ライフサイエンスコーパス: quiescence

1 to biopsies during virological and clinical quiescence.

2 ypoxia on CPC proliferation, also triggering quiescence.

3 mechanism for the control of cell death and quiescence.

4 lity food, C. elegans become sated and enter quiescence.

5 ural cells, thereby establishing endothelial quiescence.

6 inclusion was characterized by physiological quiescence.

7 ds to loss of the old hair without impairing quiescence.

8 gulate the balance between proliferation and quiescence.

9 enes in the SREBP-SCD pathway reduce satiety quiescence.

10 d hair follicle stem cells (HFSCs) during G0 quiescence.

11 ia and loss of hematopoietic stem cell (HSC) quiescence.

12 clude drug export, increased metabolism, and quiescence.

13 of the adult mouse hippocampus to return to quiescence.

14 ique measure of immune cell deactivation and quiescence.

15 decide whether to proliferate or to stay in quiescence.

16 art, attributed to rescue of age-related NSC quiescence.

17 agonized by SPRY1 to maintain satellite cell quiescence.

18 h is induced following maturation drying and quiescence.

19 s pathways that mediate lymphocyte exit from quiescence.

20 0 entry and are unable to maintain long-term quiescence.

21 nical Hippo signalling pathway maintains NSC quiescence.

22 or cyst formation following long periods of quiescence.

23 P) signaling, two key mechanisms that govern quiescence.

24 tection, defective repopulation, and loss of quiescence.

25 elegans as a model for facultative stem cell quiescence.

26 receptor would improve accumulation in tumor quiescence.

27 o extra cell divisions and delays entry into quiescence.

28 rotonin-releasing neurons induces behavioral quiescence.

29 as TGF-beta and IL-10 that promote neuronal quiescence.

30 sperse along an array of microtubules during quiescence.

31 role of PP2A in promoting the transition to quiescence.

32 ffect hematopoiesis, HSC maintenance, or HSC quiescence.

33 (CASP3) as a potential regulator of uterine quiescence.

34 ing--becomes dispensable under conditions of quiescence.

35 at normally restore haematopoietic stem-cell quiescence.

36 oA accumulation and reentry into growth from quiescence.

37 occurs during behavior and during periods of quiescence.

38 mammalian FEV/Pet1, controls satiety-induced quiescence.

39 onstitutively safeguards podocyte cell cycle quiescence.

40 ration, suggesting an inability to return to quiescence.

41 t of DREAM that cooperates with Rb to induce quiescence.

42 eurogenesis separated by a period of mitotic quiescence.

43 -complement mechanism for maintaining immune quiescence.

44 low transcriptional activity referred to as quiescence.

45 protein dynamics during proliferation versus quiescence.

46 ulation depends on the interval of signaling quiescence.

47 ulation of Cited2, a master regulator of LSC quiescence.

48 lternate between phases of cell division and quiescence.

49 ssing hair regeneration and maintaining HFSC quiescence.

50 nd box jellyfish [22, 23] exhibit periods of quiescence, a pre-requisite for sleep-like states, promp

51 n (N) deprivation, microalgae enter cellular quiescence, a reversible cell cycle arrest with drastic

52 edgehog pathway in actively maintaining this quiescence, a surprising turn of events given the pathwa

53 A proper balance among quiescence, activation and differentiation is essential

54 atellite cells are myogenic stem cells whose quiescence, activation, self-renewal, and differentiatio

55 anoma cells of origin, demonstrate that MCSC quiescence acts as a tumor suppressor, and identify the

56 (pre-BCR) expression and for reestablishing quiescence after pre-BCR-induced expansion.

57 ietic stem cells (HSCs), but how HSCs regain quiescence after stress is unclear.

58 A 5-10min period of quiescence allows for gravitational sedimentation of the

59 Further, we demonstrate that cell-cycle quiescence alters the genetic requirements for stem cell

60 They exhibit increased quiescence, an inability to enter the cell cycle in resp

61 ulate the timing of neuroblast proliferation/quiescence and a steroid hormone cue that is required fo

62 cessary and sufficient to maintain adult NSC quiescence and ablating them leads to NSC activation and

63 d how this single cell layer toggles between quiescence and activation to affect the development of s

64 nals from distal brain regions to govern NSC quiescence and activation.

65 rate inputs from multiple sources to balance quiescence and activation.

66 the bone marrow (BM) niche to maintain their quiescence and adapt blood production to the organism's

67 s causes failure of the cells to reestablish quiescence and allows premature activation.

68 ot undergo apoptosis in vivo; they return to quiescence and are recruited efficiently into humoural r

69 Maintaining quiescence and avoiding differentiation may be the ultim

70 int when cells lose the ability to return to quiescence and decide to progress through the cell cycle

71 erefore signals through CD44 to regulate NSC quiescence and differentiation, and HA accumulation in t

72 The status of long-term quiescence and dormancy guarantees the integrity of hema

73 ng alternative physiological states, such as quiescence and dormancy, and create a new view of the cy

74 The life cycle of a primary cilium begins in quiescence and ends prior to mitosis.

75 gulates cell cycle progression as cells exit quiescence and enter S-phase.

76 silencing WNT signaling, LCC cells can enter quiescence and evade innate immunity to remain latent fo

77 ic regulator of mammary epithelial stem cell quiescence and exhaustion and is necessary for long-term

78 Thus, we propose that Itpkb ensures HSC quiescence and function through limiting cytokine-induce

79 20-mediated inflammatory signals control HSC quiescence and functions.

80 luble guanylate cyclase promotes endothelial quiescence and governs vasomotor function and proportion

81 ains stem cell potency throughout hair cycle quiescence and growth, whereas paracrine Wnt inhibition

82 iche signals regulate neural stem cell (NSC) quiescence and growth.

83 y to the neurogenic niche in controlling NSC quiescence and hippocampal neurogenesis.

84 erefore, Rb proteins act as a central hub of quiescence and homeostasis by coordinating the regulatio

85 NA(hi) EVs promoted an escape from metabolic quiescence and HTR disease both in vitro and in vivo.

86 Furthermore, DR increased HSC quiescence and improved the maintenance of the repopulat

87 tic, although a few became stabilized during quiescence and in splicing mutants.

88 rotonin-releasing neurons induces behavioral quiescence and inhibits feeding and mating.

89 ator of HIV transcription, recapitulates the quiescence and latency phenotypes of hypothermia, sugges

90 pment of the vasculature, promoting vascular quiescence and long-term vessel stabilization through th

91 phatic vascular development by regulating EC quiescence and lymphatic EC fate.

92 Huwe1 to be essential for HSC self-renewal, quiescence and lymphoid-fate specification in mice.

93 Collectively, TSC2 maintains macrophage quiescence and prevents mTORC1-dependent granulomatous d

94 ovel pharmacologic avenue for regulating HSC quiescence and proliferation in response to Thpo.

95 K/AKT/MTOR signaling pathway, preserving LSC quiescence and promoting chemotherapy resistance.

96 normal rat astrocytes: CNS coculture caused quiescence and protection from methotrexate toxicity in

97 stent infections characterized by periods of quiescence and recurrent disease.

98 -deficient adult HSCs had markedly decreased quiescence and reduced cyclin-dependent kinase inhibitor

99 This is correlated with increased quiescence and reduced homing abilities of Ptk7-deficien

100 d rapid eye movement (REM), characterized by quiescence and reduced responsiveness to sensory stimuli

101 make polyP is important for survival during quiescence and resistance to diverse environmental stres

102 critical function of Pten in maintaining SC quiescence and reveal an interaction between Pten and No

103 ole for Foxm1 as a critical regulator of the quiescence and self-renewal of HSCs mediated at least in

104 port an important role for OBs in regulating quiescence and self-renewal of LTHSCs and a previously u

105 the H2 receptor on MB-HSCs to promote their quiescence and self-renewal.

106 Moreover, Sin3B inactivation impairs HSC quiescence and sensitizes mice to myelosuppressive thera

107 Microbial quiescence and slow growth are ubiquitous physiological

108 tuberculosis alternates between host-imposed quiescence and sporadic bouts of replication to complete

109 ing active, healthy mitochondria to maintain quiescence and stemness, and becomes increasingly necess

110 is characterized by alternations of network quiescence and stereotypical episodes of neuronal activi

111 r distinct vascular niches that regulate HSC quiescence and the supply of lineage-committed progenito

112 of Wnt is likely to contribute to stem cell quiescence and to explain the role of Hopx as a tumor su

113 thod, we identified a molecular signature of quiescence and used it to screen for factors that could

114 egulated by SPARCL1, which promotes the cell quiescence and vessel homeostasis contributing to the fa

115 have increased MyoD protein expression, exit quiescence, and begin proliferating.

116 f 40 kDa (PRAS40) inhibited mTORC1, promoted quiescence, and blocked tumor infiltration.

117 iting properties of self-renewal, cell cycle quiescence, and chemoresistance.

118 f cell fate choices, including self-renewal, quiescence, and differentiation into the many different

119 igher levels of warmth-liking, physiological quiescence, and less negative feelings even during socia

120 bryonic type II neuroblasts and INPs undergo quiescence, and produce embryonic-born progeny that cont

121 , adult hematopoietic stem cell survival and quiescence, and terminal maturation of select blood line

122 isms underlying the noisy process of exiting quiescence are poorly understood.

123 well as the relationship between bursts and quiescence, are still unclear.

124 associations increase at longer distances in quiescence as compared to growing cells.

125 sis, which were associated with induction of quiescence, as indicated by accumulation of cells in the

126 secutive days and nights revealed behavioral quiescence at night that is rapidly reversible, as well

127 6L1 and ZFP36L2 are critical for maintaining quiescence before precursor B cell receptor (pre-BCR) ex

128 0 ST, HPV16 E7 has the ability to override a quiescence block induced by mitogen deprivation.

129 is triggered upon entry into hypoxia-induced quiescence but facilitates subsequent cell cycle re-entr

130 onal organization of the yeast genome during quiescence by a chromosome capture technique as a means

131 Hematopoietic stem cells (HSCs) maintain quiescence by activating specific metabolic pathways, in

132 cells in non-cartilaginous airways maintain quiescence by activating the Hippo pathway and inhibitin

133 In turn, HIF-2alpha promotes MPhi quiescence by blocking a MARCO bacterial-response pathwa

134 Prolonged exit from quiescence by hematopoietic stem cells (HSCs) progressiv

135 scent ECs and functionally contributed to EC quiescence by inhibiting proliferation, migration, and s

136 ncing of select gene targets ensured uterine quiescence by preventing the decidua from expressing par

137 es enter a low-activity state of respiratory quiescence by remodeling the electron transport chain (E

138 anoids, Basak et al. (2017) induce stem cell quiescence by selective inhibition of EGF/MAPK signaling

139 at ETS-5 acts to promote roaming and inhibit quiescence by setting the internal "satiety quotient" th

140 erstand and monitor this state of alloimmune quiescence by transcriptional profiling may reveal a gen

141 As such, quiescence can be defined as a distinct state outside of

142 When deprived of nighttime quiescence, Cassiopea exhibited decreased activity and r

143 d that Cxcr4 desensitization is required for quiescence/cycling balance of murine short-term hematopo

144 us, daughter cells control the proliferation-quiescence decision by converting the memories of variab

145 acterize how p21 regulates the proliferation-quiescence decision to maintain genomic stability.

146 , suggesting the existence of a continuum of quiescence depths.

147 ed a group of miRNAs that are induced during quiescence despite markedly reduced expression of Export

148 c stem cells (HSCs), including self-renewal, quiescence, differentiation, and migration.

149 ing appears to be a key factor governing NSC quiescence, division, and fate.

150 n periods of sustained firing (UP state) and quiescence (DOWN state), a pattern the mechanisms of whi

151 rans-retinoic acid (ATRA), which induces PSC quiescence, down-regulates the ability of PSCs to mechan

152 of transcriptome and chromatin structure for quiescence driven by a highly conserved chromatin regula

153 under two conditions: developmentally timed quiescence (DTQ) occurs during larval transitions, and s

154 Feeding quiescence during DTQ results from a loss of pharyngeal

155 is implicated in the maintenance of uterine quiescence during pregnancy.

156 one marrow ECs regulated HSPC cell cycle and quiescence during regeneration.

157 ryngeal muscle excitability, whereas feeding quiescence during SIQ results from a loss of excitabilit

158 e stem cells can enter an extended period of quiescence during the resting phase but retain stem cell

159 uction and immediate division history before quiescence entry, and that such a memory is reflected in

160 tion and immediate division history prior to quiescence entry.

161 nd chromatin structure of S. cerevisiae upon quiescence entry.

162 hypercluster formation is not necessary for quiescence establishment, maintenance, and exit, raising

163 Deregulation of quiescence exit is associated with many diseases, but ce

164 Quiescence exit is highly noisy even for genetically ide

165 e the authors show that the heterogeneity of quiescence exit reflects a memory of preceding cell grow

166 Here we show that the heterogeneity of quiescence exit reflects a memory of preceding cell grow

167 mediated oxidative phosphorylation in T cell quiescence exit.

168 e switch, jointly and quantitatively explain quiescence-exit heterogeneity.

169 ding cell growth and division variations.The quiescence-exit process is noisy even in genetically ide

170 ontrolled in a cell autonomous manner, after quiescence extrinsic factors control the reactivation of

171 omologue, Tor as important regulators of GSC quiescence following exposure to ionizing radiation.

172 lochic fault during a long period of seismic quiescence, from 1450 to 1976 CE.

173 fully active and that the reported vascular quiescence function of BMP10 in vivo is due to the direc

174 terference (RNAi) as a major requirement for quiescence (G0 phase of the cell cycle) in Schizosacchar

175 Quiescence (G0) is a ubiquitous stress response through

176 during the most-recent period of basin-wide quiescence, hurricanes (and particularly major hurricane

177 such as miR-222/223, which in turn promotes quiescence in a subset of cancer cells and confers drug

178 tem and progenitor cell (HSPC) retention and quiescence in bone marrow.

179 lism identified an ACC necessary for satiety quiescence in C. elegans.

180 As in mammals, satiety signals induce quiescence in Caenorhabditis elegans Here we report that

181 ine jointly influence locomotor activity and quiescence in feeding and fasting hermaphrodites, and we

182 topoietic stem cell compartment and enhanced quiescence in hematopoietic stem and progenitor cells.

183 indicate that ERAS is important to maintain quiescence in HSCs.

184 rates with Nras(G12D/+) to promote increased quiescence in megakaryocyte-erythroid progenitors (MEPs)

185 stress compromises CPC function by inducing quiescence in part through downregulation of c-Myc.

186 f miRNAs and miRNA-processing factors during quiescence in primary human fibroblasts, we identified a

187 metabolite of vitamin A, restores mechanical quiescence in PSCs via a mechanism involving a retinoic

188 Conclusion Ischemia induces quiescence in surviving HCC cells, resulting in a depend

189 l cycle; cycling MB-HSCs fail to revert into quiescence in the absence of histamine feedback, leading

190 Here we demonstrate that quiescence in the adult lung is an actively maintained s

191 (ECM) is known to regulate neural stem cell quiescence in the adult subventricular zone (SVZ), the f

192 an active signaling mechanism that maintains quiescence in the airway epithelium.

193 erythrocytes also helps maintain neutrophil quiescence in the bloodstream.

194 n this alga to discern processes relevant to quiescence in the context of N deprivation and recovery

195 stimate of correlations between activity and quiescence in the framework of neuronal avalanches and w

196 re neuronal differentiation while preventing quiescence in the slowly dividing RGCs.

197 ted mechanism of E2F/DP action that promotes quiescence in this tissue.

198 Importantly, the mechanisms that regulate quiescence in tumor-initiating cells have not been analy

199 ntiation of premalignant cells and activates quiescence in tumor-initiating cells.

200 first response, whereas longer intervals of quiescence induce an enhanced second response.

201 We find that locomotion quiescence induced by DTQ- and SIQ-associated neuropepti

202 The biogenesis of these quiescence-induced miRNAs is independent of Exportin-5 a

203 Moreover, these quiescence-induced primary miRNAs (pri-miRNAs) are modif

204 eflects a memory of preceding cell growth at quiescence induction and immediate division history befo

205 eflects a memory of preceding cell growth at quiescence induction and immediate division history prio

206 During nitrogen-starvation-induced quiescence, inhibition of Sty1 converts non-growing, dep

207 and support the concept that pharmacological quiescence is a potentially highly effective and selecti

208 Recovering from N deprivation and quiescence is an active and orderly process as we are sh

209 This quiescence is characterized by a slowing of S phase, a b

210 The novel mutational landscape of quiescence is characterized by insertion/deletion (indel

211 SPCs exist in a quiescent state in vivo, and quiescence is correlated with latent infections in T cel

212 NR2F1-induced quiescence is dependent on SOX9, RARbeta and CDK inhibit

213 Quiescence is essential for long-term maintenance of adu

214 Quiescence is highly regulated to preserve stem cell fun

215 regeneration, it is not well understood how quiescence is maintained in organs such as the lung, whi

216 Quiescence is regulated by TGF-beta/SMAD signaling, whic

217 HSC behavior, such as self-renewal and quiescence, is regulated by a wide array of factors, inc

218 1943; Lea and Coulson, 1949), whereas during quiescence it will be expressed per unit of time.

219 ietic cellular transplantation during immune quiescence, it is unclear if prenatal tolerance becomes

220 FOXC1-deficient HFSCs spend less time in quiescence, leading to markedly shortened resting period

221 at Rb proteins, which are major enforcers of quiescence, maintain HSC homeostasis by positively regul

222 ochromatin formation at ribosomal DNA during quiescence maintenance.

223 Our approach for maintaining quiescence may be applicable to stem cells isolated from

224 amming, and that switching back to metabolic quiescence may help shield T cells from RICD as they tra

225 ntain mouse MuSC quiescence, thus defining a quiescence medium (QM).

226 a trithorax group gene network that controls quiescence, niche occupancy, and self-renewal potential

227 The quiescence of adult neural stem cells (NSCs) is regulate

228 nin activity determines the proliferation or quiescence of CRC cells based on the absence or presence

229 nt eye disease or rash 90 days or more after quiescence of disease was noted off therapy, and chronic

230 wing: an acute episode of HZO was defined as quiescence of disease within 90 days of initial presenta

231 H2AX deficiency also led to the loss of quiescence of hematopoietic stem and progenitor cells, w

232 is essential for maintaining the replicative quiescence of hematopoietic stem cells throughout life b

233 h factor 1 partially reverted the DR-induced quiescence of HSCs, whereas IL-6/IL-7 substitutions resc

234 ucing expression of FOXM1 also decreased the quiescence of human CD34(+) HSCs and progenitor cells, a

235 dapted to human cells similarly extended the quiescence of human MuSCs in vitro and enhanced their po

236 Exogenous ABA induces growth quiescence of lateral roots, which is prolonged by knock

237 /paracrine physiologic circuit that controls quiescence of MB-HSCs and hematopoietic progenitors mark

238 ough which myeloid bone marrow cells restore quiescence of myeloid-biased HSCs, with implications for

239 The equilibrium between proliferation and quiescence of myogenic progenitor and stem cells is tigh

240 HIV latency depends upon the transcriptional quiescence of the integrated provirus and the circumvent

241 Among 50 children observed to develop quiescence of uveitis under anti-TNFalpha, 39 met criter

242 L9 and PYL8 resulted in a longer ABA-induced quiescence on lateral root growth and a reduced sensitiv

243 for the majority of scenarios in a state of quiescence or homeostasis, evidence suggests that liver

244 ytic infection in a host cell or establishes quiescence or latency is influenced by events that occur

245 t Kras in Dclk1+ cells does not affect their quiescence or longevity.

246 g through the c-Mpl receptor promotes either quiescence or proliferation of hematopoietic stem cells

247 owth stabilized with increased propensity to quiescence, particularly with BEV.

248 escence, yet it has remained unclear whether quiescence plays a role in maintaining the stem cell fat

249 Although quiescence plays essential roles in cell survival and no

250 e of proliferative arrest known as "cellular quiescence" plays an important role in tissue homeostasi

251 eases proliferation on one side but promotes quiescence possibly by enhanced adhesion to the hematopo

252 Stem cell quiescence preserves the cell reservoir by minimizing ce

253 or, elevated HFSC methylation in vivo during quiescence prior to proliferation onset.

254 f seeds exhibit 'physiological dormancy' - a quiescence program initiated by either the embryo or the

255 e are quiescent and upon muscle injury, exit quiescence, proliferate to repair muscle tissue, and sel

256 he stem cell niche maintains a balance among quiescence, proliferation and regeneration of intestinal

257 These data suggest that the quiescence-proliferation transition involves global ampl

258 In nondividing yeast, a eukaryotic model of quiescence, proteasomes are depleted from the nucleus an

259 Upon exit from quiescence PSGs dissolve, and proteasomes are rapidly de

260 iscovered that all of these factors are HSPC quiescence regulators.

261 iesis, molecular mechanisms that control HSC quiescence remain largely unknown.

262 This quiescence represents a hallmark of the gametophyte-spor

263 terminal differentiation versus returning to quiescence (self-renewal) is crucial for tissue repair.

264 The homeostatic balance between quiescence, self-renewal, and differentiation of HSCs is

265 uring larval transitions, and stress-induced quiescence (SIQ) occurs in response to exposure to cellu

266 added to the plots; (b) P. corethrurus in a quiescence state in response to drought; (c) set-up of t

267 part, for telomere hypercluster formation in quiescence, suggesting that this process involves chromo

268 increase or decrease the longer cells are in quiescence, suggesting the existence of a continuum of q

269 regulator involved in maintenance of T cell quiescence, T cell subset differentiation, and memory T

270 (anagen), involution (catagen), and relative quiescence (telogen).

271 anagen), regression (catagen), and relative "quiescence" (telogen).

272 hen cells leave the division cycle and enter quiescence, telomeres gather into two to three hyperclus

273 Our findings suggest that during quiescence the canonical miRNA biogenesis pathway is dow

274 After several decades of quiescence, the disease re-emerged in Sonora and Baja Ca

275 When stem cells fail to return to quiescence, the proliferative stem cell pool becomes dep

276 For shorter intervals of signaling quiescence, the second response is blunted relative to t

277 In this study, we report that during quiescence, the unicellular haploid fission yeast accumu

278 ETC remodeling and mitochondrial respiratory quiescence through glycogen synthase kinase 3 (GSK3).

279 issues to promote developmentally controlled quiescence through the regulation of Cyclin E/Cdk2 activ

280 n for factors that could maintain mouse MuSC quiescence, thus defining a quiescence medium (QM).

281 ial in vivo, which they conserve by coupling quiescence to adhesion-mediated niche maintenance, there

282 pathways that accompany the transition from quiescence to proliferation and differentiation.

283 pathway and autophagy is essential to enter quiescence to survive extended periods of nutrient limit

284 C. elegans exhibits satiety quiescence under certain conditions that mimics many asp

285 kemia, is also essential for maintaining HSC quiescence under stress.

286 Cs are typically used sparingly and exist in quiescence unless activated for tissue growth.

287 anism used by hair follicle SCs to reinforce quiescence upon self-renewal and suggest a unique abilit

288 role for PP2A in promoting the transition to quiescence upon terminal differentiation in vivo.

289 Induction of quiescence was associated with a decrease in the express

290 y affect the likelihood of reactivation when quiescence was maintained for >/=1.5 years.

291 Skin hypomethylation during quiescence was necessary for subsequent progression of h

292 When we extended the study to 3 months of quiescence, we confirmed the replication-independent mut

293 at FOXO1 acts as a gatekeeper of endothelial quiescence, which decelerates metabolic activity by redu

294 toward glycolysis triggering their return to quiescence, while inhibition of LDH activity rescued AMP

295 foxo is required for entry in quiescence, while Tor is essential for cell cycle reentr

296 e that MSC-derived EVs prompt a loss of HSPC quiescence with concomitant expansion of murine myeloid

297 The mechanisms balancing HSC quiescence with expansion and differentiation into hemat

298 poietic stem cells (HSCs) are mostly kept in quiescence with only minor contribution to steady-state

299 t signalling couples hair follicle stem cell quiescence with reduced H3 K4/K9/K27me3 levels for prope

300 lt stem cells exist in a state of cell-cycle quiescence, yet it has remained unclear whether quiescen