signaling to safeguard naive pluripotency.

14 Cdx2, suggesting that Sox21 helps safeguard pluripotency.

15 s sufficient to drive reprogramming to naive pluripotency.

16 e resulting cells recapitulate in vivo naive pluripotency.

17 expression to establish and maintain primed pluripotency.

18 backdrop for future analysis of naive human pluripotency.

19 s as they exhibit their own 'latent' form of pluripotency.

20 viding in vivo functional validation of hPSC pluripotency.

21 show that Sall4 is dispensable for mouse ESC pluripotency.

22 ciently reprograms primed cells toward naive pluripotency.

23 mouse epiblast stem cells (EpiSCs) to naive pluripotency.

24 program of epigenetic reprogramming to naive pluripotency.

25 GLUT2-dependent fashion but did not regulate pluripotency.

26 PRESS1 controls a gene network that promotes pluripotency.

27 ociated with acquisition of naive and primed pluripotency.

28 ltivation in colonies to maintain growth and pluripotency.

29 neating developmental progression from naive pluripotency.

30 ing the importance of mitotic bookmarking in pluripotency.

31 cell fate transitions into and out of human pluripotency.

32 at modulates the dynamics of exit from naive pluripotency.

33 usceptible to reactivation upon induction of pluripotency.

34 ESCs) ensures NANOG expression and stem cell pluripotency.

35 ions and a switch to Activin/Nodal-dependent pluripotency.

36 tem cells also release Bmp4 but retain their pluripotency.

37 , and cMyc (OSKM) reprogram somatic cells to pluripotency.

38 regulates transcriptional outputs during ESC pluripotency.

39 e involved in regulating the human and mouse pluripotency.

40 enous Nanog expression or culturing in naive pluripotency '2i' media, suggesting that the self-renewa

41 nitially found to reprogram somatic cells to pluripotency, a "second generation" of cellular reprogra

42 on facilitates the acute extinction of naive pluripotency, a pre-requisite for rapid progression from

43 in males they delay meiosis and instead lose pluripotency, activate an irreversible program of prospe

44 Mechanistically, exit from naive pluripotency activates an Oct4-governed transcriptional

45 of over 1,500 transcripts in cells acquiring pluripotency, although only a fraction changed protein l

46 ell-cell contact and Activin/Nodal-dependent pluripotency and a peptide is described that enhances ST

47 m diploidization by impeding exit from naive pluripotency and by shortening the S-G2/M phases.

48 hybrids underwent reprogramming, expressing pluripotency and cardiac precursor genes latent in paren

49 pmental regulators that couple metabolism to pluripotency and cell fate determination.

50 -to-nucleus signaling pathways that regulate pluripotency and cell fate.

51 understanding of miRNAs in the regulation of pluripotency and cell reprogramming in the laboratory ra

52 During early embryogenesis, cells must exit pluripotency and commit to multiple lineages in all germ

53 adult neuronal genomes with reprogramming to pluripotency and development.

54 ursting, with implications for regulation of pluripotency and development.Polycomb repressive complex

55 role for Satb1 in the lineage choice between pluripotency and differentiation and further our underst

56 inorganic elements are relevant to cellular pluripotency and differentiation in human pluripotent st

57 erm "epigenetic landscape" as a metaphor for pluripotency and differentiation, but methylation landsc

58 /AKT/mTOR signalling plays in the control of pluripotency and differentiation, with a particular focu

59 -fate decisions by modulating the balance of pluripotency and differentiation.

60 fine balance between the alternate states of pluripotency and differentiation.

61 ehavior, including processes such as induced pluripotency and differentiation.

62 , reflecting divergence in the regulation of pluripotency and early development.

63 f active enhancers associated with key naive pluripotency and early germline genes.

64 ells, DAZL and BOULE, regulate the exit from pluripotency and entry into meiosis.

65 cers of developmental regulators to maintain pluripotency and for subsequent activation in differenti

66 o-repressor protein, CBFA2T2, that regulates pluripotency and germline specification in mice.

67 ethylation plays vital roles in both loss of pluripotency and governance of the transcriptome during

68 itochondrial function associated with primed pluripotency and in regulating one-carbon metabolism, nu

69 de a comprehensive analysis of the exit from pluripotency and lineage commitment at the single cell l

70 In contrast, exit from pluripotency and lineage commitment have not been studie

71 ular Cell, that chromatin-bound MDM2 impacts pluripotency and metabolism to promote survival and prol

72 n uncovered as being crucial for DNA repair, pluripotency and oncogenesis.

73 ation, play an important role in maintaining pluripotency and regulating the differentiation of stem

74 a LIF-independent manner to promote ES cell pluripotency and self-renewal.

75 vation of Foxd3 required for exit from naive pluripotency and subsequent PGC specification.

76 TP63 is required to maintain stem cell pluripotency and suppresses the metastatic potential of

77 erties in common with naive cells, including pluripotency and the ability to migrate to the lymph nod

78 o development to modulate the acquisition of pluripotency and the formation of the inner cell mass.

79 d in vivo, including during reprogramming to pluripotency and the onset of differentiation, and we di

80 stem cells and in mice results in changes in pluripotency and the primed state of cells.

81 howed their involvement in the regulation of pluripotency and the reprogramming process in rats.

82 To study the role of Oct1 in ESC pluripotency and transcriptional control, we constructed

83 Our analysis reveals pluripotency and transdifferentiation regulatory princip

84 their unique combination of two properties: pluripotency and unlimited proliferative capacity.

85 e within microColonies, both in the state of pluripotency and when cells are differentiated, and that

86 everal KLFs are also crucial for maintaining pluripotency and, hence, have been linked to reprogrammi

87 ociated with genes involved in regulation of pluripotency, and these genes display early changes in e

88 t of the modulation of expression of several pluripotency- and differentiation-related genes by Satb1

89 The standard assays for pluripotency are based on genomic approaches, which take

90 Maintenance and dissolution of pluripotency are tightly controlled by phosphorylation.

91 neity in vitro have fostered a conception of pluripotency as an intrinsically metastable and precario

92 is also required to constrain levels of the pluripotency-associated factor NANOG in EPI cells.

93 potent stem cells, characterized by enhanced pluripotency-associated gene expression and self-renewal

94 s stabilized by an interconnected network of pluripotency-associated genes, integrates external signa

95 Collectively, we report that potassium is a pluripotency-associated inorganic element in human cells

96 Expression of known pluripotency-associated miRNAs, such as the miR-290-295

97 Here, we discover that the pluripotency-associated pioneer factor OCT4 binds chroma

98 whereby enhancer binding by Sall4 and other pluripotency-associated transcription factors is respons

99 ription factor binding and expression of the pluripotency-associated transcriptome.

100 individual TE-derived human lincRNAs, human pluripotency-associated transcripts 2, 3 and 5 (HPAT2, H

101 as the gold standard for assessing stem cell pluripotency, based on their capacity to test donor cell

102 iPSC-CMs largely lost the markers of pluripotency, became positive for cardiac-specific marke

103 in embryonic development, tumorigenesis, and pluripotency, but their exact functions are poorly under

104 he metabolic transition from naive to primed pluripotency by directly repressing oxidative metabolism

105 suggest that the potent stimulation of naive pluripotency by LIF/Stat3 is attributable to parallel an

106 We conclude that YAP maintains hESC pluripotency by preventing WNT3 expression in response t

107 Two phases of pluripotency, called naive and primed, have previously b

108 By contrast, pluripotency can be captured and stabilized indefinitely

109 y, but also closely correlate with stem cell pluripotency, cancer drug resistance, GSL storage disord

110 T) activity has been implicated in stem cell pluripotency, cancer metastasis, and tumorigenesis.

111 ls significantly differs when their cellular pluripotency changes.

112 litated plasticity in a manner distinct from pluripotency, characterized by increased expression of S

113 oRNA levels but did not rescue the exit from pluripotency defect.

114 Embryonic stem cell (ESC) pluripotency, defined as the ability to differentiate in

115 onfirmed to harbor an appropriate gene edit, pluripotency, differentiation potential, and genomic sta

116 Pluripotency enhancer selection is a stepwise process th

117 argeting, somatic-enhancer inactivation, and pluripotency enhancer selection.

118 irect both somatic-enhancer inactivation and pluripotency-enhancer selection to drive reprogramming.

119 Most pluripotency enhancers are selected later in the process

120 thesised to be enabling for the execution of pluripotency, entailing remodelling of transcriptional,

121 rely blocks transcriptional switch to primed pluripotency, even in the absence of p53 activity induce

122 d discuss our hypothesis that redundancy and pluripotency evolved in tick salivary immunomodulators t

123 Stem-like CK14 + and TBX3 + and pluripotency-expressing OCT4 + and NANOG + cells expande

124 smantles a significant fraction of the naive pluripotency expression program through decommissioning

125 By studying genes regulated by pluripotency factor and nucleosome remodelling deacetyla

126 e pathway cooperate to inactivate the LIN-28 pluripotency factor in seam cells, a stem-like cell type

127 Nanog, a core pluripotency factor in the inner cell mass of blastocyst

128 These data establish a new link between the pluripotency factor NANOG and autophagy involved in resi

129 We found that both GLI3 and GLI1 bind to the pluripotency factor NANOG.

130 Here we identify the pluripotency factor Oct4 as a key regulator of trunk len

131 How the zebrafish pluripotency factor Pou5f3 (homologous to mammalian Oct4

132 rocytes in the TZ activate expression of the pluripotency factors [Sox2, Oct4 (Pou5f1), Nanog], and c

133 nd can be reversed in vivo and in vitro when pluripotency factors are re-expressed.

134 nt growth and elevated the expression of the pluripotency factors CD133, Nanog, and Oct4.

135 nexpectedly included genes encoding putative pluripotency factors expressed at the onset of ZGA.

136 to support crosstalk between LKB1, Stat3 and pluripotency factors in breast cancer and effective anti

137 Hypoxia upregulates the core pluripotency factors NANOG, SOX2, and OCT4, associated w

138 are important for HNK-mediated inhibition of pluripotency factors since LKB1-silencing and AMPK-inhib

139 Selective downregulation of pluripotency factors upon Spt6 depletion may be mechanis

140 with high expression of neural crest genes, pluripotency factors, and lineage markers.

141 nly after near-complete elimination of naive pluripotency factors, but precedes appearance of lineage

142 lating mESC functions through control of key pluripotency factors, including Octamer-binding protein

143 onic stem cells (ESCs) reduced expression of pluripotency factors, increased expression of cell-linea

144 at3 resulted in suppression of expression of pluripotency factors.

145 t by SRSF5 is required for the expression of pluripotency factors.

146 s, including CCCTC-binding factor (CTCF) and pluripotency factors.

147 cellular reprogramming by degradation of key pluripotency factors.

148 form mammospheres and elevated expression of pluripotency-factors (Oct4, Nanog and Sox2), properties

149 the formation of mammosphere, expression of pluripotency-factors and aldehyde dehydrogenase activity

150 ntional two-dimensional differentiation from pluripotency fails to recapitulate cell interactions occ

151 othesis, we define 12 key hallmarks of naive pluripotency, five of which are specific to primates.

152 e size was the most important determinant of pluripotency, followed by high wave number and high feat

153 eir temporal trends, indicating that loss of pluripotency, formation of primitive streak and mesoderm

154 oduced from hiPSCs after transition of their pluripotency from the primed state using various methods

155 cell division and could efficiently maintain pluripotency gene expression over time.

156 Increased expression of the pluripotency gene Klf4 in these phenotypically switched

157 The pluripotency gene Nanog is not expressed in normal adult

158 scription factor subunits at the core of the pluripotency gene regulatory network and will enhance ou

159 s but is not required for maintenance of the pluripotency gene regulatory network.

160 on and dynamic DNA demethylation to activate pluripotency gene transcription.

161 Many pluripotency gene-enhancer interactions are anchored by

162 for future/embryonic expression, while core pluripotency genes (OCT4 and NANOG) were transcriptional

163 ing nonintegrating plasmids containing all 6 pluripotency genes (OCT4, SOX2, KLF4, NANOG, LIN28, and

164 The signal(s) triggering expression of the pluripotency genes are unknown, but we demonstrate that

165 of lineage specific genes and repression of pluripotency genes drives differentiation of embryonic s

166 For complete repression of pluripotency genes during ESC differentiation, chromatin

167 Pluripotency genes engaged in both "fully-reprogrammed"

168 Unexpectedly, some NPC interactions around pluripotency genes persist in our iPSC clone.

169 We find that most pluripotency genes reconnect to target enhancers during

170 binds directly to upstream regions of these pluripotency genes to promote their expression and repre

171 CD55 regulated self-renewal and core pluripotency genes via ROR2/JNK signaling and in paralle

172 uripotent stem cells including expression of pluripotency genes, epigenetic reprogramming, and differ

173 ated CBX4 and CBX6 repress the expression of pluripotency genes, such as Sox2 and Nanog, through PRC1

174 tes reprogramming by reactivating endogenous pluripotency genes.

175 regulatory elements and transcription of key pluripotency genes.

176 e H3K56 and H3K9 acetylation at promoters of pluripotency genes.

177 ion of stem-like cells and the expression of pluripotency genes.

178 ty of terminally differentiated cells toward pluripotency has completely altered the outlook for biom

179 esult, key signalling pathways that regulate pluripotency have been identified and their functions we

180 e the principles that establish and regulate pluripotency have been well defined in the mouse, it has

181 variant, indicating that they are markers of pluripotency in a malignant setting.

182 unctions as a barrier toward achieving naive pluripotency in both mouse and human ESCs.

183 Similarly, exit of epiblasts from naive pluripotency in cultured human post-implantation embryos

184 r mesendoderm specification during exit from pluripotency in embryos and in culture.

185 specific and not a required step for exit of pluripotency in hPSCs and identifies MYC and MYCN as dev

186 l insights into the manipulation of cellular pluripotency in hPSCs by regulating intracellular potass

187 provide stringent criteria to evaluate naive pluripotency in human and other primate cells.

188 es to elucidate the regulatory principles of pluripotency in human embryos and stem cells, and highli

189 tigate epigenetic mechanisms of stemness and pluripotency in lung cancers.

190 where differences exist in the regulation of pluripotency in mice and humans.

191 ure of the signalling network that maintains pluripotency in mouse embryonic stem cells, and find an

192 AhR depletion induces undifferentiation and pluripotency in normal and transformed cells.

193 ssion, genomic integrity, and maintenance of pluripotency in stem cell populations.

194 vidual family members display redundancy and pluripotency in their action to ameliorate or evade host

195 uct hepatocyte-like lineage progression from pluripotency in two-dimensional culture.

196 ins their self-renewal capacity in vitro and pluripotency in vivo.

197 signalling pathways that regulate stem-cell pluripotency, including the TGFbeta superfamily, all of

198 Pluripotency-independent conversion of endothelial cells

199 Pluripotency is a state that exists transiently in the e

200 enetic remodeling, cellular reprogramming to pluripotency is also accompanied by a rewiring of metabo

201 Embryonic stem (ES) cell pluripotency is governed by OCT4-centric transcriptional

202 hrough mitosis and that conversion to primed pluripotency is linked to lineage priming in the G1 phas

203 sis article, a third phase, called formative pluripotency, is proposed to exist as part of a developm

204 n order of acquisition of chromatin marks at pluripotency loci, and multivalent states (comprising pr

205 eage bias, with faster aggregation promoting pluripotency loss and ectoderm, and slower aggregation f

206 2 genes in human embryonic stem cells causes pluripotency loss and spontaneous differentiation toward

207 ment, metabolism, and cell cycle to the core pluripotency machinery.

208 mice were associated with downregulation of pluripotency maintaining factors (c-Myc, Nanog and Oct4)

209 cadherin and transcription factors Slug, and pluripotency maintaining factors Nanog, c-Myc, and Oct4.

210 hibited the expression of stem cell markers, pluripotency maintaining transcription factors, cell cyc

211 acteristic of stem cells that contributes to pluripotency maintenance.

212 development to the maintenance of stem cell pluripotency, many biological signaling pathways exhibit

213 ted with a significant downregulation of key pluripotency marker expression, disruption of mesenchyma

214 BAF155 leads to increased expression of the pluripotency marker Nanog and its ectopic expression in

215 ower proportion of stem cells expressing the pluripotency marker Oct3/4 and increased cell survival.

216 on cell proliferation and expression of the pluripotency marker Oct4 24 h after seeding.

217 in to the appropriate subcellular structure, pluripotency-marker expression, and multilineage differe

218 +) sorted cells maintained the expression of pluripotency markers and that ESC adherent to the amnion

219 Gene expression of pluripotency markers decreased similarly for EBs of both

220 Expression of pluripotency markers Nanog, Oct4, Sox2, and Klf4 was sig

221 lting cell population expressed both CSC and pluripotency markers, and the sphere-forming CSC-like ce

222 observed pronounced changes in expression of pluripotency markers, including Sox2, Nanog, and Otx2.

223 n of multiple core transcription factors and pluripotency markers.

224 x between the lineages and the expression of pluripotency markers.

225 , including tumorigenesis relevant genes and pluripotency markers.

226 pression profiling and the expression of key pluripotency markers.

227 We find that the exit from pluripotency marks the start of a lineage transition as

228 nsgenic system we exhibit that in mESCs, the pluripotency master regulator Oct4, counteracts pro-diff

229 ere is concern that the stresses of inducing pluripotency may lead to deleterious DNA mutations in in

230 ts establish a direct connection between the pluripotency network and chromatin organization and emph

231 library to screen for key regulators of the pluripotency network and discovered three combinations o

232 , because of the complexity of both the core pluripotency network and the process of cell fate comput

233 Its depletion destabilizes the pluripotency network and triggers differentiation.

234 t after the dissolution of the naive ES-cell pluripotency network during establishment of EpiLCs, the

235 the self-renewal defect is mediated through pluripotency network independent pathways.

236 sights into the underlying principles of the pluripotency network may provide unprecedented opportuni

237 mutual repression between Hoxa1 and the core pluripotency network provides a molecular mechanism that

238 ctor NANOG as a key regulator connecting the pluripotency network with constitutive heterochromatin o

239 apidly reactivated upon re-expression of the pluripotency network.

240 ctor of Tcf7l1 mRNA, a core component of the pluripotency network.

241 , identifies HPAT5 as a key component of the pluripotency network.

242 f the pioneer factor OCT4 and regulating the pluripotency network.

243 ay be due in part to the divergence in their pluripotency networks and early post-implantation develo

244 The pluripotency of iPSCs was confirmed by quantitative reve

245 Inherent challenges, however, are the pluripotency of IVIG and its xenogeneicity in animals.

246 Pluripotency of stem cells also relies on normal proteas

247 ons, such as maintenance of self-renewal and pluripotency of stem cells.

248 Reversible synchronization has no effect on pluripotency or differentiation.

249 etic events can drive reprogramming to naive pluripotency or if distinct chromatin states are instead

250 anscriptional factor essential for stem cell pluripotency, plays a role in maintaining KSHV latent in

251 transition to a distinct formative phase of pluripotency preparatory to lineage priming.

252 mESCs must be released from Oct4-maintained pluripotency prior to ectopically induced differentiatio

253 ly, MEK1 activity was necessary to clear the pluripotency protein Ventx2 at the onset of gastrulation

254 ent stem cells (PSCs) integrate haploidy and pluripotency, providing a novel system for functional ge

255 2, owing to their antagonistic effect on the pluripotency regulator Nanog.

256 omotive effect of Icaritin on cell cycle and pluripotency regulators are eliminated by siRNA knockdow

257 We suggest that asymmetric clearance of pluripotency regulators may represent an important mecha

258 A number of important pluripotency regulators, including the transcription fac

259 Execution of pluripotency requires progression from the naive status

260 demonstrated that cellular reprogramming to pluripotency reverses cellular age, but alteration of th

261 Using a fluorescent reporter for naive pluripotency (Rex1-GFP), we established that the acutely

262 ccount for the 'stemness' - self-renewal and pluripotency - shared between embryonic stem cells (ESCs

263 and neural crest stem cells express distinct pluripotency signatures.

264 In summary, we describe a p53-regulated, pluripotency-specific lncRNA that safeguards the hESC st

265 ristics, such as self-renewal capacity and a pluripotency-specific molecular signature.

266 Moreover, SRSF5 is bound to pluripotency-specific transcripts such as Lin28a and Pou

267 reprogramming from primed to naive states of pluripotency, Stat3 similarly upregulates mitochondrial

268 hat DGCR8 is essential for the exit from the pluripotency state.

269 Although naive and primed pluripotency states have been characterized molecularly,

270 Recent evidence of alternative pluripotency states indicates the regulatory flexibility

271 matin modifications that are lost along with pluripotency, suggesting a mechanism by which cancer cel

272 s is reversible and occurs without affecting pluripotency, suggesting that Myc-depleted stem cells en

273 tem cells also require PRMT5 for maintaining pluripotency, suggesting that similar mechanisms might r

274 ers can compromise the behavior of important pluripotency-sustaining positive feedback loops, and ind

275 mprised of combinations of binding sites for pluripotency TFs and measured their expression in mouse

276 Somatic and pluripotency TFs modulate reprogramming efficiency when

277 that a specific set of interactions between pluripotency TFs plays a large role in setting the level

278 e live-cell imaging uncovered that two naive pluripotency TFs, STAT3 and ESRRB, interrogate chromatin

279 ater in the process and require OS and other pluripotency TFs.

280 s a key transcriptional regulator for primed pluripotency that also functions as a barrier toward ach

281 y a major role in stem cell self-renewal and pluripotency, their integration with signalling pathways

282 As human pluripotent stem cells (hPSCs) exit pluripotency, they are thought to switch from a glycolyt

283 map bifurcating lineage choices leading from pluripotency to 12 human mesodermal lineages, including

284 of plant development and on the switch from pluripotency to differentiation in different plant organ

285 tinoic acid driven mESC differentiation from pluripotency to lineage commitment, using an unbiased si

286 ancy during the transition from naive/primed pluripotency to multipotent primary neural progenitor ce

287 Pluripotency (TRA-1-81, SSEA3, OCT4, NANOG, SOX2) remain

288 e editing to investigate the function of the pluripotency transcription factor OCT4 during human embr

289 by regulating cell cycle machinery and core pluripotency transcription factors mediated by ERalpha.

290 This coincides with upregulation of key pluripotency transcription factors OCT4, NANOG, KLF4 and

291 They show that the histone mark H3K27ac and pluripotency transcription factors remain associated wit

292 ically dependent on interactions between key pluripotency transcription factors, epigenetic regulator

293 dult dermal fibroblasts by overexpression of pluripotency transcription factors.

294 he maintenance and establishment of cellular pluripotency via multiple mechanisms in bona fide hPSCs

295 he critical window immediately after loss of pluripotency when cells make the earliest developmental

296 comb repressive complex 2 is dispensable for pluripotency when human embryonic stem cells are convert

297 The state of pluripotency, which is stabilized by an interconnected n

298 Cs) were shown to exist in a state of primed pluripotency, while mouse embryonic stem cells (mESCs) d

299 genetic variability and improved functional pluripotency will have great utility in regenerative med

300 ree combinations of ATFs capable of inducing pluripotency without exogenous expression of Oct4 (POU d