ライフサイエンスコーパス: quiescence

1 is essential for NSC reactivation (exit from quiescence).

2 ainly due to discontinuation after sustained quiescence.

3 tresses persist, cells favor a transition to quiescence.

4 processes when cells begin their entry into quiescence.

5 e between self-renewal, differentiation, and quiescence.

6 ritical functions of Hopx in maintaining HSC quiescence.

7 in untubulated atrial cells, despite Ca(2+) quiescence.

8 ion and degradation of mRNA to secure T cell quiescence.

9 is, which is critical for maintenance of HSC quiescence.

10 vide only four times to then enter permanent quiescence.

11 s, which jointly prevent the recovery of HSC quiescence.

12 istinct from mitogen removal and spontaneous quiescence.

13 uppresses neurogenic competence and restores quiescence.

14 cycle progression in vivo after cells leave quiescence.

15 ression of cell cycle-dependent genes during quiescence.

16 on factors but shared features of decreasing quiescence.

17 a protective, nondividing cellular state or quiescence.

18 rs-fMRI normalization is a biomarker for SOZ quiescence.

19 ting Ascl1 protein degradation and stem cell quiescence.

20 in compaction represses transcription during quiescence.

21 st of Tie2, a receptor that signals vascular quiescence.

22 veal region-specific regulation of stem cell quiescence.

23 signaling through JAK-STAT5 to maintain HFSC quiescence.

24 dentify the LSEC mediator that maintains HSC quiescence.

25 nt function in hematopoietic stem cell (HSC) quiescence.

26 signals and the Wnt antagonist sFRP5 induce quiescence.

27 arrest, while more ventral NSCs undergo G(2) quiescence.

28 that lack of Eng impairs reentry of HSCs to quiescence.

29 on, functions as a key regulator of cellular quiescence.

30 of reversible cell cycle arrest, also called quiescence.

31 activation, and the acquisition of metabolic quiescence.

32 ion stress increases over repeated rounds of quiescence.

33 -beta signaling to ensure maintenance of HSC quiescence.

34 bolically active, proliferative state toward quiescence.

35 fate specification and promote proliferative quiescence.

36 (ISC) proliferation and subsequent return to quiescence.

37 at the IME1 locus, those diploids can enter quiescence.

38 to biopsies during virological and clinical quiescence.

39 s pathways that mediate lymphocyte exit from quiescence.

40 ypoxia on CPC proliferation, also triggering quiescence.

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

42 ulation during the transition from growth to quiescence.

43 nt kinase inhibitors, by blocking entry into quiescence.

44 nhibition of cell proliferation to establish quiescence.

45 e kinase 1 (ALK-1) promotes endothelial cell quiescence.

46 undance is a crucial feature for maintaining quiescence.

47 regenerative potential while maintaining HSC quiescence.

48 2 (BTG1/2) as factors responsible for T cell quiescence.

49 function of adult LT-HSCs by promoting their quiescence.

50 mentin, NSCs have a reduced capacity to exit quiescence, a time when NSCs are required to clear a wav

51 he transcriptional dynamics of McSCs through quiescence, activation, and melanocyte maturation.

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

53 the Smad protein Mad, and for the return to quiescence after a regenerative episode.

54 molecular mechanisms that restore microglial quiescence after acute stimulation remain largely unexpl

55 survival during embryogenesis and exit from quiescence after hatching, although how they do so is un

56 ts of TNF to allow restoration of microglial quiescence after peripheral endotoxin challenge.

57 c protein) are known to regulate endothelial quiescence after secretion from the liver and right atri

58 tically significant differences in achieving quiescence after the switch.

59 ory T cells, directly and indirectly balance quiescence and activation programmes in conventional T c

60 ranscriptional regulators involved in T cell quiescence and activation, but recent findings highlight

61 The balance between stem cell quiescence and activity determines not only the rate of

62 t mice, and is accompanied by prolonged HFSC quiescence and by delayed entry and progression into the

63 ss, namely self-renewal, control of cellular quiescence and cellular senescence.

64 Wnt4 transitions SCs into a deeper state of quiescence and delays muscle repair.

65 ess into an intermediate stage that precedes quiescence and differentiation.

66 s switches fate, in that it rescues cellular quiescence and disrupts the ability to sporulate.

67 injury, muscle stem cells (MuSCs) exit from quiescence and divide to reconstitute the stem cell pool

68 e morphogenetic protein 9 (BMP9), a vascular quiescence and endothelial-protective factor, binds sENG

69 ry diseases, is characterized by episodes of quiescence and exacerbation (flares).

70 ic adaptations promote increased CD8(+) T(M) quiescence and fitness but also impart the reacquisition

71 ch posits that nontax revenue causes citizen quiescence and hampers government accountability.

72 findings demonstrate that HIC1 regulates MP quiescence and identifies MP subpopulations with transie

73 kpoints that actively maintain tolerance are quiescence and ignorance.

74 he chromosome interactions of yeast cells in quiescence and in exponential growth, and (ii) the brain

75 transcriptional programming to overcome HSC quiescence and increase differentiation and output of ma

76 HMGN1 overexpression is linked to decreased quiescence and increased HSC activity in bone marrow tra

77 d endothelial cells (ECs) regulates cellular quiescence and inflammation, we hypothesized that the di

78 checkpoint that maintains peripheral T cell quiescence and inhibits anti-tumor immune responses.

79 ur current understanding of neural stem cell quiescence and its regulation by intrinsic and systemic

80 5 to be required and sufficient to drive HSC quiescence and long-term self-renewal.

81 iopoietin and a key regulator of endothelial quiescence and maintenance of EC barrier function result

82 is critical for steady-state maintenance of quiescence and peripheral tolerance.

83 restraining lysosomal activity preserves HSC quiescence and potency and may be therapeutically releva

84 n or inhibition of p38 signaling rescued HSC quiescence and prevented DNA damage accumulation.

85 neural stem cells (NSCs) to transit between quiescence and proliferation is crucial for brain develo

86 ostasis, cells transition between cell cycle quiescence and proliferation.

87 oted zebrafish epithelial cells to exit from quiescence and re-enter the cell cycle.

88 et1 plays a critical role in maintaining the quiescence and reconstitution capacity of HSCs and that

89 accharides (cPOS) were found to both inhibit quiescence and reduce the population of persister cells

90 ally exploited to selectively reverse T-cell quiescence and reduce the size of the latent viral reser

91 ulates Bmi1-Cre(ER) cell survival, exit from quiescence and regenerative potential upon gamma radiati

92 ep-wake regulatory pathway induce behavioral quiescence and rest-activity arrhythmia, and facilitate

93 Zinc deficiency induces quiescence and resupply stimulates synchronized cell-cyc

94 tional mechanisms for the maintenance of NSC quiescence and reveal a role for Id4 as a quiescence-ind

95 This suggests a novel pathway to quiescence and reveals essential micronutrients play a r

96 fore, a critical checkpoint that governs HSC quiescence and self-renewal by Rheb-mediated restriction

97 we show that Foxm1 is required for survival, quiescence and self-renewal of MLL-AF9 (MA9)-transformed

98 g in the NEO1(+) fraction and association of quiescence and self-renewal-related transcription factor

99 or (HB-EGF) as the signal that maintains HSC quiescence and show that immature LSECs are unable to sh

100 During quiescence and slow wave sleep, bouts of synchronized ac

101 dy reveals a key mechanism underlying T cell quiescence and suggests that low mRNA abundance is a cru

102 NSC as a means of enhancing appropriate NSC quiescence and survival during transplantation into the

103 role in neural stem cell (NSC) maintenance, quiescence and survival.

104 ns of SGP wrapping that are critical for PGC quiescence and survival.

105 t advances in our understanding of stem cell quiescence and techniques enabling more refined analyses

106 ) are well-known activators of proliferative quiescence and terminal differentiation.

107 cription factors, as necessary for stem cell quiescence and thorn identity.

108 ntral nerve cord neuroblasts reactivate from quiescence and ventral nerve cord glia expand their memb

109 ation and to determine how LSECs promote HSC quiescence and why "capillarized LSECs" lose control of

110 st exist that rigorously preserve macrophage quiescence and yet, allow nimble pro-inflammatory macrop

111 tion, impaired hematopoietic stem cell (HSC) quiescence, and a poor prognosis for acute myeloid leuke

112 ted leukemogenesis as well as the abundance, quiescence, and activity of AML stem cells.

113 l role in mediating stem cell proliferation, quiescence, and differentiation.

114 el pathway, that antagonized MyD88-dependent quiescence, and engaged Weckle and Yorkie downstream.

115 ting its degradation, thereby preserving LSC quiescence, and promoting LSC self-renewal in MLL-rearra

116 l maintains a balance between proliferation, quiescence, and regeneration via interactions with the m

117 at the second larval stage due to cell cycle quiescence, and that relief of this block during the thi

118 The ability of these mutants to enter quiescence, and their long-term survival in the quiescen

119 These same signatures evaluated at clinical quiescence are correlated with disease activity in patie

120 Cell proliferation and quiescence are intimately coordinated during metazoan de

121 Cell cycle entry and quiescence are regulated by the E2F transcription factor

122 Our study identifies quiescence as a key feature of old NSCs imposed by the n

123 ivity that restricts cells from returning to quiescence as cells approach S phase.

124 potential reactivation after they return to quiescence as memory T cells.

125 tibular SCs in mammals transition to lasting quiescence as they develop massively thickened circumfer

126 1 enforces iNKT cellular and transcriptional quiescence associated with maturation and commitment to

127 its removal induces preosteoclast metabolic quiescence, associated with impaired tricarboxylic acid

128 e-specific deletion of the gene encoding the quiescence-associated factor HIC1 reveals additional pat

129 o estimate the incidence rate ratio (IRR) of quiescence between the 2 treatments.

130 tion of Plk1 in MuSCs does not perturb their quiescence but depletes activated MuSCs as they enter th

131 ying dysfunctional mitochondria can re-enter quiescence but fail to synchronize the transcriptional c

132 rapidly inactivate CDK4/6 to return cells to quiescence but with reduced probability as cells approac

133 Drosophila Hippo pathway maintains NSC quiescence, but its regulation during brain development

134 W303 haploids can enter quiescence, but their diploid counterparts cannot.

135 t norepinephrine signaling, HFSCs enter deep quiescence by down-regulating the cell cycle and metabol

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

137 e and tensin homolog (PTEN) pathway reversed quiescence by inducing cyclin-dependent kinase 2 (CDK2)

138 Quiescence characteristics in rest-activity rhythms were

139 , and its cell size did not become larger in quiescence compared to log phase, resulting in failure t

140 work is not repaired after HSC re-entry into quiescence, contrary to hematopoietic progenitors.

141 other cell, which controls the proliferation-quiescence decision in daughter cells and thereby couple

142 nic signals are converted into proliferation-quiescence decisions is poorly understood.

143 gression and lead to temporary developmental quiescence (diapause), exemplified by the dauer larva st

144 nderlicensing after cell cycle re-entry from quiescence distinguishes a higher-risk first cell cycle

145 hematopoietic stress, including loss of HSC quiescence, DNA damage accumulation in HSCs, and reduced

146 rug-exposed population enters into metabolic quiescence (dormancy) as persister forms.

147 ) determines whether NSCs enter G(0) or G(2) quiescence during embryogenesis.

148 We find that laminin also preserves PGC quiescence during embryogenesis.

149 critical roles in both maintaining Treg cell quiescence during homeostasis and regulating Treg suppre

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

151 Epcr-transduced Mpl(-/-) HSCs enter quiescence earlier after transplantation than control-tr

152 t EC and NSC co-encapsulation maintained NSC quiescence, enhanced NSC viability, and facilitated NSC

153 maintenance remains unknown, particularly at quiescence exit when HSCs must also dynamically shift me

154 unicate in a bidirectional manner to promote quiescence exit.

155 ggresomes to control NSC proteostasis during quiescence exit.

156 mediated oxidative phosphorylation in T cell quiescence exit.

157 eismometers in populated areas, this seismic quiescence extends for many kilometers radially and hund

158 etic protein 9) is a circulating endothelial quiescence factor with protective effects in pulmonary a

159 How microglia regain quiescence following challenges remains less understood.

160 Exit from quiescence following laminin depletion requires glp-1/No

161 ents modulate timing of HFSC activation from quiescence for proper tissue homeostasis of adult skin.

162 e in a state of reversible growth arrest, or quiescence, for prolonged periods of time.

163 As a key regulator of T-cell quiescence, FOXO1 promotes latency and suppresses produc

164 Quiescence (G0) is a transient, cell cycle-arrested stat

165 Although quiescence has long been viewed as a dormant, low-activi

166 matopoietic stem cell (HSC) self-renewal and quiescence; however, how these 2 seemingly opposing func

167 checkpoints throughout the life of a T cell: quiescence, ignorance, anergy, exhaustion, senescence an

168 stem cells face greater barriers to exiting quiescence, imposed by the niche through inflammation an

169 adverse event in 34 patients, and sustained quiescence in 25 patients.

170 and becomes uncoupled from glycolysis during quiescence in a Notch-dependent manner.

171 n, MIA and NGAL treatment increased cellular quiescence in both C4-2b and C4-2B4 PCa cells.

172 at Calvarial-CM treatment increased cellular quiescence in C4-2B4 PCa cells.

173 m has been optimized to measure activity and quiescence in Caenorhabditis larvae and adults and in Dr

174 Abrogating quiescence in dauer results in post-dauer sterility.

175 We discovered recently that NSCs undergo quiescence in either G(0) or G(2) in the Drosophila brai

176 protein, Mpt5 (Puf5), have parallel roles in quiescence in haploids.

177 we report that tamoxifen promotes mechanical quiescence in hepatic stellate cells (HSCs), stromal fib

178 l regulator of mitochondrial homeostasis and quiescence in iNKT cell development and effector lineage

179 The perturbation of quiescence in mice that lack Beclin 1 or FIP200 in myelo

180 Dormant M. tuberculosis induced quiescence in MSCs and promoted their long-term survival

181 The inhibition of FAO/OXPHOS also induces quiescence in naive human ESCs.

182 s, we captured the fast release of metabolic quiescence in organello and devised quantitative iodoace

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

184 s a critical switch from active sprouting to quiescence in part through phosphorylation of ATG16L1, w

185 al contractility via AMPK to promote uterine quiescence in pregnancy.

186 we also demonstrated that these cells induce quiescence in surrounding wild-type NSCs in a cell-cell

187 sting that HNF4alpha maintains proliferative quiescence in the liver, at least, in part, via repressi

188 techniques enabling more refined analyses of quiescence in vivo.

189 Consistent with this, S. carpocapsae IJ quiescence increased from 30 min to 24 h at <=20 degrees

190 -) HSCs exhibit enhanced mobility, decreased quiescence, increased apoptosis, and defective reconstit

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

192 In endocrine lineage cells, the cellular quiescence induced by short-term NEUROG3 expression requ

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

194 cription factors, which maintain and restore quiescence, induces Muller glia to proliferate and gener

195 SC quiescence and reveal a role for Id4 as a quiescence-inducing factor, in contrast with its role of

196 ature produces BMP4, a well-established HFSC quiescence-inducing factor, thus contributing to a proli

197 ound that transformed NSCs are refractory to quiescence-inducing signals.

198 formation but it is correlated with nucleus quiescence instead.

199 n of protein synthesis during the entry into quiescence is a consequence of the direct interaction of

200 Whether quiescence is a conserved protective response pathway in

201 Quiescence is a fundamental property that maintains hema

202 Quiescence is a hallmark of CD4(+) T cells latently infe

203 Increased neural stem cell (NSC) quiescence is a major determinant of age-related regener

204 Quiescence is a state of reversible proliferative arrest

205 Quiescence is a stress-resistant state in which cells re

206 Hematopoietic stem cell (HSC) quiescence is a tightly regulated process crucial for he

207 While reversing this quiescence is an effective approach to reactivate latent

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

209 Regulation of quiescence is critical for the maintenance of adult hema

210 Quiescence is essential for stem cell maintenance, and i

211 Quiescence is essential for the long-term maintenance of

212 The ability to enter quiescence is highly reproducible but shows broad natura

213 We further show that HSC quiescence is maintained by an abundance of large lysoso

214 adult stem cells but how stem cells maintain quiescence is poorly understood.

215 ease: besides regulating malignant stem cell quiescence, it promotes nuclear factor kappaB (NF-kappaB

216 actually activate its replicative phase from quiescence/latency.

217 nt, resulting in the disruption of stem cell quiescence maintenance and activation.

218 acts non-autonomously to control blast cell quiescence may be relevant to its function as a tumor su

219 f Gprasp1 or Gprasp2 increased the survival, quiescence, migration, niche retention, and hematopoieti

220 ion including Hif-1alpha, Hif-2alpha and HSC quiescence modulators.

221 After 53 years of quiescence, Mount Agung awoke in August 2017, with inten

222 T cell activation can cause disease, T cell quiescence must be preserved.

223 include expression of stress-response genes, quiescence, necrotrophy, and metabolic advantages obtain

224 ally, we demonstrate zinc deficiency-induced quiescence occurs independently of DNA-damage response p

225 the somatic gonad to maintain developmental quiescence of both SGBs and GSCs.

226 sinusoidal endothelial cells (LSECs) promote quiescence of hepatic stellate cells (HSCs).

227 ical characteristics related to stemness and quiescence of leukemic cells in acute myeloid leukemia (

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

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

230 Megakaryocytes promote quiescence of neighboring HSCs.

231 pend on coordinated activation and return to quiescence of resident muscle stem cells (MuSCs).

232 n due to reduced proliferation and increased quiescence of the cell cycle.

233 ghlights the roles of Hopx in maintenance of quiescence of the hematopoietic stem cells through CXCL1

234 t require DAF-2/insulin receptor or maintain quiescence of the nearby sex myoblasts, and developmenta

235 actors, promotes xylem identity and cellular quiescence of the organizer cells.

236 The signals maintaining quiescence of the reproductive endocrine axis during chi

237 The genes required for quiescence of tissue-resident macrophages are not well u

238 omponents ATG5, ATG16L1 or ATG7-in mediating quiescence of tissue-resident macrophages by limiting th

239 y, have a key function in maintaining immune quiescence of tissue-resident macrophages, resulting in

240 effects of Cxcl12 expression in maintaining quiescence of TKI-resistant LSC populations.

241 The primary outcome was quiescence of uveitis before and after the switch.

242 support abrupt entry of HSCs into permanent quiescence or sudden loss of regeneration potential afte

243 eighbors the HFSC activation zone during the quiescence phase (telogen).

244 CSP-alpha knockout mice, RGL stem cells lose quiescence postnatally and enter into a high-proliferati

245 MuSCs require ZEB1 to maintain their quiescence, prevent their premature activation following

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

247 ntiation and highlight that establishment of quiescence programs underlies iNKT cell development and

248 es have revealed how signals regulating cell quiescence, proliferation, and differentiation also indu

249 diminished expression of genes repressed by quiescence-promoting E2F4/DREAM complex.

250 tin production in adipose tissue, augmenting quiescence-promoting hematopoietic niche factors in lept

251 patients rapidly enter a state of behavioral quiescence proportionate to their illness severity with

252 is elegans quiescent behavior, post-response quiescence (PRQ), which is modulated by the C. elegans r

253 ies-specific gene networks controlling glial quiescence, reactivity, and neurogenesis.

254 ophila) offer insights into brain repair and quiescence regulation that are difficult to obtain using

255 ell cycle and metabolism while up-regulating quiescence regulators Foxp1 and Fgf18.

256 is of HSC gene expression suggested that the quiescence regulators were significantly up-regulated, s

257 rine agents and niche cells that maintain SC quiescence remain unknown.

258 ity state, increasing evidence suggests that quiescence represents states of poised potential and act

259 In addition, nlp-22-induced locomotion quiescence requires the receptor gnrr-6.

260 Preventing CENP-A deposition during quiescence results in significantly reduced CENP-A level

261 6 can result in different cell fates such as quiescence, senescence, or apoptosis.

262 cts in somatic gonad cells to produce a "pro-quiescence" signal (or signals) that acts inter se and b

263 hich in turn triggers reversible pluripotent quiescence specifically in the ground-state ESCs.

264 Using single-cell assays of HSC quiescence, stemness, differentiation potential, and epi

265 have emerged in the regulation of stem cell quiescence, survival, self-renewal, proliferation, senes

266 letion of Yap1 and Taz induces a loss of HSC quiescence, symmetric self-renewal ability, and renders

267 contributes to maintaining the proliferative quiescence that appears to underlie the permanence of se

268 y may be harnessed to overcome proliferative quiescence that limits regeneration in mammalian ears.

269 tected from full depletion by an increase in quiescence that makes old NSCs more resistant to regener

270 When a black hole emerges from quiescence (that is, it 'turns on' after accreting mater

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

272 cells that plays a critical role in vascular quiescence through its endothelial receptor activin rece

273 t4 produced by the muscle fiber maintains SC quiescence through RhoA.

274 omotes entry, maintenance, and recovery from quiescence through the Rlm1 transcription factor.

275 m cells (MuSCs) experience a transition from quiescence to activation that is required for regenerati

276 oceanica CCMP1779 during the transition from quiescence to autotrophy.

277 progenitor cells during the transition from quiescence to cellular activation with N-(4-hydroxypheny

278 ted upon EBV infection as naive B cells exit quiescence to enter a germinal center-like differentiati

279 On antigen stimulation, T cells exit quiescence to initiate clonal expansion and effector dif

280 Since the switchover from quiescence to reactivation provides a remarkable case of

281 In zebrafish and chick, the transition from quiescence to reactivity is essential for retinal regene

282 HSCs remain in quiescence to sustain their long-term self-renewal poten

283 The molecular basis for the neural stem cell quiescence-to-activation transition has become an import

284 In addition, RGL cells lose quiescence upon specific conditional targeting of CSP-al

285 The IRR for quiescence was 0.91 (95% confidence intervals [CI]: 0.7-

286 Mean number of injections to reach quiescence was 9+/-3 for pPDR in the high-risk character

287 N deprivation-induced quiescence was accompanied by a strong reorganization of

288 We found that metabolic quiescence was acquired at the follicular B cell stage i

289 Reduced HSC quiescence was confirmed in thalassemic patients, along

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

291 uality control is required for stem cells in quiescence when RNA content, protein synthesis, and meta

292 Many bacteria exist in a state of metabolic quiescence where energy consumption must be minimized so

293 es involved in the G2/M cycle and subsequent quiescence, whereas cells with large filopodia are relat

294 in response to tissue stresses, and promotes quiescence, whereas Igfbp5 preferentially labels a rapid

295 gnaling pathways: NLP-22 promotes behavioral quiescence, whereas NLP-2 promotes movement during letha

296 lipid, and purine metabolism, and inhibited quiescence, which explains the life span shortening.

297 Some wild diploids can only enter cellular quiescence, which indicates that there are conditions in

298 standing the programmes that regulate T cell quiescence will be key for developing novel approaches t

299 o do have flares after switching may achieve quiescence with increased biosimilar dosage.

300 cell-to-cell interactions balance stem cell quiescence with proliferation and direct neurogenesis in