ライフサイエンスコーパス: cell fate

1 s for DUSP5 in controlling ERK signaling and cell fate.

2 have emerged as important regulators of stem cell fate.

3 in CcdA provides a mechanism for regulating cell fate.

4 inase (RTK) and major determinant of somatic cell fate.

5 ins are translated selectively and influence cell fate.

6 s to various cellular stresses and regulates cell fate.

7 gy, and may be involved in the regulation of cell fate.

8 ess is important for specifying differential cell fate.

9 epatic drug and energy metabolism as well as cell fate.

10 axis specifies innate and adaptive lymphoid cell fate.

11 e of a Ddx5-miR125b-Rybp axis in controlling cell fate.

12 e of surface topography and chemical cues on cell fate.

13 pears to be a central switch that determines cell fate.

14 n of genes and pathways, and thus ultimately cell fate.

15 re two well-controlled mechanisms regulating cell fate.

16 otent progenitor cells commit to the desired cell fate.

17 of a Notch repressor to assign non-neuronal cell fate.

18 djacent germ cells to maintain germline stem cell fate.

19 oderm-derived I4 neuron adopts a muscle-like cell fate.

20 le is known about the metabolic control of B cell fate.

21 t bimodal transcriptional effects to control cell fate.

22 velopment for competency for primordial germ cell fate.

23 miRNA locus critical for adipose progenitor cell fate.

24 dm16, which determines beige/brown adipocyte cell fate.

25 ulate myelopoiesis that collectively dictate cell fate.

26 on and migration by inducing a mesoderm-like cell fate.

27 riptional regulators of plant root epidermal cell fate.

28 ly or negatively control AS events linked to cell fate.

29 gene expression with the potential to modify cell fate.

30 y checkpoint that controls cell division and cell fate.

31 opment is critical to endocrine and exocrine cell fate.

32 t is now established that Bcl11b specifies T cell fate.

33 ate inputs from multiple pathways to control cell fate.

34 multipotent progenitors become restricted in cell fate.

35 ame time generating a gradient that patterns cell fates.

36 d sufficient to confer particular regulatory cell fates.

37 peding the activation of genes for alternate cell fates.

38 omatin reorganization that accompanies these cell fates.

39 NEUROG3 but do not adopt alternate endocrine cell fates.

40 y adopt distinct polar, stalk, and main body cell fates.

41 at results in the acquisition of specialized cell fates.

42 red for commitment to differentiated somatic cell fates.

43 rogram to correctly specify pancreatic islet cell fates.

44 opment of nonconventional tolerance-inducing cell fates.

45 on is involved in the acquisition of gonadal cell fates.

46 on and fission determining mitochondrial and cell fates.

47 m through coordinated integration of diverse cell fates across developmental space and time, yet unde

48 composition support a probabilistic model of cell fate allocation and in silico simulations predict a

49 nate lymphoid, myeloid, and dendritic, and B-cell fate alternatives are excluded by different mechani

50 Cell fate analysis using a Sox2 (neural) enhancer reveal

51 erstanding of how MCPH1 controls neural stem cell fate and brain development.

52 respond to injury by adopting an osteogenic cell fate and creating damaging calcific deposits, which

53 that pyruvate metabolism dictates intestinal cell fate and differentiation decisions downstream of ap

54 role of ES to regulate neural crest-derived cell fate and differentiation in vivo, knockdown of FIG4

55 nted stem cells must be optimized to control cell fate and enhance therapeutic efficacy.

56 as a novel post-transcriptional regulator of cell fate and establish a direct, previously unappreciat

57 th epigenetics and transcription to modulate cell fate and function.

58 ess where spatial and temporal cues regulate cell fate and functional organization of the rudiment of

59 al Hedgehog signaling pathway that specifies cell fate and morphogenesis.

60 activity is an important regulator of CD8+ T cell fate and raise the possibility that increasing prot

61 Hedgehog (Hh) signaling regulates cell fate and self-renewal in development and cancer.

62 E2A and HEB orchestrated T cell fate and suppressed the ILC transcription signature

63 thelium, is crucial for maintaining prostate cell fate and suppressing tumor initiation.

64 by which PRC2 controls urothelial progenitor cell fate and the timing of differentiation, and further

65 the state transition toward each alternative cell fate and their relationships with specific phenotyp

66 tures and associated enhancers that regulate cell fate and tumorigenesis in the CNS.

67 that have shown promise in controlling stem cell fate and which have also been fully synthesized the

68 regulated the formation of terminal-effector cell fates and memory-precursor cell fates, respectively

69 ity and defects can lead to altered daughter cell fates and numbers.

70 l metal pools can modulate protein function, cell fate, and organism health and disease, has broadene

71 cial structural genomic elements determining cell fate, and they are also involved in the determinati

72 Extracellular cues regulate cell fate, and this is mainly achieved through the engag

73 ablishment and maintenance of these distinct cell fates are driven by massive gene expression program

74 perivascular cells similarly regulate tumor cell fate at metastatic sites.

75 of CRL3(GCL) function and regulation defines cell fate at the single-cell level.

76 y did not increase c-kit-derived endothelial cell fates but instead induced cardiomyocyte differentia

77 uence the specification of distinct CD8(+) T cell fates, but the observation of equivalent expression

78 se findings suggest that Nanos promotes germ cell fate by downregulating maternal RNAs and proteins t

79 ata indicate that TET proteins regulate iNKT cell fate by ensuring their proper development and matur

80 emonstrate that Wnt signaling regulates stem cell fate by promoting neuronal fate choices.

81 ted that TEX1 repressed the megaspore mother cell fate by promoting the biogenesis of TAS3-derived tr

82 tidylcholine (LysoPC) controls P. falciparum cell fate by repressing parasite sexual differentiation.

83 Mechanistically, Id proteins specify cardiac cell fate by repressing two inhibitors of cardiogenic me

84 e et al. (2017) show that GCL blocks somatic cell fate by specifically destroying the Torso Receptor

85 that sequential inductions generate distinct cell fates by changing landscape in sequence and hence n

86 for fractional killing, which predicts that cell fate can be altered in three possible ways: alterat

87 Stem-cell fate can be influenced by metabolite levels in cult

88 this manner, the effects of each isoform on cell fate can be simultaneously assessed through simple

89 Our data reveals a programmed cell fate change in postnatal skeleton and unravels a re

90 essing factor Nudt21 as a novel regulator of cell fate change using transcription-factor-induced repr

91 lls, suggesting a broader role for Nudt21 in cell fate change.

92 The first cell fate choice in mouse development is the segregation

93 the lateral inhibition that underlies binary cell fate choice is extensively studied, but the context

94 At the molecular level, FOXP1 regulated cell-fate choice of MSCs through interactions with the C

95 at regulate prohemocyte maintenance and some cell fate choices between hemocyte lineages.

96 ditis elegans, implies a phase diagram where cell-fate choices are displayed in a plane defined by EG

97 Tfh-Teff cell fate commitment is regulated by mutual antagonism b

98 nd epigenomes acting in concert with initial cell fate commitment remains poorly characterized.

99 Cell fate commitment represents a critical state transit

100 We present a theoretical model of stem cell fate computation that is based on Halley and Winkle

101 of obtaining a deeper understanding of stem cell fate computation, in order to influence experimenta

102 physical asymmetric division mechanisms and cell fate consequences have been investigated, the speci

103 rly thymic progenitors (ETPs) could escape T cell fate constraints imposed normally by a Notch-induct

104 centration, BMP4 gives rise to only a single cell fate, contrary to its role as a morphogen in other

105 f regulating the epigenetic landscape during cell fate conversion but also provide a framework to imp

106 mbryonic stem cells (mESCs) are resistant to cell fate conversion induced by the melanocyte lineage m

107 rentiation and transcription-factor-mediated cell fate conversion produces haematopoietic stem and pr

108 efficiency of fluorescent cell labeling and cell fate conversion.

109 e of safeguarding mechanisms that counteract cell fate conversion.

110 KLF4 is critical for cell fate decision and has an ambivalent role in tumorig

111 -transcriptional factors functioning in this cell fate decision are mostly unknown.

112 The cell fate decision between interferon-producing plasmacy

113 ammalian embryo is fundamental for the first cell fate decision that sets aside progenitor cells for

114 ch loss of function during the sheath-neuron cell fate decision, suggesting the miRNAs facilitate Not

115 chick as these cells offer a window into the cell fate decision-making process.

116 mena, particularly in biology, including the cell-fate decision in developmental processes as well as

117 Here we describe a genetic program for cell-fate decision in the opportunistic human pathogen S

118 lecules are essential to the coordination of cell-fate decision making in multicellular organisms.

119 y achieve robust functionality, for example, cell-fate decision-making and signal transduction, throu

120 rovides a mechanistic basis for the observed cell fate decisions and accounts for the precision and d

121 regulated by extracellular signals, control cell fate decisions and determine the size and compositi

122 Notch receptor activation initiates cell fate decisions and is distinctive in its reliance o

123 The Notch signalling pathway mediates cell fate decisions and is tumour suppressive or oncogen

124 d the co-receptors LRP5 and LRP6 to regulate cell fate decisions and the growth and repair of several

125 tal for elucidating the mechanisms governing cell fate decisions and tissue homeostasis.

126 Cell fate decisions are controlled by the interplay of t

127 mmune system should provide insight into how cell fate decisions are made during infections and poten

128 the Akt substrate networks associated with T cell fate decisions are qualitatively different.

129 Ras signaling mediates cell fate decisions as well as proliferation during deve

130 pulation level reflects collective unipotent cell fate decisions by single stem cells.

131 ctuation-driven patterning mechanism for how cell fate decisions can be initiated through a random ye

132 gulatory networks that drive the sequence of cell fate decisions during development.

133 tion factor (TF) Eomes is a key regulator of cell fate decisions during early mouse development.

134 tent of IRE1alpha activity and may determine cell fate decisions during ER stress conditions.

135 rgize with the activities of another family, cell fate decisions during pathogenic encounters are unp

136 regulatory mechanisms that guide trophoblast cell fate decisions during placenta development remain i

137 Transcriptional regulation during CD4(+) T cell fate decisions enables their differentiation into d

138 ha (C/EBPalpha), which is mainly involved in cell fate decisions for myeloid differentiation.

139 intricate microfibrillar networks influence cell fate decisions in a contextual manner, more informa

140 trast to a prior emphasis on the finality of cell fate decisions in developmental systems, cellular p

141 However, their roles in cell fate decisions in early embryonic development remai

142 ral integration site (MEIS) proteins control cell fate decisions in many physiological and pathophysi

143 essential morphogenetic signal that dictates cell fate decisions in several developing organs in mamm

144 molecular mechanisms that regulate the first cell fate decisions in the human embryo are not well und

145 of posttranscriptional regulation in cardiac cell fate decisions remain largely unknown.

146 ng the regulatory interactions that underlie cell fate decisions requires characterizing TF binding s

147 as gained attention as a key determinant for cell fate decisions, but the contribution of DNA replica

148 ich to study regulatory mechanisms governing cell fate decisions, extracellular signaling, cell and t

149 rotein Notch, which is crucial for embryonic cell fate decisions, has 36 extracellular EGF domains th

150 ssion is critically shaped by IL-4, altering cell fate decisions, which are likely important for the

151 s of Bicoid activity alter the most anterior cell fate decisions, while prolonged inactivation expand

152 essential roles in embryonic development and cell fate decisions.

153 e pluripotent stem cell cycle contributes to cell fate decisions.

154 t TET2 is an important regulator of CD8(+) T cell fate decisions.

155 e causative role of Fus3 dynamics in driving cell fate decisions.

156 , it is unclear how Akt controls alternate T cell fate decisions.

157 ories can unveil how gene regulation governs cell fate decisions.

158 expression of Musashi isoforms may influence cell fate decisions.

159 ansport these lipids to promote inflammatory cell fate decisions.

160 ependent signals that determine inflammatory cell fate decisions.

161 ion to mediate cellular responses, including cell fate decisions.

162 hich lysine methylation signaling impacts on cell fate decisions.

163 proteins as central regulators of murine NKT cell fate decisions.

164 ic roles of polycomb repressive complex 2 in cell fate decisions.Polycomb repressive complex 2 (PRC2)

165 s unclear how networks that control critical cell-fate decisions (e.g., cell division and apoptosis)

166 between the two TOR complexes that controls cell-fate decisions in response to nutrient availability

167 a rate-limiting step in regulating critical cell-fate decisions in various inflammatory scenarios.

168 hresholds required for driving morphogenetic cell-fate decisions.

169 and consequently altering SHH-guided neural cell-fate decisions.

170 foster our understanding of lymphoid/myeloid cell-fate decisions.

171 Although Numb is well-recognized as a cell-fate determinant in stem/progenitor cells, accumula

172 endothelial-specific deletion of osteoblast cell-fate determinant OSX compared with bigenic mice (Os

173 pidermis-targeted coexpression of sT and the cell fate-determinant atonal bHLH transcription factor 1

174 and it relies on the correct partitioning of cell fate determinants.

175 e most critical genes acting in the steps of cell fate determination and early differentiation of var

176 es a synthetic biology framework to approach cell fate determination and suggests a landscape-based e

177 ipheral taste system: embryonic chemosensory cell fate determination and the specification of lingual

178 gulation of gene expression is essential for cell fate determination and tissue development.

179 enabled us to identify key genes involved in cell fate determination and to obtain new insights about

180 ring development, extracellular cues guiding cell fate determination are provided by morphogens.

181 Cell fate determination by lateral inhibition via Notch/

182 Dachshund homolog 1 (DACH1), a key cell fate determination factor, contributes to tumorigen

183 The process of cell fate determination has been depicted intuitively as

184 This reveals a role for nmy-2 in cell fate determination not obviously linked to the prim

185 ble, which enables direct study of quadruple cell fate determination on an engineered landscape.

186 e and cellular metabolism both contribute to cell fate determination, but their interplay remains poo

187 neuromuscular junction formation, and neuron cell fate determination, typically during the pupal stag

188 in disease states with opposing responses in cell fate determination, yet its contribution in pro-sur

189 cycle to allow ample time for DNA repair and cell fate determination.

190 provides new insights into the mechanisms of cell fate determination.

191 aste cell proliferation, differentiation and cell fate determination.

192 the proteomic dynamics during the process of cell fate determination.

193 hancer-mediated transcription attenuation in cell fate determination.

194 emodeling and unravel the complexity of stem cell fate determination.

195 f signal transduction in cells are vital for cell fate determination.

196 and exhibit multilevel cross-talk regulating cell fate-determining and fibrogenic pathways.

197 mbda, is paradigmatic for gene regulation in cell-fate development, yet insight about its mechanisms

198 spontaneous expression differences underlie cell fate diversity in both differentiation and disease

199 ntify TNF as a pivotal factor in determining cell fate during a viral infection and delineate a MAVS/

200 ption factors are implicated in establishing cell fate during mammalian development.

201 pindle orientation is a major determinant of cell fate during tissue regeneration.

202 stone demethylases that both regulate normal cell fates during development and contribute to the epig

203 repertoire of vertebrate trunk neural crest cell fates during normal development, highlight the like

204 This protocol specifies cell fate efficiently into cardiac and endothelial linea

205 s cells undergoing one of two very different cell fates: either transdifferentiating into myofibrobla

206 nd to suggest specific hypotheses to improve cell fate engineering protocols.

207 regulation at key regulators of neural stem cell fate ensuring adequate NSPCs self-renewal and maint

208 Therefore, cell fates exposed to higher Bicoid concentration requir

209 controlling a molecular switch that dictates cell fate following exposure to adverse environments.

210 a useful target to alter leukemia-initiating cell fate for differentiation therapy.

211 lling to favour adaptive responses and shift cell fate from apoptosis to survival under chronic stres

212 ence indicates that both cell number and the cell fates generated by each neuroblast are very precise

213 Understanding of cell fate has been advanced by studying single-cell RNA-

214 et of rapamycin signaling drives intraclonal cell fate heterogeneity.

215 mediate post-fission randomization of sister cell fates highlights the potential of stochastic fluctu

216 motes early acquisition of a memory CD8(+) T cell fate in a cell-intrinsic manner without disrupting

217 modification with ubiquitin chains controls cell fate in all eukaryotes.

218 occurring in vivo forces for improving stem cell fate in clinical regenerative therapies.

219 ur work reveals that HEC function stabilizes cell fate in distinct zones of the shoot meristem thereb

220 checkpoint maintenance and determination of cell fate in mitosis.

221 ug itraconazole (ITA) as an inhibitor of MFB cell fate in resident fibroblasts derived from multiple

222 re delamination and selection of a proneural cell fate in the early Drosophila embryo.

223 help coordinate gene expression to modulate cell fate in the hematopoietic system.

224 ays, and transcription factors that direct B cell fate in the periphery.

225 In addition to rejection, probing of T and B cell fate in vivo provides insights into the underlying

226 sted a potential strategy to control cardiac cell fates in development and diseases.

227 n an expanding B cell clone assumes multiple cell fates, including class-switched B cells, antibody-s

228 Multiple cell fates, including renewed stem cells and committed d

229 luripotent cells competent to respond to all cell fate inducers tested.

230 s orchestrated at the cellular level and how cell fate is affected by severe tissue damage.

231 Cell fate is established through coordinated gene expres

232 Differential gene expression specifying cell fate is governed by the inputs of intracellular and

233 lead multipotent cells to acquire different cell fates makes a quantitative understanding of differe

234 of this proposal by using a genetic knock-in cell fate mapping strategy in different murine SCI model

235 acking system that combines Cre/lox-assisted cell fate mapping with a thymidine kinase (sr39tk) repor

236 define fetal and adult hematopoiesis, while cell-fate mapping studies have revealed complex developm

237 xtended timespan, combining cell tracing and cell fate marker expression over time.

238 , Hh, and Notch signalling reporters and the cell fate markers Eyes Absent (Eya) and Castor (Cas) to

239 in promoting the maintenance of floral stem cell fate, not by repressing AG transcription, but by an

240 rophages toward an alternate and detrimental cell fate of necroptosis.

241 ferent pathological stimuli induce different cell fates of c-kit(+) cells in vivo.

242 l stimuli differentially affect the eventual cell fates of c-kit(+) cells.

243 dentification of miRNAs which influence stem cell fate offers new approaches for application of miRNA

244 high affinity memory B cells into the plasma cell fate, our findings provide fundamental insights int

245 When differentiated to dorsal forebrain cell fates, our fragile X syndrome human pluripotent ste

246 itical role in regulating activation-induced cell fate outcomes.

247 is elegans, thereby ensuring proper temporal cell fate patterning.

248 als maintain developmental states and create cell fate patterns in vivo and influence differentiation

249 Cell fate perturbations underlie many human diseases, in

250 hibitor, and H heterozygotes exhibit bristle cell fate phenotypes reflecting gain-of-Notch signaling,

251 However, the cell fate plasticity of endogenous pericytes in vivo rem

252 iR-34a restricts the acquisition of expanded cell fate potential in pluripotent stem cells, and it re

253 he postnatal olfactory epithelium, revealing cell fate potentials and branchpoints in olfactory stem

254 rized cardiac PW1-expressing cells and their cell fate potentials in normal hearts and during cardiac

255 latory steps involved in successful terminal cell fate programming remain obscure.

256 l to hyperactive signaling in a diversity of cell fate programs.

257 mediate cell-cell communication and control cell fate, proliferation, and survival.

258 compounds' unique abilities to regulate stem cell fate provides opportunities for developing improved

259 exes with Smad4 to target specific genes for cell fate regulation.

260 vestigations reveal that the plasma membrane cell fate regulator, SCRAMBLED (SCM), is mislocalized in

261 the hair cell, which appears to control both cell fate regulators and abiotic stress responses.

262 but the signaling networks controlling beta-cell fate remain poorly understood.

263 nal-effector cell fates and memory-precursor cell fates, respectively.

264 effects are manifest as profound changes in cell fates [short hair cells (HCs) are missing], ribbon

265 which allows time-restricted perturbation of cell fate, shows that depletion of Smarcb1 activates the

266 These results highlight the complexity of cell fate specification by cell-cell interactions in a r

267 nally, by controlling the timing and pace of cell fate specification, the embryo temporally modulates

268 totic precision fundamentally contributes to cell fate specification, tissue development and homeosta

269 sis, auditory hair cell differentiation, and cell fate specification.

270 tial and temporal mechanisms governing their cell-fate specification and differential integration int

271 he relationships among cell types in diverse cell-fate specification processes.

272 scence microscopy to study processes such as cell-fate specification, cell death, and transdifferenti

273 mrt5 as a novel regulator of the neuron-glia cell-fate switch in the developing hippocampus.

274 Regulation of the neuron-glia cell-fate switch is a critical step in the development o

275 nuates MSC senescence by orchestrating their cell-fate switch while maintaining their replicative cap

276 ulated network that controls the neuron-glia cell-fate switch.SIGNIFICANCE STATEMENT We identify Dmrt

277 c mIg/BCR dosage may play a larger role in B cell fate than previously anticipated.

278 fter YAP/TAZ), which together control breast cell fate through intrinsic and paracrine mechanisms.

279 x or cyclosome (APC/C), in the regulation of cell fate through modulation of Wingless (Wg) signaling.

280 ssing endogenous DNA damage, and may control cell fate through the regulation of CHK1.

281 tch signaling, which coordinates neighboring cell fates through direct cell-cell signaling.

282 s local minima and signal inductions dictate cell fates through modulating the shape of the multistab

283 developmental processes yet produce distinct cell fates through specific downstream transcription fac

284 ines the axis of division and is crucial for cell fate, tissue morphogenesis, and the development of

285 Control of stem cell fate to either enter terminal differentiation versu

286 x, in which TGFbeta can induce two disparate cell fates, to a new epithelial disease state.

287 Using in vivo and in vitro cell fate tracing concomitant with specific cell ablatio

288 induction of Irf4 expression redirected Tfh cell fate trajectories toward those of Teff.

289 a conserved role for YTHDC2 in this critical cell fate transition.

290 Whether cell fate transitions can be induced during various deve

291 Here we dissect cell fate transitions during colonic regeneration in a m

292 epigenomic remodeling events associated with cell fate transitions into and out of human pluripotency

293 tions of histone modifications in initiating cell fate transitions, with particular focus on their co

294 hastic oncogene activation or nonphysiologic cell fate transitions.

295 However, the mechanisms that regulate stem cell fates under such widely varying conditions are not

296 he network architectures underlying distinct cell fates using a reverse engineering method and uncove

297 maging to correlate signaling histories with cell fates, we demonstrate that interactions between nei

298 ow that GLYCINE-RICH PROTEIN 8 promotes hair cell fate while alleviating phosphate starvation stress.

299 a microRNA-dependent manner to inhibit hair cell fate, while also terminating growth of root hairs m

300 transcription factors (TFs) aims to control cell fate with the degree of precision needed for clinic