ライフサイエンスコーパス: cell fate decision

1 ment and differentiation phases of the first cell fate decision.

2 (TFs) that regulates the rod versus bipolar cell fate decision.

3 rstanding of mechanisms underlying the first cell fate decision.

4 etabolism, which correlates with a defective cell fate decision.

5 eural cell types and promotes a Muller glial cell fate decision.

6 y conserved MAPK signaling pathway regulates cell fate decision.

7 and EGF/EGFR in HPC self-renewal and binary cell fate decision.

8 lved in DNA repair itself, and mediates this cell fate decision.

9 hich lysine methylation signaling impacts on cell fate decisions.

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

11 idermal differentiation, suggesting aberrant cell fate decisions.

12 intracellular signaling, and drive CD4(+) T cell fate decisions.

13 of interest to investigate cell potency and cell fate decisions.

14 ation, duration of exposure also coordinates cell fate decisions.

15 CD4-associated Lck is important for CD4(+) T cell fate decisions.

16 tem cells control developmental programs and cell fate decisions.

17 have dramatic consequences on epidermal stem cell fate decisions.

18 CD3 complex is the primary determinant for T cell fate decisions.

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

20 signaling pathways directing these critical cell fate decisions.

21 a population of cells that needs to balance cell fate decisions.

22 otch(OFF) or Notch(ON) neurons during binary cell fate decisions.

23 dorsal telencephalic neuronal and astroglia cell fate decisions.

24 anslate parallel signalling information into cell fate decisions.

25 tivates or represses many genes that control cell fate decisions.

26 omatin regulators have multifaceted roles in cell fate decisions.

27 essential roles in embryonic development and cell fate decisions.

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

29 the Bmp and Wnt/beta-catenin pathways during cell fate decisions.

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

31 nctional role of Nanog heterogeneity on stem cell fate decisions.

32 mune signals and metabolic cues, to direct T-cell fate decisions.

33 infection are essential in shaping CD8(+) T cell fate decisions.

34 hese processes may help to gain control over cell fate decisions.

35 are crucial for endodermal morphogenesis and cell fate decisions.

36 ction and angiogenesis, and mesenchymal stem cell fate decisions.

37 ch as chromatin remodeling to achieve stable cell fate decisions.

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

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

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

41 expression of Musashi isoforms may influence cell fate decisions.

42 ansport these lipids to promote inflammatory cell fate decisions.

43 ependent signals that determine inflammatory cell fate decisions.

44 ate Ag and cytokine receptor signals to make cell fate decisions.

45 ssures the correct order of these sequential cell fate decisions.

46 f morphogen exposure is critical for correct cell fate decisions.

47 ernative splicing are important factors in T cell fate decisions.

48 1 as a critical effector of mTORC1 to govern cell fate decisions.

49 m cells and participate in the regulation of cell fate decisions.

50 post-transcriptional regulation of epidermal cell fate decisions.

51 etworks and epigenetic modifiers to instruct cell fate decisions.

52 cells provide instructive inputs that govern cell fate decisions.

53 l shifts in the epigenetic landscape driving cell fate decisions.

54 and has also been shown to regulate various cell-fate decisions.

55 otent states, which might affect other early cell-fate decisions.

56 h contribute to a remarkably large number of cell-fate decisions.

57 ion/epigenetic control of a vast majority of cell-fate decisions.

58 very, allowing enhanced control over diverse cell-fate decisions.

59 rate such signals over time to make critical cell-fate decisions.

60 hresholds required for driving morphogenetic cell-fate decisions.

61 processes including cell differentiation and cell-fate decisions.

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

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

64 levels of mitochondrial damage and mediates cell fate decisions accordingly is incompletely understo

65 important regulators of gene expression and cell fate decisions, although their functions in HSCs ar

66 mplex is a master regulator of developmental cell-fate decisions, although the key target pathways ar

67 n this study, we add to the role of Notch in cell fate decision and demonstrate that the Notch signal

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

69 Notch signaling plays a pivotal role in cell fate decision and lineage commitment of lymphocytes

70 racterized by context-dependent key roles in cell fate decision and tumorigenesis.

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

72 n mammals, are involved in the regulation of cell fate decisions and cell proliferation in various or

73 s to investigate the roles of DKK1 in embryo cell fate decisions and competence to establish pregnanc

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

75 hown to play an essential role in regulating cell fate decisions and differentiation during cardiogen

76 anscriptional RNA-regulatory machine impacts cell fate decisions and differentiation is poorly unders

77 the control of gene expression, supervising cell fate decisions and differentiation.

78 otch signaling regulates a broad spectrum of cell fate decisions and differentiation.

79 to maintain multipotency but also stabilize cell fate decisions and direct lineage restriction.

80 resent an invaluable platform to investigate cell fate decisions and disease.

81 , and glutaminolysis preferentially fuel the cell fate decisions and effector functions of immune cel

82 icroRNAs have emerged as key regulators of B cell fate decisions and immune function.

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

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

85 es, which help with symmetry breaking during cell fate decisions and lineage commitment.

86 ation--provides a foundation for the initial cell fate decisions and morphogenetic movements of embry

87 pioneer transcription factors in adult stem cell fate decisions and plasticity, which ensure that se

88 gulates several cellular processes including cell fate decisions and proliferation in both invertebra

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

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

91 ssues, to provide positional information for cell fate decisions and to enable robust programmes of d

92 The cell-fate decisions and lineage relationships that under

93 that PGE2 may act as a morphogen to regulate cell-fate decisions and outgrowth of the embryonic endod

94 he idea that metabolic changes underlie many cell-fate decisions and p53-mediated tumour suppression,

95 cooperation in controlling anti-tumorigenic cell-fate decisions and reveal these activities to be di

96 rminants coordinate to enhance robustness of cell fate decision, and they provide a safeguard mechani

97 key pathway that contributes to development, cell fate decisions, and differentiation, including that

98 a chromatin signature of genes that mediate cell fate decisions, and its expression is highly upregu

99 properties may be engineered to dictate stem cell fate decisions, and overview a subset of the operat

100 contribute to explain stochasticity in stem cell fate decisions, and that the standard model for lat

101 n the lymphoid organ T zone support distinct cell fate decisions, and they establish a function for d

102 n patterns driving embryonic development and cell fate decisions, and variations in their sequences a

103 Notch signaling regulates cell-fate decisions, and expression studies suggested th

104 pathways that control cutaneous development, cell-fate decisions, and keratinocyte growth and differe

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

106 Cell fate decisions are controlled by the interplay of t

107 Cell fate decisions are fundamental to the development o

108 Our data provide new insights into how cell fate decisions are imposed by the expression of a s

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

110 In contrast to such situations in which cell fate decisions are made in rapidly dividing populat

111 In metazoans, cell fate decisions are more complex: organismal homeost

112 Germ cell fate decisions are poorly understood, despite their

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

114 In particular, how alternate cell fate decisions are regulated in nascent mesoderm re

115 Our results demonstrate that cell fate decisions are tightly associated with the cell

116 How these cell-fate decisions are regulated is unclear, but eviden

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

118 larly important roles in early developmental cell fate decisions, as previously shown for Elf5.

119 of kidney and vein progenitors by regulating cell fate decisions at the lateral boundary of the IM.

120 efine a BMP regulatory network that controls cell fate decisions at the neural plate border.

121 e Nde1-Lis1 complex regulates individualized cell fate decisions based on the geographical location w

122 or discovering pathways regulating the first cell fate decisions because of the ease with which early

123 Thus, nuclear calcium controls the T cell fate decision between a proliferative immune respon

124 The cell fate decision between interferon-producing plasmacy

125 d by the expression of proteins that dictate cell fate decisions between intervein and vein during de

126 Mitochondria control bioenergetics and cell fate decisions, but how they influence nuclear gene

127 nergistic or antagonistic manner to regulate cell fate decisions, but it is less clear whether insolu

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

129 r inhibitor of DNA binding (Id)2 modulates T cell fate decisions, but the molecular mechanism underpi

130 nges in mitochondrial dynamics regulate stem cell fate decisions by driving a physiological reactive

131 Notch receptors guide mammalian cell fate decisions by engaging the proteins Jagged and

132 enance of the blood system requires balanced cell fate decisions by hematopoietic stem and progenitor

133 ical WNT signaling but also alters granulosa cell fate decisions by maintaining epithelial-like trait

134 tch-1 signaling pathway involved in critical cell fate decisions by modulating cell proliferation.

135 odifications, may affect gene expression and cell fate decisions by modulating multiple RNA-related c

136 ce, we determined that ADAM10 controls these cell fate decisions by regulating Notch signaling.

137 d stress granules actively signal to mediate cell fate decisions by signaling to the translation appa

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

139 nome-wide analyses showed that Tet3 mediates cell-fate decisions by inhibiting Wnt signaling, partly

140 ion, as early as the 4-cell stage, initiates cell-fate decisions by modulating the balance of pluripo

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

142 These data demonstrate that cell fate decisions can be made in newly postmitotic ret

143 monocytes to successfully traverse the 48-h cell fate decision checkpoint and commence macrophage ma

144 In this article, we survey microbial cell fate decisions demonstrated to involve a random ele

145 tyrosine kinases (RTKs) determine different cell-fate decisions despite sharing the same signalling

146 Mechanisms of initial cell fate decisions differ among species.

147 erlying these structures and how they affect cell fate decision during embryonic development are poor

148 tonomous signals often play crucial roles in cell fate decisions during animal development.

149 Notch signaling controls a wide range of cell fate decisions during development and disease via s

150 ling pathways are also essential to myogenic cell fate decisions during development and tissue repair

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

152 n factors are well-established regulators of cell fate decisions during development.

153 lfate (HS) has been implicated in regulating cell fate decisions during differentiation of embryonic

154 g paradigm has far-reaching implications for cell fate decisions during early embryonic development.

155 rder to understand the mechanisms that guide cell fate decisions during early human development, we c

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

157 Cell fate decisions during embryogenesis and adult life

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

159 e assessment of the role of the AhR critical cell fate decisions during hematopoiesis.

160 The first cell fate decisions during mammalian development establi

161 Cell fate decisions during multicellular development are

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

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

164 otch ligands and receptors determines binary cell fate decisions during progenitor cell divisions, wi

165 on and cell division events, BRs also govern cell fate decisions during stomata development in Arabid

166 entified mouse Ptf1a as a novel regulator of cell-fate decisions during both early and late brainstem

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

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

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

170 Cell fate decisions following TLR signaling parallel dea

171 mplex organ that requires multiple rounds of cell fate decision for development and homeostasis throu

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

173 ling regulation through HES1, which dictated cell fate decisions from bipotent precursors either to t

174 s or environmental cues signaled by BRs into cell fate decisions governed by the YODA-MKK4/5-MPK3/6 m

175 ents, holds implications for Notch regulated cell-fate decisions governing differentiation.

176 nd differentiation, in vitro control of stem cell fate decisions has been difficult.

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

178 is will allow new levels of understanding of cell fate decisions, identity, and function in normal de

179 embryo coordinate epithelial plasticity with cell fate decision in a fast changing cellular environme

180 e signaling centers, yet each makes a unique cell fate decision in a spatiotemporally restricted patt

181 S) stem cells reflect the first, irrevocable cell fate decision in development that is reinforced by

182 blast stem cells (TSCs) arise from the first cell fate decision in the developing embryo and generate

183 these two pathways to regulate the earliest cell fate decision in the FSC lineage.

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

185 pplied to uncover novel regulators governing cell fate decisions in a variety of systems.

186 cycle and mechanisms required for executing cell fate decisions in a wide-range of developmental con

187 have profound implications for understanding cell fate decisions in cancer stem cells.

188 gene expression and epigenetic regulation of cell fate decisions in cardiac lineages.

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

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

191 ular factors coordinate chromatin status and cell fate decisions in hESCs.

192 ortant to understand the basic regulation of cell fate decisions in hESCs.

193 at cell cycle regulators Cyclin D1-3 control cell fate decisions in human pluripotent stem cells by r

194 croRNAs (miRNAs) are important regulators of cell fate decisions in immune responses.

195 nscriptional regulatory networks controlling cell fate decisions in mammalian embryonic development r

196 kinase (PI3K)/Akt signaling pathway controls cell fate decisions in many cell types by modulating the

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

198 ysis of transcriptional thresholds governing cell fate decisions in metazoan development.

199 rotein Kinase C (aPKC) is a key regulator of cell fate decisions in metazoans [5-7].

200 ize the major pathways that govern the first cell fate decisions in mouse development.

201 to act as a maternal determinant regulating cell fate decisions in mouse development.

202 riming gene regulatory networks for critical cell fate decisions in rapidly proliferating postimplant

203 d NF-kappaB survival pathways in driving the cell fate decisions in response to antiestrogens in ER(+

204 PML and PML NBs can also regulate mTOR and cell fate decisions in response to cellular stresses.

205 udy the dynamics of single adult neural stem cell fate decisions in response to competing juxtacrine

206 in operates as a molecular switch to dictate cell fate decisions in response to different cellular st

207 witch that governs cellular-context-specific cell fate decisions in response to variable stress stimu

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

209 lucidate mechanisms controlling the earliest cell fate decisions in spermatogenesis.

210 Notch has a well-defined role in controlling cell fate decisions in the embryo and the adult epidermi

211 hestrate gene expression programs and direct cell fate decisions in the hematopoietic system.

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

213 show that phyB acts systemically to regulate cell fate decisions in the leaf epidermis.

214 ls, identifies Fbw7 as a master regulator of cell fate decisions in the pancreas, and reveals adult p

215 igated whether Kremen1 functions to modulate cell fate decisions in the prosensory domain of the deve

216 f neural precursor production and for binary cell fate decisions in the ventral neuroectoderm.

217 nodes where signal input will direct desired cell fate decisions in vitro or in vivo.

218 dition, it has been shown that m(6)A affects cell fate decisions in yeast and plant development.

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

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

221 extensively characterized as a regulator of cell-fate decisions in a variety of organisms and tissue

222 noisy input into a toggle switch for robust cell-fate decisions in CCSCs.

223 Such bursting has important consequences for cell-fate decisions in diverse processes ranging from HI

224 en linked on a cell biological basis to stem cell-fate decisions in human HSCs and emerges as an impo

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

226 um and spinal cord, the mechanisms mediating cell-fate decisions in the brainstem, which regulates a

227 pe diversity in metazoa, results from binary cell-fate decisions in the branching pedigree of develop

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

229 Using this system, we aimed to model cell-fate decisions including specification, expansion a

230 Several factors contribute to these cell fate decisions, including the amount and duration o

231 factor 4 (KLF4) is an important regulator of cell-fate decision, including cell-cycle regulation, apo

232 KLF4 is an important regulator of cell-fate decision, including DNA damage response and ap

233 The mechanism of these cell fate decisions involved mutual repression of NANOG

234 In mammals the first cell fate decision involves segregation of the pluripote

235 ains an open question when and how the first cell fate decision is made in mammals.

236 ons strongly suggest that the TH1 versus TH2 cell fate decision is regulated at multiple levels and s

237 s that control energy homeostasis may affect cell fate decisions is largely unknown.

238 Notch signaling also underlies adult hepatic cell fate decisions is largely unknown.

239 ations here suggest that the role of Tcf3 in cell-fate decision is more complex than previously appre

240 s, although how dendritic cells promote this cell-fate decision is not fully understood.

241 mplicate the role of substrate stiffness for cell fate decisions, it is difficult in these matrices t

242 o elucidate the regulatory mechanisms behind cell fate decisions, it is highly desirable to synthesiz

243 5 and 8 of development) promotes the first 2 cell fate decisions leading to increased differentiation

244 Cell fate decision making in HSCs, as indeed in other ce

245 inase signaling to regulate pluripotency and cell fate decision making in mouse embryonic stem cells

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

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

248 etwork allows for stochastic yet unambiguous cell fate decision-making.

249 ional coupling of cell cycle progression and cell fate decision-making.

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

251 Quantitative live imaging of asymmetric cell-fate decision-making and their live shape manipulat

252 tic or lysogenic pathway is followed; hence, cell-fate decision-making appears not to be correlated w

253 The cell fate decision of a mesenchymal precursor cell is un

254 secreting alveolar cell lineage by driving a cell fate decision of the mammary luminal progenitor cel

255 that these ICOS signals critically impacted cell fate decisions of Ag-specific CD8(+) T cells, resul

256 How cell fate decisions of stem and progenitor cells are reg

257 genitor cells, implicate Su(H) in regulating cell fate decisions of these progenitors, and document t

258 Such transitions, including cell fate decisions, often employ positive feedback regu

259 hput screening of gene networks that trigger cell fate decisions or phenotypic changes.

260 the field of tumor biology in order to study cell-fate decisions or to trace cancer cells in the mous

261 They have also been shown to underlie cell fate decisions (or cellular memory).

262 nge of biological processes, including early cell fate decisions, organogenesis and adult tissue home

263 as being important for the induction of Tfh cell fate decision, other molecules may play key roles i

264 This bifurcation marks a cell-fate decision point whereby cells with relatively h

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

266 ne the global stability and kinetic speed of cell fate decision process for development.

267 otch signaling pathway, a known regulator of cell fate decisions, proliferation, and apoptosis, has r

268 Notch is a key regulator of cell fate decision relevant in many immunological pathwa

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

270 the molecular mechanisms that mediate these cell fate decisions remain unclear.

271 This cell fate decision requires the transcription factor Pro

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

273 e system in the priming of naive T cells, in cell fate decisions such as effector and memory cell dif

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

275 of Set1 in neural stem cells does not affect cell fate decisions, suggesting a differential requireme

276 We formulate and analyze an algorithm of cell fate decision that describes the way in which divis

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

278 refully controlled set of cell divisions and cell fate decisions that lead to a mature embryo contain

279 One of the first embryonic cell fate decisions (that is, mesendoderm determination)

280 -transcriptional regulators of hematopoietic cell-fate decisions, though little remains known about t

281 ibiting the BMP4/Activin A-regulated vaginal cell fate decision through a downregulation of RUNX1.

282 thus control low rates of near irreversible cell fate decisions through a balancing act between nois

283 microRNAs regulate developmental cell-fate decisions, tissue homeostasis, and oncogenesis

284 ironmental signals that determine macrophage cell fate decisions to establish appropriate inflammator

285 This molecular circuitry may inform distinct cell fate decisions to Notch1 in epithelial tissues, whe

286 developing mesothelium and allow appropriate cell fate decisions to occur in this multipotent mesoder

287 Stem cell fate decisions to remain quiescent, self-renew or d

288 flammation and immune tolerance by skewing T-cell fate decisions toward either the T-helper 17 (Th17)

289 ral encoding has a role in HIF signaling and cell fate decisions triggered by hypoxic conditions.

290 tein is essential for the initiation of this cell fate decision, ultimately providing the malaria com

291 etween endosomes was sufficient to reprogram cell-fate decision upon EGF stimulation.

292 introducing molecular switches that regulate cell fate decisions via mTOR.

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

294 ogramming provides fundamental insights into cell fate decisions, which in turn reveal strategies to

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

296 and may facilitate correlating hematopoietic cell fate decisions with the extrinsic cues that elicite

297 However, they often have opposing effects on cell-fate decisions with each pathway promoting an alter

298 ar and studied the proneural requirement for cell fate decision within this population.

299 Bam and COP9 signalosome components regulate cell fate decisions within the Drosophila ovarian germli

300 We conclude that cell fate decisions within the inner cell mass are depen