ライフサイエンスコーパス: fate

1 and explored their sources and environmental fate.

2 icting these cells to a vascular endothelial fate.

3 rotransmitter identity and suppress the GABA fate.

4 emporally seamless tracing of transient cell fate.

5 ces impact mesenchymal progenitor cell (MPC) fate.

6 ion of RLP44: the control of procambial cell fate.

7 ected lineage decision toward a cardiac cell fate.

8 entalized Src-kinase activity may drive cell fate.

9 of targeting combine to determine substrate fate.

10 e both a pathogenic and an anti-inflammatory fate.

11 d no overt signs of shifting to an epidermal fate.

12 ling network that ultimately determines cell fate.

13 adapt cellular physiology, and dictate cell fate.

14 within the SVZ stem cell niche controls NSPC fate.

15 ar metabolism, organelle integrity, and cell fate.

16 lipids act to prevent this nonapoptotic cell fate.

17 of translational homeostasis regulates cell fate.

18 ing the protein machinery that govern T cell fate.

19 ltipotent NKX2-1(+) progenitors to lose lung fate.

20 M14 might be dispensable for human germ cell fate.

21 signaling directs pancreatic endocrine cell fate.

22 g are interlinked and how they regulate cell fate.

23 o be important for maintaining germline cell fate.

24 ration and determined the implications on SC fate.

25 tes photoreceptor fate and VSX2 bipolar cell fate.

26 omothorax (Hth), a negative regulator of eye fate.

27 dent activity on HSC asymmetric division and fate.

28 types with multiple possible differentiation fates.

29 erm while repressing alternative mesectoderm fates.

30 isplay increasingly restricted subpopulation fates.

31 nt parts of the organism taking on different fates.

32 izes, digestive tract targets, and metabolic fates.

33 s (RPBs) direct nascent proteins to distinct fates.

34 unprecedented opportunity to understand cell fates.

35 gulatory programs determining different cell fates.

36 mbled on protein substrates, modifying their fates.

37 he gene expression program of alternative Th fates.

38 e complex patterns of binary and graded cell fates.

39 individual naive T cells to adopt different fates.

40 tenin promotes mesodermal rather than neural fate(7), this ultimately leads to activation of mesoderm

41 Stochasticity strongly influences fate acquisition at the single cell level and results in

42 the processes of stem-cell function and cell-fate acquisition in the maize seedling and provide a val

43 ow cooperative signaling pathways drive cell fate acquisition.

44 hes a bipotential ovary and initiates female fate acquisition.

45 st dataset of sage-grouse nest locations and fates across wildfire-altered sagebrush ecosystems of th

46 he cellular basis of islet morphogenesis and fate allocation remain unclear.

47 ng environmental signals that guide vascular fate and assembly, thereby further informing our underst

48 ides providing a better understanding of the fate and behavior of typical marine microplastics, these

49 Crucial decisions involving cell fate and connectivity that shape the distinctive develop

50 tegories and polymer groups to determine the fate and danger of plastic contamination.

51 a dynamic process that depends on the cell's fate and developmental stage and that is adjusted for op

52 ncode transcription factors controlling cell fate and differentiation in many developmental and adult

53 tered scavenger community composition on the fate and efficiency of carrion removal within ecosystems

54 n germ cells is critical to maintaining cell fate and fertility.

55 However, the origin, fate and functions of PROM1(+) cells in AH and HCC are u

56 d by postmitotic ON SACs and promotes the ON fate and gene expression program while repressing the OF

57 revealed that dermal adipocytes alter their fate and generate ECM-producing myofibroblasts within wo

58 e of achieving a better understanding of the fate and impact of micro- and/or nanoplastics (MP/NP) on

59 ponse to environmental cues to regulate cell fate and maintain normal homeostasis.

60 tment plant, we determined the environmental fate and mass inventories of contact lenses in the Unite

61 unanswered questions about the environmental fate and metabolism of this herbicide; the genes and enz

62 eir release into the environment where their fate and persistence will be influenced by photochemical

63 rnative way for understanding transient cell fate and plasticity in biological processes.

64 ide valuable insights into the environmental fate and potential bioremediation strategies of these no

65 expression program while repressing the OFF fate and program.

66 ar serine is a critical determinant of EpdSC fate and provide insight into how nutrient availability

67 Reliable predictions of the environmental fate and risk of engineered nanomaterials (ENMs) require

68 ng the basic mechanisms that coordinate cell fate and tissue shape will generate an integrated unders

69 a window into the molecular biology of cell fate and tissue shape, mechanistic studies of our own de

70 effects of gold nanoparticles, such as their fate and toxicity, which remain challenging questions no

71 ment systems as well as their effects on the fate and transport of pollutants in natural and engineer

72 ays an important role in governing stem cell fate and tumorigenesis.

73 tion, such that PRDM1 promotes photoreceptor fate and VSX2 bipolar cell fate.

74 but also for repression of specific retinal fates and alternative gene regulatory networks.

75 would allow us to better predict population fates and design mitigation strategies.

76 cted regulatory networks that influence cell fates and lineage commitment.

77 signaling is associated with particular cell fates and states, we generated a targeted mouse line exp

78 can play a role in determining the ultimate fates and unique characteristics of distinctive subpopul

79 how mitochondrial metabolism determines HSC fate, and especially focus on the links between mitochon

80 sion changes that favour a premalignant cell fate, and, in an assay for nephrogenesis using murine ce

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

82 To determine how OTX2+ cell fates are regulated in mice, we deleted Prdm1 and Vsx2 o

83 We hypothesize that POMC and NPY/AgRP cell fates are specified and maintained by distinct intrinsic

84 homeostasis, but how these distinct cellular fates are triggered by environmental cues is poorly unde

85 Cell fate assays showed that multicolor flow cytometry and tr

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

87 rentiation trajectories reveal an early cell fate bifurcation.

88 chanisms controlling commitment to the sperm fate, but how this fate is subsequently executed remains

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

90 In metazoan tissues, cells decide their fates by sensing positional information provided by spec

91 erochromatin and gene repression during cell-fate change(5), whereas histone H3 lysine 4 (H3K4) trime

92 ing SC viability, fibronectin deposition, or fate change.

93 Combined, these fate changes suggest that photoreceptors are a default f

94 explore the idea that stochasticity of cell fate choice during tissue development could be harnessed

95 requires that different models of stem cell fate choice predict sufficiently different clonal statis

96 wn to govern progenitor proliferation and PC fate choice, and PGC1alpha, which we show controls PC ma

97 co-regulator of HRAS proliferation and cell fate choice.

98 le of 3D niche biomechanics in regulating SC fate choice.

99 has transformed our ability to examine cell fate choice.

100 at ultimately govern stiffness-dependent NSC fate commitment are not fully understood.

101 Cell fate commitment involves the progressive restriction of

102 tanding of regulatory events leading to cell fate commitment.

103 n serving as a potential early marker of ASC fate commitment.

104 gene expression, genomic stability, and cell fate commitment.

105 This ultimately induces osteogenic fate commitment.

106 many cellular mechanisms that regulate mRNA fate, covalent nucleotide modification has emerged as a

107 ir niche (niche exit) and control the binary fate decision (secretory vs enterocyte lineage) by repre

108 Compared with the third division, cell-fate decision in the second division requires a lower le

109 ansition of ISCs to progenitors and how this fate decision is established.

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

111 tem; however, its relationship with cellular fate decision remains an open question.

112 y dynamically important cell states, such as fate decision states in differentiation.

113 vide compelling evidence for early stage TRM fate decisions and the existence of committed TRM precur

114 t highlights their maturation, function, and fate decisions at homeostasis.

115 neity drives organ-scale patterning and cell-fate decisions during cardiac trabeculation in zebrafish

116 nt availability is integrated with stem cell fate decisions during tumour initiation.

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

118 (6)A for gene expression regulation and cell fate decisions has been well acknowledged in the past fe

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

120 sm mediating inflammatory responses and cell fate decisions in various organs including the liver.

121 Cell fate decisions involved in vascular and hematopoietic em

122 d from single naive precursors, we find that fate decisions made during the acute phase of murine CMV

123 spholipase D leads to defects in binary cell-fate decisions that are compatible with ectopic Notch ac

124 otein Connexin 43 (Cx43) contributes to cell fate decisions that determine the location of fin ray jo

125 multitude of developmental pathways and cell fate decisions that include MNT's ability to fortify or

126 opmental biology is to learn the sequence of fate decisions that leads to each mature cell type in a

127 anding of the contribution of mTOR to T-cell fate decisions will ultimately aid in the therapeutic ta

128 or understanding gene regulation during cell fate decisions, inflammation and stem cell heterogeneity

129 tion and discuss how this can impact on cell-fate decisions.

130 c hormone is shown to direct local stem cell fate decisions.

131 on to cell polarization, ACD and binary cell fate decisions.

132 sign and offer important insight into B cell fate decisions.

133 identical cells, that may acquire different fates depending on the feedback between SHR's availabili

134 ssible mechanism for biased delivery of cell fate determinants.

135 naling is a cellular pathway regulating cell-fate determination and adult tissue homeostasis.

136 stone demethylase discovered, regulates cell-fate determination and is overexpressed in multiple canc

137 novel role of ETBR in NPCs and mitochondrial fate determination in cerebral ischemia, and in improvin

138 o control cytoplasmic Cdc42 activity and HSC fate determination in vivo.

139 hat RAS-induced senescence represents a cell fate determination-like process characterised by a uniqu

140 targets of PNT participate in the posterior fate determination.

141 tem cell maintenance, niche interactions and fate determination.

142 rimary neuron trajectories, whereas temporal fate diversifies terminal elaborations.

143 lation has a profound influence on stem cell fate during normal development in maintenance of physiol

144 Here, we show a transition of these two cell fates during aging of telomerase deficient zebrafish.

145 and bone marrow-derived RMs (BMRMs), but the fate, dynamics, replenishment, functions and metabolic s

146 Cells lining the OF margin can maintain RPE fate ectopically and fail to transition from neuroepithe

147 of mRNAs to control embryogenesis, stem cell fate, fertility and neurological functions in Drosophila

148 MYC is transiently induced in cells fated for GC expansion and plasma cell (PC) formation, s

149 ever, ectopic DPP cannot rescue the anterior fate formation, suggesting additional targets of PNT par

150 r cancer datasets show that most of the cell fate genes are perturbed by the differentially expressed

151 Lineage identity plus Notch-mediated sister fate govern primary neuron trajectories, whereas tempora

152 r, how apoptotic caspases regulate GC B cell fate has not been fully characterized.

153 developmental progenitors presenting a fixed fate imbalance of self-renewing divisions with an ever-d

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

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

156 igates the mechanisms that control stem cell fate in development and disease.

157 listic assessment of nanoformulation shells' fate in soil and in the environment after release, as we

158 em cells, known as i-cells, to the germ cell fate in the clonal cnidarian Hydractinia symbiolongicarp

159 We present an overview of cyanotoxin fate in the environment, biological incorporation into S

160 wever, little is known about their long-term fate in the organism as it is generally admitted that th

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

162 of T cell help may affect follicular B cell fate, including death, survival, anergy, and recruitment

163 rturbations that drive cells toward specific fates, including several annotated in an existing scRNA-

164 ur results indicate that the fetal germ-cell fate is based on discrete cell-heritable identities.

165 tructive signaling pathways controlling cell fate is poorly understood.

166 g commitment to the sperm fate, but how this fate is subsequently executed remains less clear.

167 roducing motor neurons to OPCs with distinct fates is poorly understood.

168 tent of the disadvantages conferred by other fates is sufficient to account for the observed rate of

169 ld help elucidate determinants of fruit cell fate maintenance.

170 tor homolog of Blimp-1 in T cells (Hobit) to fate map the T(RM) progeny in secondary responses.

171 re, by combining multicolour 'Brainbow' cell-fate mapping and sequencing of immunoglobulin genes from

172 iated gene manipulation in microglia and for fate mapping of microglia but not CAMs.

173 Here, we used in mice a cell fate mapping strategy based on reporter protein expressi

174 hese topics are reviewed through the lens of fate mapping using genetically engineered mouse models a

175 cribe how this can be achieved using in situ fate mapping.

176 Here, we generated a genetic fate-mapping system for temporally seamless tracing of t

177 Using multiple fate-mapping systems, we show that snMacs do not derive

178 d enhancers in a monocyte-to-macrophage cell fate model.

179 ne and further develop current environmental fate models by integrating biological aspects, to improv

180 tes of antibiotics, suggesting that common e-fate models remain valid under varying salinity.

181 We analyzed substrate composition and fate of 216 P. unifilis nests along 88 km of rivers.

182 ronment exposed to antibiotics, however, the fate of a bacterial population depends on diverse factor

183 tion-reduction (redox) conditions impact the fate of a Green fluorescent protein (Gfp)-tagged AR plas

184 ver, we lack direct observation of the early fate of a horizontally transferred gene to prove this th

185 In this research, the fate of AA during roasting followed by drip brewed-like

186 ced sulfur (S) has a contrasting role in the fate of arsenic (As) in peatlands.

187 on and faunal change on the one hand and the fate of Australopithecus afarensis and the evolution of

188 crobial community functions like BGE and the fate of carbon in ecosystems.

189 ction of this scavenger guild influences the fate of carrion resources and efficiency of carrion remo

190 nd could possibly influence the dynamics and fate of cold subducting slabs.

191 h can be applied to assess the environmental fate of dsRNA biopesticides at concentrations relevant t

192 However, the fate of FFA diverges in these populations.

193 inhibitors and has influenced the metabolic fate of fluorinated compounds.

194 The fate of hematopoietic stem and progenitor cells (HSPC) i

195 matin are well documented in cancer, but the fate of higher-order chromosomal structure remains obscu

196 geochemical simulation model that traces the fate of individual carbon atoms as they interact with th

197 nomous metabolic mechanism that controls the fate of injured axons.

198 ined transcription factor(s) determining the fate of LTi progenitors versus non-LTi ILC progenitors.

199 t for parameterizing models that predict the fate of marine oil spills.

200 ber of other factors appear to influence the fate of mature B cells responding to antigen in vivo.

201 ed with their seasonal variations, drive the fate of metastable ENMs.

202 IFNs play a complex role in determining the fate of microbial pathogens and may also be deleterious

203 e that the spatial distribution and ultimate fate of microplastics are strongly controlled by near-be

204 ove accuracy in predicting the environmental fate of micropollutants.

205 Paired blood exchange tracked the fate of monocytes recruited to the injured kidney.

206 or of immune cell homeostasis by shaping the fate of myeloid and lymphoid cells.

207 The origin and fate of new mutations within species is the fundamental

208 spite these concerns, the concentrations and fate of NPAHs and OPAHs in the atmospheric environment a

209 l taxa and their activities that control the fate of oil spills.

210 The fate of organic micropollutants in host-parasite systems

211 als that a shared common structure links the fate of otherwise different types of memories together a

212 Despite decades of research on the fate of phenolic compounds when water is disinfected wit

213 Auxin determines the developmental fate of plant tissues, and local auxin concentration is

214 The fate of plastic waste is a pressing issue since it forms

215 To date, however, the fate of potentially toxic plastic additives has received

216 bundance, phenotype, functional capacity and fate of pre-existing and induced SARS-CoV-2-specific CD8

217 In addition, the fate of RO(2) produced from VOC oxidation can be kept re

218 The fate of scientific hypotheses often relies on the abilit

219 The subcellular fate of splicing variants AtUPS5L (long) and AtUPS5S (sh

220 ns with distinct linkages that can alter the fate of substrate proteins in unique ways.

221 hotspots is an important determinant of the fate of sulfur in the ocean.

222 r limitation to understanding the origin and fate of T cells in tumour immunity is the lack of quanti

223 In this study, we investigated the fate of the flame retardant hexabromocyclododecane (HBCD

224 udies) can be correlated to the pathological fate of the native fold; the low fold stability of the n

225 However, the role and fate of the oxide ligands in such intriguing additional

226 ity and new links in marine food webs to the fate of the plastics in the water column.

227 However, the fate of the recently described adaptive NK cell populati

228 rutiny, the concentration, chemical form and fate of the retained gadolinium species remain unknown.

229 ion (4%) of the climatic refugia of KMD, the fate of the species will be determined by the interplay

230 their special physical characteristics, the fate of the thermally treated nanomaterials may differ o

231 However, the composition and fate of the thousands of pollutants reaching the marine

232 teins (TPPs), understanding of the metabolic fate of TPPs is critical for their preclinical and clini

233 her of these substituents, the environmental fate of triclosan would be markedly different.

234 erature on the persistence and environmental fate of trifluralin with a focus on biodegradation pathw

235 m plays an important role in determining the fate of tumor cells.

236 ibosomal proteins, yet the cellular role and fate of ubiquitylated proteins remain unclear.

237 Our results suggest that the fate of Y. pestis infection of the lung is decided extre

238 sults of this study highlighted that (i) the fate of Zn in water-soil-plant compartments was similar,

239 The function and fate of Zta may be determined by the specific lysine res

240 hese activities is controlled to dictate the fates of cellular RNAs remains poorly understood.

241 tion in RNP granules differentially controls fates of mRNAs localized within the same cytoplasmic dom

242 the decision between endocrine and exocrine fates of multipotent progenitors in the developing pancr

243 lineage tracing experiments to determine the fates of peribiliary mesenchymal cells (PMCs) that surro

244 DEDD deadenylase TOE1 in distinguishing the fates of small nuclear (sn)RNAs of the spliceosome from

245 this functional dichotomy, the intracellular fates of two naturally occurring misfolded N-glycosylate

246 sic stability of the CA lattice in vitro and fates of viral core components in infected cells.

247 ng of individual cells revealed two distinct fates: one set of biofilm cells expanded ballistically o

248 ing molecular features that may inform their fate or function.

249 es suggest that photoreceptors are a default fate outcome in OTX2+ cells and that VSX2 must be presen

250 In order to assess their fate, possible transformations and ecotoxicology-essenti

251 We identified states of primed fate potential and located them on a continuous transcri

252 Cell fate potential is programmed in tissue-specific configur

253 dules and concurrent repression of competing fate programs precede cell fate stabilization and final

254 the control of dioxygenase activity and cell fate programs.

255 This article presents a cell fate regulatory network model that contributes to unders

256 hat the top 20 miRNAs regulate multiple cell fate related function modules and interact tightly based

257 al system, yet the pathways specifying these fates remain poorly defined.

258 roteins (RBPs) mediated control of stem cell fate remains to be defined.

259 subsets induce distinct autoreactive T cell fates remains unclear.

260 rmed soil carbonate minerals whose long-term fate requires assessment through field trials.

261 ient to promote a subcerebral or commissural fate, respectively.

262 In contrast, late-born V3 INs became fate-restricted to ventral laminae and displayed mostly

263 wnregulation of M1BP function suppresses eye fate resulting in a reduced eye or a "no-eye" phenotype.

264 It also suggests that the neuronal fate selector function of GATAs is modulated by their co

265 TA2 and GATA3 operate as serotonergic neuron fate selectors and regulate the differentiation of serot

266 on by distal enhancers is essential for cell-fate specification and maintenance of cellular identitie

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

268 rk for understanding early tracheoesophageal fate specification at the genome-wide level.

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

270 In contrast to paradigmatic models of fate specification in mostly motionless cell packings, t

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

272 in regulating human cortical neuron subtype fate specification, which is disrupted by a psychiatric-

273 nd transcriptional networks controlling cell-fate specification.

274 terspersed in euchromatin that regulate cell fate specifiers.

275 sion of competing fate programs precede cell fate stabilization and final commitment.

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

277 This glia-to-neuron cell fate switch occurs during male sexual maturation under t

278 tions revealed that the neurogenic/apoptotic fate switch was mediated through cell-cycle regulation b

279 osamine (O-GlcNAc), in NSCs promotes a glial fate switch.

280 e allocation of oligodendrocyte lineage cell fates.This article has an associated 'The people behind

281 We used sci-fate to study the cortisol response in >6,000 single cul

282 Fate tracking and transcriptome assessment in reporter m

283 ic stem cell (HSC) lineage and the data from fate tracking of EMP and HSC lineages indicated the poss

284 and its A-to-I editing activity during cell fate transitions and delineates a key regulatory layer u

285 The connection between cell fate transitions and metabolic shifts is gaining momentu

286 hanging the epigenetic landscape during cell fate transitions in early development.

287 echanism and identify critical cues for cell fate transitions in the root SCN.

288 derstand the cellular mechanisms controlling fate transitions.

289 y cellular process coupling cell division to fate transitions.

290 iry (H), which is needed to repress trichome fate, underlies variation in trichome patterns between a

291 elopment, cells gradually assume specialized fates via changes of transcriptional dynamics, sometimes

292 ivergent impact of estrogen on hepatobiliary fate was confirmed in a human hepatoblast cell line, ind

293 Using a new model to track neutrophil fates, we found short but variable lifetimes across mult

294 To better understand their fate when soil redox conditions change, that is, from fl

295 n be reprogrammed toward diverse lung cancer fates when exposed to the appropriate set of driver muta

296 ranscription factor of mesenchymal stem cell fate, where its loss or loss of Wnt signaling diverts di

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

298 iferation, neurogenesis, migration, and cell fate, while in trimester three and early postnatally (Ep

299 imulation, B cells assume heterogeneous cell fates, with only a fraction differentiating into antibod

300 ecruitment is thought to determine substrate fate, yet it has been generally assumed that all Hsp70 p