ライフサイエンスコーパス: cell fate

1 temperature change and genetic variation on cell fate.

2 n factor access to the genome and determines cell fate.

3 in B lymphocytes and maintains the adult B-2 cell fate.

4 oot hair cells to instead adopt the non-hair cell fate.

5 fferentially determine adult stem/progenitor cell fate.

6 ing as key mediators of metabolic control of cell fate.

7 re it regulates gene expression pertinent to cell fate.

8 e region with concomitant acquisition of RPE cell fate.

9 behavior, but do not affect proliferation or cell fate.

10 etic state of enhancers determines senescent cell fate.

11 ariety of cellular functions and can dictate cell fate.

12 C and MIZ1 form a module that regulates GC B cell fate.

13 d a primary mediator of its effects on liver cell fate.

14 egulates biochemical signaling and therefore cell fate.

15 Fbeta signaling in maintenance of the tendon cell fate.

16 he 'super-enhancers' that regulate mammalian cell fate.

17 tions for DNA repair fidelity and subsequent cell fate.

18 adhesion which ultimately help to determine cell fate.

19 thways are also important in regulating stem cell fate.

20 of unattached kinetochores, cell volume, and cell fate.

21 anscriptional networks that diversify neuron cell fate.

22 for temporally seamless tracing of transient cell fate.

23 function of RLP44: the control of procambial cell fate.

24 y affected lineage decision toward a cardiac cell fate.

25 partmentalized Src-kinase activity may drive cell fate.

26 signaling network that ultimately determines cell fate.

27 ress, adapt cellular physiology, and dictate cell fate.

28 ther lipids act to prevent this nonapoptotic cell fate.

29 ellular metabolism, organelle integrity, and cell fate.

30 ation of translational homeostasis regulates cell fate.

31 trolling the protein machinery that govern T cell fate.

32 t PRDM14 might be dispensable for human germ cell fate.

33 ch RA signaling directs pancreatic endocrine cell fate.

34 naling are interlinked and how they regulate cell fate.

35 ght to be important for maintaining germline cell fate.

36 promotes photoreceptor fate and VSX2 bipolar cell fate.

37 am regulatory programs determining different cell fates.

38 nding lymphocytes to generate a multitude of cell fates.

39 linked Flp/frt reporter to track individual cell fates.

40 ning cells linked to distinct differentiated cell fates.

41 at later stages and fails to acquire correct cell fates.

42 mechanisms that maintain these programs and cell fates.

43 ervasive epigenetic priming steers endocrine cell fates.

44 nerate complex patterns of binary and graded cell fates.

45 ell proliferation, differentiation, or other cell fates.

46 tiation toward neuronal and oligodendrocytic cell fates.

47 across three divisions to specify different cell fates.

48 that are necessary to reproduce the observed cell fates.

49 e an unprecedented opportunity to understand cell fates.

50 ing how cooperative signaling pathways drive cell fate acquisition.

51 into the processes of stem-cell function and cell-fate acquisition in the maize seedling and provide

52 Here, we report on the fastest evolving cell fate among vulva precursor cells in Caenorhabditis

53 Cell fate analysis showed a greater number of BrdU-label

54 and identify the molecular trajectories of B cell fate and ASC formation.

55 ls alveolar regeneration by controlling stem cell fate and behavior.

56 Crucial decisions involving cell fate and connectivity that shape the distinctive de

57 ed by all three receptors directly instructs cell fate and developmental progression.

58 hat encode transcription factors controlling cell fate and differentiation in many developmental and

59 ey regulatory histidine kinases that control cell fate and differentiation.

60 levels to orchestrate appropriate choices of cell fate and differentiation.

61 ing in germ cells is critical to maintaining cell fate and fertility.

62 r Six1 is essential for induction of sensory cell fate and formation of auditory sensory epithelium,

63 ates metabolic pathways as key regulators of cell fate and function.

64 prokaryotes and eukaryotes alike to control cell fate and generate cell diversity.

65 2 is a master regulator of Ly6C(hi) monocyte cell fate and inflammation in response to TLR signaling.

66 f how a system like NF-kappaB that regulates cell fate and inflammatory signalling in response to div

67 n response to environmental cues to regulate cell fate and maintain normal homeostasis.

68 whether and how TET2 regulates mammary stem cell fate and mammary tumorigenesis in vivo remains to b

69 alternative way for understanding transient cell fate and plasticity in biological processes.

70 Genetic lineage tracing unravels cell fate and plasticity in development, tissue homeosta

71 hylation is an epigenetic mark that dictates cell fate and response to stimuli.

72 anisms enabling these metabolites to control cell fate and review evidence that nutrient availability

73 at supports a role for the crosstalk between cell fate and tissue shape during early human embryogene

74 secting the basic mechanisms that coordinate cell fate and tissue shape will generate an integrated u

75 offer a window into the molecular biology of cell fate and tissue shape, mechanistic studies of our o

76 on plays an important role in governing stem cell fate and tumorigenesis.

77 How diverse cell fates and complex forms emerge and feed back to eac

78 We studied fetal germ-cell fates and discovered that both apoptosis and differ

79 connected regulatory networks that influence cell fates and lineage commitment.

80 ipulation of cellular DNA sequences to alter cell fates and organism traits, has the potential to bot

81 tial signaling is associated with particular cell fates and states, we generated a targeted mouse lin

82 govern LPM specification, organization, its cell fates and the inferred evolutionary trajectories of

83 and respond to external forces, influencing cell fate, and enabling new mechanistic studies.

84 ng many genes that are important for luminal cell fate, and supported the transcription of these gene

85 xpression changes that favour a premalignant cell fate, and, in an assay for nephrogenesis using muri

86 B cell and plasma cell fates are controlled by different transcriptional n

87 but links between specific dietary fats and cell fates are poorly understood.

88 To determine how OTX2+ cell fates are regulated in mice, we deleted Prdm1 and V

89 We hypothesize that POMC and NPY/AgRP cell fates are specified and maintained by distinct intr

90 Cell fate assays showed that multicolor flow cytometry a

91 age single-cell RNA sequencing analyses, and cell fate assays to chart basophil and mast cell differe

92 idge top (rdg), with expanded ventral neural cell fates at E10.5.

93 imately contribute to our ability to control cell fates at will.

94 pre-memory transcriptional reprogramming and cell-fate bias.

95 differentiation trajectories reveal an early cell fate bifurcation.

96 s a pivotal chromatin factor to control stem cell fate by modulating chromatin architecture and DNA d

97 erase SUV420H2 regulates embryonic stem (ES) cell fate by patterning the epigenetic landscape.

98 Second, we uncover changes in cell fate caused by transcription factor mutations.

99 h heterochromatin and gene repression during cell-fate change(5), whereas histone H3 lysine 4 (H3K4)

100 Here, we show that models of cell fate choice can, in homeostatic tissues, be categor

101 re we explore the idea that stochasticity of cell fate choice during tissue development could be harn

102 newal requires that different models of stem cell fate choice predict sufficiently different clonal s

103 e complex regulatory mechanisms that control cell fate choice.

104 omics has transformed our ability to examine cell fate choice.

105 ntral co-regulator of HRAS proliferation and cell fate choice.

106 is context, OTX2 functions to repress sister cell fate choices.

107 anics to generate complex forms and modulate cell-fate choices, and these multiscale regulatory inter

108 Cell fate commitment involves the progressive restrictio

109 tablish the first gene regulatory network of cell fate commitment that integrates temporal protein st

110 ic regulation of gene expression during stem cell fate commitment through the utilization of metaboli

111 ting gene expression, genomic stability, and cell fate commitment.

112 nderstanding of regulatory events leading to cell fate commitment.

113 evolving model of progressive restriction of cell fate competence through inherited transcriptional i

114 ived cells, preprogrammed towards a specific cell fate, contribute to fibro-fatty infiltration of sub

115 ory connection between stress conditions and cell fate control in plants.

116 elf-reinforced recruitment, derailing normal cell-fate control during development and leading to an o

117 Cell-fate conversion generally requires reprogramming ef

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

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

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

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

122 al commitment that orchestrates this crucial cell fate decision.

123 tical modeling to analyze transitions during cell fate decision.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

142 Cell fate decisions involved in vascular and hematopoiet

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

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

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

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

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

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

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

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

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

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

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

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

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

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

157 nduce changes in accessibility that underpin cell fate decisions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

172 Cell-fate-determinant molecule NUMB-interacting protein

173 a possible mechanism for biased delivery of cell fate determinants.

174 Cell fate determination requires faithful execution of g

175 Ddx3x as essential for hindbrain patterning, cell fate determination, and as a tumor suppressor gene

176 s in plant morphogenesis, hormone signaling, cell fate determination, nutrient deficiency, nitrogen m

177 rocesses, including embryo development, stem cell fate determination, trichome branching, leaf morpho

178 est that RAS-induced senescence represents a cell fate determination-like process characterised by a

179 ging from metabolism to redox homeostasis to cell fate determination.

180 utrient-triggered mitochondrial dynamics and cell fate determination.

181 ells, as well as its function in C. albicans cell fate determination.

182 h signaling is a cellular pathway regulating cell-fate determination and adult tissue homeostasis.

183 ine 27 (H3K27me3) regulates gene repression, cell-fate determination and differentiation.

184 ytic-independent role of DOT1L in modulating cell-fate determination and in transcriptional elongatio

185 st histone demethylase discovered, regulates cell-fate determination and is overexpressed in multiple

186 rfamily pathways, that are involved in their cell-fate determination from pre-specified embryonic for

187 T, provide the only phosphate source for the cell fate-determining transcription factor CtrA(9-18).

188 such as CD27, in the regulation of CD8(+) T cell fate during acute infection with lymphocytic chorio

189 anize tissue repair and the specification of cell fate during development.

190 beta-catenin/Wnt-dependent specification of cell fate during gastrulation illustrates the insights g

191 regulation has a profound influence on stem cell fate during normal development in maintenance of ph

192 Here, we show a transition of these two cell fates during aging of telomerase deficient zebrafis

193 Morphogen gradients specify cell fates during development, with a classic example be

194 play essential roles in determining distinct cell fates during the development of multicellular organ

195 sly in B and CD4(+) T cells to control their cell fate dynamics and thus, the character of the antibo

196 suggest a role for signal timing to minimize cell-fate errors, analogous to kinetic proofreading of s

197 work of mRNAs to control embryogenesis, stem cell fate, fertility and neurological functions in Droso

198 Studies of cell fate focus on specification, but little is known ab

199 ly relevant roles for FLIP(L) in determining cell fate following p53 activation.

200 MYC is transiently induced in cells fated for GC expansion and plasma cell (PC) format

201 ults in de facto p53 protein loss, switching cell fate from apoptosis toward mitosis.

202 liver cancer datasets show that most of the cell fate genes are perturbed by the differentially expr

203 r calculating the global impact of miRNAs on cell fate genes based on the shortest path.

204 owever, how apoptotic caspases regulate GC B cell fate has not been fully characterized.

205 sufficient specificity to control different cell fates has been a long-standing problem in developme

206 nt, yet how it precisely controls pancreatic cell fates has remained obscure.

207 is necessary for the specification of dorsal cell fate in a stage-dependent manner.

208 stem acts as an organizer that promotes stem cell fate in adjacent cells and patterns the surrounding

209 rval stage, leading to the retention of seam cell fate in both daughter cells.

210 nvestigates the mechanisms that control stem cell fate in development and disease.

211 le, pathogen-specific, antiinflammatory Th17 cell fate in human T cells in vitro.

212 lt stem cells, known as i-cells, to the germ cell fate in the clonal cnidarian Hydractinia symbiolong

213 map for further dissecting cis regulation of cell fate in the intestine.

214 and cancer, herein we investigated slan(+) -cell fate in tonsils by using a molecular-based approach

215 (Shh) signal transduction specifies ventral cell fates in the neural tube and is mediated by the Gli

216 iming of T cell help may affect follicular B cell fate, including death, survival, anergy, and recrui

217 crucial role in determining tissue-specific cell fate, including differentiation of B-cell lineages.

218 ions of tTreg, one in which the regulatory T cell fate is associated with unique properties of the TC

219 Our results indicate that the fetal germ-cell fate is based on discrete cell-heritable identities

220 It remains unclear how the meristematic cell fate is maintained.

221 e instructive signaling pathways controlling cell fate is poorly understood.

222 Cell fate maintenance is an integral part of plant cell

223 ell autonomous role for TGFbeta signaling in cell fate maintenance.

224 he control of cell cycle genes, and thus, in cell fate maintenance.

225 prevents the former from acting in vascular cell fate maintenance.

226 n could help elucidate determinants of fruit cell fate maintenance.

227 Here, we used in mice a cell fate mapping strategy based on reporter protein exp

228 Here, by combining multicolour 'Brainbow' cell-fate mapping and sequencing of immunoglobulin genes

229 In this study, we first construct a cell fate miRNA-gene regulatory network.

230 yeloid enhancers in a monocyte-to-macrophage cell fate model.

231 ther signaling pathways and regulates proper cell fates of mesenchymal progenitor cell populations.

232 lator of tissue growth, but can also control cell fate or tissue morphogenesis.

233 ilization of target programs shifts leukemia cell fate out of self-renewal into differentiation.

234 omatin lineage-priming and use it to predict cell fate outcomes.

235 Cell fate potential is programmed in tissue-specific con

236 Here we investigate B cell fate programming and heterogeneity during ASC diffe

237 s an inflammatory signature, and maintains B cell fate programming.

238 s in the control of dioxygenase activity and cell fate programs.

239 stem, we analyzed the relative importance of cell fate-promoting mechanisms versus negating fate-supp

240 P granule exit for two mRNAs coding for germ cell fate regulators.

241 This article presents a cell fate regulatory network model that contributes to u

242 ows that the top 20 miRNAs regulate multiple cell fate related function modules and interact tightly

243 ing proteins (RBPs) mediated control of stem cell fate remains to be defined.

244 mTEC subsets induce distinct autoreactive T cell fates remains unclear.

245 In this study, we find that the mouse tendon cell fate requires continuous maintenance in vivo and id

246 ring development to allow rapid yet accurate cell fate resolution.

247 similar competitive fitness collide, mutant cell fate reverts towards homeostasis, a constraint that

248 regulators for the onset of polarization and cell fate segregation in the mouse.

249 Embryonic cell fate specification and axis patterning requires int

250 e same transcription factors can function in cell fate specification and differentiated cell behavior

251 addition, we revealed a role for Neurog2 in cell fate specification and differentiation of ventromed

252 recocious polarization as well as subsequent cell fate specification and morphogenesis.

253 Notch signalling is required for T-cell fate specification and must be maintained throughou

254 ling pathways that control unique aspects of cell fate specification and tissue morphogenesis.

255 isms controlling hypothalamic patterning and cell fate specification are poorly understood.

256 The protein co-factor Ldb1 regulates cell fate specification by interacting with LIM-homeodom

257 Here, we report that this first cell fate specification event is controlled by glucose.

258 at tissue-level forces can directly regulate cell fate specification in early human development.

259 Developmental cell fate specification is a unidirectional process that

260 To determine whether prdm8 controls pMN cell fate specification, we used zebrafish as a model sy

261 ams, actively repressed by GSX2/DLX-mediated cell fate specification.

262 ivation by distal enhancers is essential for cell-fate specification and maintenance of cellular iden

263 duction and functions to canalize aspects of cell-fate specification, animal size regulation, and mol

264 ity and transcriptional networks controlling cell-fate specification.

265 ns interspersed in euchromatin that regulate cell fate specifiers.

266 epression of competing fate programs precede cell fate stabilization and final commitment.

267 Inhibition of CDK4/6 can result in different cell fates such as quiescence, senescence, or apoptosis.

268 production, and neurogenic vs. gliogenic BP cell fate, suggesting that Sox9 may have contributed to

269 egrees and this may sensitize cells toward a cell fate switch at increased temperature.

270 s a molecular explanation for root epidermal cell fate switch in response to ribosomal defects and, m

271 opic non-hair cells and determined that this cell fate switch is generally linked to defects in ribos

272 This glia-to-neuron cell fate switch occurs during male sexual maturation un

273 We discovered that this cell fate switch relied on MYB23, a MYB protein encoded

274 entity and the regulation of the neuron-glia cell fate switch.

275 re cases with marked chronic inflammation, a cell-fate switch from a transparent corneal epithelium t

276 ed differentiation correlated with a luminal cell fate that could be reversed by inhibition of PDGFR

277 o allocate antigen-dependent B- and CD4(+) T-cell fates that collaborate to control the quantity and

278 es the allocation of oligodendrocyte lineage cell fates.This article has an associated 'The people be

279 Diffusion pseudotime analysis revealed cell-fate trajectories among four different categories t

280 We observe bifurcating cell-fate trajectories as primordial lung progenitors di

281 e autoregulation, but did not cause hallmark cell fate transformations associated with loss of lin-12

282 gle-cell resolution may be adopted for other cell fate transition systems beyond EMT.

283 ADAR1 and its A-to-I editing activity during cell fate transitions and delineates a key regulatory la

284 The connection between cell fate transitions and metabolic shifts is gaining mo

285 Cell fate transitions are frequently accompanied by chan

286 Cell fate transitions are key to development and homeost

287 Stem and progenitor cell fate transitions constitute key decision points in

288 in changing the epigenetic landscape during cell fate transitions in early development.

289 uch mechanism and identify critical cues for cell fate transitions in the root SCN.

290 Together, this stepwise mapping to cell fate transitions shows how an inflammatory niche co

291 However, if not reprogrammed properly during cell fate transitions, it can also disrupt cellular iden

292 as subcellular changes) that accompany human cell fate transitions.

293 is allows us to identify genes that regulate cell-fate transitions and maintain the balance between r

294 ell behavior for up to four days and analyze cell fates utilizing a newly developed image-data analys

295 uced acquisition of an antiinflammatory Th17 cell fate was confirmed in vivo in an experimental autoi

296 cal transcription factor of mesenchymal stem cell fate, where its loss or loss of Wnt signaling diver

297 rough this process, replicative H3 maintains cell fate while, in contrast, the replacement H3.3 varia

298 proliferation, neurogenesis, migration, and cell fate, while in trimester three and early postnatall

299 at segregated EPH-EFN expression coordinates cell fate with compartmentalisation during early embryon

300 on stimulation, B cells assume heterogeneous cell fates, with only a fraction differentiating into an