ライフサイエンスコーパス: cell fate decision

1 al commitment that orchestrates this crucial cell fate decision.

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

3 tical modeling to analyze transitions during cell fate decision.

4 m cell regeneration, tissue homeostasis, and cell fate decision.

5 ibution to cell polarization, ACD and binary cell fate decisions.

6 n is tightly controlled and coordinated with cell fate decisions.

7 have the potential to regulate hematopoietic cell fate decisions.

8 are central regulators of cell division and cell fate decisions.

9 iptome will provide invaluable insights into cell fate decisions.

10 hich lysine methylation signaling impacts on cell fate decisions.

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

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

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

14 essential roles in embryonic development and cell fate decisions.

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

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

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

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

19 expression of Musashi isoforms may influence cell fate decisions.

20 ansport these lipids to promote inflammatory cell fate decisions.

21 ependent signals that determine inflammatory cell fate decisions.

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

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

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

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

26 1 as a critical effector of mTORC1 to govern cell fate decisions.

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

28 post-transcriptional regulation of epidermal cell fate decisions.

29 etworks and epigenetic modifiers to instruct cell fate decisions.

30 cells provide instructive inputs that govern cell fate decisions.

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

32 idermal differentiation, suggesting aberrant cell fate decisions.

33 tochondrial plasticity is a key regulator of cell fate decisions.

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

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

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

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

38 tem cells control developmental programs and cell fate decisions.

39 have dramatic consequences on epidermal stem cell fate decisions.

40 of early DC progenitor versus late-stage DC cell fate decisions.

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

42 signaling pathways directing these critical cell fate decisions.

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

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

45 dorsal telencephalic neuronal and astroglia cell fate decisions.

46 anslate parallel signalling information into cell fate decisions.

47 ne design and offer important insight into B cell fate decisions.

48 nduce changes in accessibility that underpin cell fate decisions.

49 to affect cellular signaling, secretion, and cell fate decisions.

50 ve rather than bystander roles in regulating cell fate decisions.

51 ange rapidly compared to the time for making cell fate decisions.

52 gage alternate signaling networks to control cell fate decisions.

53 stemic hormone is shown to direct local stem cell fate decisions.

54 rd mitochondrial dynamics in regulating stem cell fate decisions.

55 ment is essential for inferring the earliest cell fate decisions.

56 l architecture to regulate tissue growth and cell fate decisions.

57 ctuations in acetyl-CoA levels function in T cell fate decisions.

58 go a programme of independent and stochastic cell fate decisions.

59 newal and balancing neural versus mesodermal cell fate decisions.

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

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

62 hresholds required for driving morphogenetic cell-fate decisions.

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

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

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

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

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

68 ing, activate signaling pathways, and direct cell-fate decisions.

69 pretation and discuss how this can impact on cell-fate decisions.

70 g of cellular stress, they drive contrasting cell-fate decisions.

71 cur gradually rather than abruptly to direct cell-fate decisions.

72 ific transcription factors (LS-TFs) underlie cell-fate decisions.

73 a key mediator of developmental programs and cell-fate decisions.

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

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

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

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

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

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

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

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

82 ed epigenetic machineries that regulate stem cell fate decisions and development, and are also implic

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

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

85 Alternative splicing (AS) is involved in cell fate decisions and embryonic development.

86 hanistic understanding of how BCOR regulates cell fate decisions and how loss of function contributes

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

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

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

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

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

92 gulatory dynamics to present a new model for cell fate decisions and their regulators in NPCs during

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

94 6l1 as a molecular nexus for balancing glial cell-fate decision and controlling gliomagenesis.

95 intuitive role for early p21 dynamics in the cell-fate decision and pinpoints a source of proliferati

96 force on the downstream signal transduction, cell-fate decisions and effector function of immune cell

97 Notch receptors play critical roles in cell-fate decisions and in the regulation of skeletal de

98 The cell-fate decisions and lineage relationships that under

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

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

101 examples of the connection among metabolism, cell fate decisions, and organismal physiology.

102 ng MAP kinase cascade signaling dynamics and cell fate decisions, and that signaling outcome can be m

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

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

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

106 Because aberrant cell fate decisions are at the heart of tissue degenerat

107 Cell fate decisions are controlled by the interplay of t

108 physiological consequences of these distinct cell fate decisions are discussed.

109 Cell fate decisions are fundamental to the development o

110 Cell fate decisions are governed by sequence-specific tr

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

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

113 n, but their joint functions in coordinating cell fate decisions are poorly understood.

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

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

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

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

118 pment, homeostasis, activation, and effector-cell fate decisions, as well as its important impacts on

119 that Cx43-GJIC is responsible for regulating cell fate decisions associated with appropriate joint fo

120 g on how BMP4 and Nodal signaling govern the cell-fate decisions associated with gastrulation.

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

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 indicate that NOG is a critical regulator of cell fate decisions between esophageal and pulmonary mor

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

127 portant cell biological regulators including cell fate decisions but are often ignored in human genet

128 lation regulate cellular differentiation and cell fate decisions, but how these changes affect erythr

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

130 sm may be responsible for the earliest T(FH) cell-fate decision, but a critical aspect of the TCR has

131 plex mTORC1 as a central regulator of T(H)17-cell fate decisions by coordinating metabolic and transc

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

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

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

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

136 ch RNA-binding protein HuR orchestrates Th17 cell fate decisions by posttranscriptionally regulating

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

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

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

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

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

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

143 Cell fate decision circuits must be variable enough for

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

145 of receptor tyrosine kinases (RTKs), crucial cell fate decisions depend on the duration and dynamics

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

147 Mechanisms of initial cell fate decisions differ among species.

148 rminant of BHC complex recruitment to enable cell fate decisions driven by GFI1B.

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

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

151 d site-specific demethylation, they regulate cell fate decisions during development and in embryonic

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

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

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

155 he Hedgehog (Hh) family of morphogens direct cell fate decisions during embryogenesis and signal to m

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

157 The first cell fate decisions during mammalian development establi

158 We tie cell-cycle progression with early cell fate decisions during neurogenesis, demonstrating t

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

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

161 s) provide a unique experimental platform of cell fate decisions during pre-implantation development,

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

163 utrient availability is integrated with stem cell fate decisions during tumour initiation.

164 hatidic acid regulates Notch-mediated binary cell-fate decisions during asymmetric cell divisions, an

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

166 erogeneity drives organ-scale patterning and cell-fate decisions during cardiac trabeculation in zebr

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 ng by the scaffold protein, PAG1, influences cell fate decisions following RTK activation.

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

172 Functionally vital cell fate decisions from a range of phenotypic choices a

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

174 of m(6)A for gene expression regulation and cell fate decisions has been well acknowledged in the pa

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

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

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

178 The speed at which a cell fate decision in nematode worms evolves is due to t

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

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

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

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

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

184 sults highlight how temperature can modulate cell fate decisions in an invertebrate model of stem cel

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

186 ption factor TCF-1 (Tcf7) regulates CD8(+) T cell fate decisions in double-positive (DP) thymocytes t

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

188 stem cell biology have enabled the study of cell fate decisions in early human development that are

189 ng plays key roles in tissue homeostasis and cell fate decisions in embryonic and post-embryonic deve

190 of ACD is therefore necessary to understand cell fate decisions in health and disease.

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

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

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

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

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

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

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

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

199 mming in the mammary gland, which can affect cell fate decisions in progenitor cell pools.

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

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

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

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

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

205 l use of PhysiBoSS, we studied heterogeneous cell fate decisions in response to TNF treatment.

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

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

208 he transcriptional repressor Blimp1 controls cell fate decisions in the developing embryo and adult t

209 lling cues regulate germ cell versus somatic cell fate decisions in the early posterior epiblast.

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

211 Cell fate decisions in the fly embryo are rapid: hunchba

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

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

214 chanism mediating inflammatory responses and cell fate decisions in various organs including the live

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

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

217 Compared with the third division, cell-fate decision in the second division requires a low

218 ein (SSDP) (ChiLS) complex controls numerous cell-fate decisions in animal cells, by mediating transc

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

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

221 ystem for studying the principles underlying cell-fate decisions in stem cells.

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

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

224 and external cues from the environment drive cell fate decisions. In budding yeast, the decision to e

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

226 tumor suppressor protein p53 is critical for cell fate decisions, including apoptosis, senescence, an

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

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

229 cal for understanding gene regulation during cell fate decisions, inflammation and stem cell heteroge

230 Cell fate decisions involved in vascular and hematopoiet

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

232 e molecular mechanisms that coordinate these cell fate decisions is an active area of investigation.

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

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

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

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

237 5 and 8 of development) promotes the first 2 cell fate decisions leading to increased differentiation

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

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

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

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

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

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

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

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

246 cell is initially specified in a stochastic cell fate decision mediated by Notch signaling.

247 Organ cell diversity depends on binary cell-fate decisions mediated by the Notch signalling pat

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

249 Our results suggest that the cell fate decision of the initial cell is determined in

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

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

252 tor of inflammation controlled hematopoietic cell fate decisions of HSCs.

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

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

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

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

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

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

259 r epigenetically primed or remodelled before cell-fate decisions, providing the molecular framework f

260 Mechanical cues have important roles in cell fate decisions regarding proliferation, survival, a

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

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

263 ical impact of GATA2 expression on human AML cell fate decisions remains ambiguous.

264 pite recent efforts, the nature of the early cell fate decisions remains contentious.

265 Cell divisions and cell-fate decisions require stringent regulation for pro

266 This cell fate decision requires the transcription factor Pro

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

268 ring lineage specification could affect stem cell fate decisions resulting in pathology.

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

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

271 on protein Connexin 43 (Cx43) contributes to cell fate decisions that determine the location of fin r

272 tarting point for the predictive modeling of cell fate decisions that include AKT1-driven senescence,

273 ns a multitude of developmental pathways and cell fate decisions that include MNT's ability to fortif

274 m Phospholipase D leads to defects in binary cell-fate decisions that are compatible with ectopic Not

275 A clear example is the series of binary cell-fate decisions that take place during asymmetric ce

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

277 the search for an early onset of the second cell-fate decision, the specification of the inner cell

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

279 undary between tendon and bone by regulating cell fate decisions through a mechanism that employs Not

280 ein (CBP) and beta-catenin, resulting in the cell fate decision to differentiate rather than prolifer

281 In stem cells, EtOH may shift cell fate decisions to alter developmental outcomes by i

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

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

284 m cells (ESCs) that balance self-renewal and cell-fate decisions to establish a protective barrier, w

285 hanistic paradigm for regulating live-or-die cell-fate decisions under stress conditions.

286 ctivation of innate responses and subsequent cell-fate decisions under stress conditions.

287 regulator of chaperones(1,2), is integral to cell-fate decisions underlying survival or death.

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

289 any of these functions ultimately impinge on cell fate decisions via apoptosis-dependent or -independ

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

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

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

293 s gene regulatory changes directing mesoderm cell fate decisions, which lead to the differentiation o

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

295 Disentangling the role of heterogeneity in cell fate decision will likely rely on the refined integ

296 derstanding of the contribution of mTOR to T-cell fate decisions will ultimately aid in the therapeut

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

298 bolites and dietary manipulations can impact cell fate decisions, with a focus on the regulation of a

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

300 ese more efficient schemes complete reliable cell fate decisions within the short embryological times