ライフサイエンスコーパス: cell cycle

1 y (SPB) of budding yeast duplicates once per cell cycle.

2 tly incorporated in the mammalian genome per cell cycle.

3 nes were tightly linked to regulation of the cell cycle.

4 l metabolism, oxidative stress response, and cell cycle.

5 istones or histone PTMs in each stage of the cell cycle.

6 and subtle mass fluctuations throughout the cell cycle.

7 with cdk1 as the essential regulators of the cell cycle.

8 ation of gene transcription, DNA repair, and cell cycle.

9 overexpressed to study antiapoptosis and the cell cycle.

10 MP receptors and distinct modulations of the cell cycle.

11 molecule tracking in different phases of the cell cycle.

12 lated to B cell lineage, IL-7 signaling, and cell cycle.

13 s through regulation of the cytoskeleton and cell cycle.

14 n essential conserved role for DONSON in the cell cycle.

15 g factor of the unconventional P. falciparum cell cycle.

16 pend most of their life in interphase of the cell cycle.

17 ome organization and dynamics throughout the cell cycle.

18 litate passage to the succeding stage of the cell cycle.

19 early, mid, and late S phase of the mitotic cell cycle.

20 of gametocyte development in the subsequent cell cycle.

21 growth zone) display significantly different cell cycling.

22 P1 exhibit delays in growth of cell size and cell cycling.

23 erences in the cytokinin receptors mediating cell cycle activation in feeding sites induced by BCN an

24 tory protein that is itself inhibited by the cell-cycle activator, their interaction network presents

25 raction networks, composed of phase-specific cell-cycle activators and inhibitors.

26 However, the constitutive cell cycle activity of these niches remains to be charac

27 the majority of injury-induced cardiomyocyte cell cycle activity results in binucleation, not prolife

28 Stromal coculture did not prevent leukemia cell cycle activity, but a specific sensitivity profile

29 Precise control of the cell cycle allows for timely repair of genetic material

30 ining with anti-alpha-tubulin antibodies and cell cycle analysis indicated that tubulin and/or microt

31 nd break (DSB) repair pathway throughout the cell cycle and accounts for nearly all DSB repair outsid

32 nd 6 (CDK4/6) are fundamental drivers of the cell cycle and are required for the initiation and progr

33 and CDK6) regulate entry into S phase of the cell cycle and are validated targets for anticancer drug

34 b induces cells to enter the G0 phase of the cell cycle and become quiescent.

35 ls of dNTPs are tightly regulated during the cell cycle and depend on the balance between dNTP biosyn

36 genitor cells of the retina from exiting the cell cycle and differentiating.

37 LXCXE-mimic) predicted to interact with the cell cycle and differentiation regulator RETINOBLASTOMA-

38 preventing epithelial cells from exiting the cell cycle and entering a quiescent state.

39 Transcriptional targets include cell cycle and epigenetic regulators (e.g., Foxo3, Plk1,

40 genetic pathways, including cell signaling, cell cycle and immune evasion, in their development.

41 pathway delays cells in the G1 phase of the cell cycle and improves cell survival in response to gro

42 pair of the offending damage to complete the cell cycle and maintain cell survival.

43 and comprised gene clusters associated with cell cycle and mitosis and with the presence or absence

44 man FL-HCC, which included genes that affect cell cycle and mitosis regulation.

45 ation of gene expression, genomic stability, cell cycle and nuclear architecture.

46 Associated with these cell cycle and pro-apoptotic effects, we observed increa

47 This bacterium modulates the cell cycle and programed cell death, contributing to per

48 expressed in bone marrow ECs regulated HSPC cell cycle and quiescence during regeneration.

49 ve/cytotoxic effects upon Caco-2 cells (MTT, cell cycle and reactive oxygen species (ROS)) were evalu

50 is smaller pool of OPCs results from altered cell cycle and reduced cell proliferation.

51 led to cell accumulation in G1 phase of the cell cycle and reduced expression of cell cycle regulato

52 intimately linked to a dysregulation of the cell cycle and signalling pathways.

53 esults establish a critical role of TRIB1 in cell cycle and survival that is mediated via the modulat

54 hat phospholipid metabolism is linked to the cell cycle and that changes in membrane composition can

55 SK stem cell population exhibiting increased cell cycling and a myelomonocytic differentiation bias.

56 alysis identified miR-28 targets involved in cell-cycle and B-cell receptor signaling.

57 In striking contrast, the regulation of cell-cycle and differentiation gene programs by MEF2C wa

58 survival, and further observe alterations in cell-cycle and immune checkpoint regulation genes in pos

59 ion of pathways mediating energy metabolism, cell cycle, and B cell receptor signaling.

60 in, which has roles including NE reassembly, cell cycle, and chromatin organization in cells, and sub

61 to transcription factors, neurogenesis, the cell cycle, and neuronal differentiation, and m(6)A tagg

62 sites, which are targeted by Cdks during the cell cycle, and that calcineurin opposes Fus3 to activat

63 uxin export, both preceding the induction of cell cycle- and cytoplasmic growth-associated genes.

64 in various cellular processes, including the cell cycle, apoptosis, migration and invasion.

65 The mechanics of DNA replication and cell cycling are well-characterized in model organisms,

66 ecule-1, calbindin), followed by a marker of cell cycle arrest (urine insulin-like growth factor-bind

67 liferation and colony formation, and induced cell cycle arrest accompanied by increased expression of

68 esistant EOC cells through induction of G2/M cell cycle arrest and apoptotic cell death.

69 PSMB6, which together induces autophagy and cell cycle arrest and benefits virus replication.

70 reatment with this enzyme selectively causes cell cycle arrest and death in cancer cells due to deple

71 UV-induced PAF also activates cell cycle arrest and disrupts DNA repair, in part by in

72 upon glutamine deprivation, thus triggering cell cycle arrest and promoting cell survival.

73 NA damage in IGF-1R-negative cells caused G1 cell cycle arrest and S phase fork stalling.

74 kdown of FEN1 resulted in G1/S or G2/M phase cell cycle arrest and suppressed in vitro cellular proli

75 n and invasion as well as in vitro growth by cell cycle arrest at S phase with increased cell size an

76 iR-200a in metastatic melanoma cells induces cell cycle arrest by targeting CDK6 and decreases the le

77 enitor (GMP) cells, accompanied by increased cell cycle arrest in CMPs.

78 etinoblastoma tumour suppressor, inducing G1 cell cycle arrest in tumour cells.

79 tic silencing of S-phase genes and permanent cell cycle arrest or cellular senescence.

80 t the RR inhibitor 3-AP actively induces PEL cell cycle arrest through inhibiting the activity of the

81 th drugs were mediated by induction of G0/G1 cell cycle arrest through upregulation of p27 and downre

82 Cell cycle arrest was reversible at any point by exogeno

83 lgae enter cellular quiescence, a reversible cell cycle arrest with drastic changes in metabolism all

84 s DNA damage, checkpoint activation, S-phase cell cycle arrest, and cell death in sensitive breast ca

85 cancer cells by inducing both apoptosis and cell cycle arrest, and that reducing DHX33 levels throug

86 ed in multiple cellular responses, including cell cycle arrest, DNA repair, apoptosis, metabolism, au

87 However, PI3K inhibitors primarily induce cell cycle arrest, leaving a significant reservoir of tu

88 tates and later antagonizes TGFbeta-mediated cell cycle arrest, yet remains critical for the patholog

89 , HKL decreased CDK2 activity, leading to G1 cell cycle arrest.

90 tion fork, causing replicative stress and/or cell cycle arrest.

91 of tubulin polymerization, and induction of cell cycle arrest.

92 s of hUPF1 induces a DNA damage response and cell cycle arrest.

93 eads to suppression of protein synthesis and cell cycle arrest.

94 ing cell proliferation through initiation of cell cycle arrest.

95 ell proliferation/viability and by promoting cell-cycle arrest and apoptosis.

96 e latter mechanism involves p38-dependent G1 cell-cycle arrest and subsequent intrinsic mitochondrial

97 aled that CDK4/6 inhibition failed to induce cell-cycle arrest or senescence.

98 solid tumors, ABBV-075 triggers prominent G1 cell-cycle arrest without extensive apoptosis.

99 and inactivates CRLs and, in turn, triggers cell-cycle arrest, apoptosis, senescence and autophagy i

100 ed ATR-dependent phosphorylation of Chk1 and cell-cycle arrest, consistent with replication checkpoin

101 ional target genes that induce apoptosis and cell-cycle arrest.

102 these results establish circadian clock and cell cycle as interdependent coupled oscillators and ide

103 Ps) from categories including metabolism and cell cycle, as well as RNA- and protein-modifying enzyme

104 We reveal inducible changes in expression of cell cycle-associated proteins including MCM2 and cyclin

105 Crucially, abolishing cell cycle asynchrony consistently disrupted the spindle

106 ts demonstrate how an evolutionary conserved cell cycle asynchrony maintains the invariant cleavage p

107 Foci form soon after cells exit the cell cycle, before other hallmarks of senescence appear.

108 e propose that microRNA-200a functions as a "cell cycle brake" that is lost during melanoma progressi

109 tion is inhibited during the G1 phase of the cell cycle, but both pathways are active in the S and G2

110 Although mitotic cell cycles can take place in the absence of centrosomes

111 ability of ATR inhibition to abrogate the G2 cell cycle checkpoint both contributed to the synergisti

112 We showed here that E7 abrogated the G1 cell cycle checkpoint under hypoxia and analyzed key cel

113 igger a characteristic 'VSG synthesis block' cell-cycle checkpoint, as some cells reinitiated S phase

114 ys that maintain genomic stability including cell cycle checkpoints, DNA repair, protein ubiquitinati

115 n actionable dependence on ATR/CHK1-mediated cell cycle checkpoints.

116 pt and irreversible nature of three specific cell-cycle checkpoints.

117 vealed upregulation of genes associated with cell cycle, chromatin, cytoskeleton/motility, immunity,

118 bitor p21 that almost exclusively determines cell-cycle commitment in daughter cells.

119 d recovery from anemic stress and persistent cell cycling consistent with a role for KLF3 in dampenin

120 ced proliferative fitness and stably rewired cell cycle control pathways.

121 s regulating diverse cellular processes from cell cycle control to developmental fate, deregulation o

122 tumour suppressor gene), CDC14B (involved in cell cycle control) and NTRK3 (tyrosine receptor kinase

123 ss, impaired checkpoint signaling, defective cell cycle control, and genomic instability, which was r

124 ppression of DNA damage signaling is key for cell-cycle control and needed for normal development.

125 Loss of cell-cycle control is a hallmark of human cancer.

126 rough suppression of the transcriptional and cell cycle defects was observed upon depletion of the ce

127 n genes, whose downregulation coincides with cell cycle defects, senescence and/or apoptosis.

128 its retinal differentiation independently of cell-cycle defects.

129 le progression in human cells, and it causes cell-cycle deficits of radial glial cells in the embryon

130 Here, we investigate size control and the cell cycle dependence of bacterial growth using multigen

131 flammatory response following DNA damage are cell-cycle dependent.

132 Cell cycle-dependent formation and activation of this tr

133 and opens up tremendous scope for analysing cell cycle dynamics and developing interventions targett

134 e fungal pathogen Candida albicans to couple cell cycle dynamics with responses to cell wall stress i

135 Mechanisms that control cell-cycle dynamics during tissue regeneration require e

136 Unbalancing epicardial cell-cycle dynamics with chemical modulators indicated a

137 roach can be extended to other models of the cell cycle engine and other biomolecular networks.

138 re report that SOCE and calcineurin regulate cell cycle entry of quiescent T cells by controlling gly

139 n activity by inhibiting differentiation and cell cycle entry.

140 In normal cells, Ki-67 was a late marker of cell-cycle entry; Ki-67 mRNA oscillated with highest lev

141 ns how these larger fluctuations in archaeal cell cycle events contribute to cell size variability an

142 fication that can be used to fine-tune these cell cycle events, frequently through processes that do

143 Senescence is a state of stable cell cycle exit with important implications for developm

144 rospero accumulation that, in turn, promotes cell cycle exit.

145 ing this approach, we found that Gsx2 delays cell-cycle exit and reduces Pax6 expression, whereas Ebf

146 Further cell cycle fingerprint analysis and 3D chemical structur

147 maciclib combination led to more significant cell cycle G0/G1 arrest of tumor cells.

148 D1 is essential for H3K9me2 demethylation at cell cycle gene loci.

149 n neuronal gene expression and a decrease in cell-cycle gene expression.

150 , including WNT/beta-catenin alterations and cell-cycle-gene (CDK4 and CDK6) mutations.

151 with loss of chromatin accessibility around cell cycle genes during postnatal maturation.

152 Finally, we showed that histone and cell cycle genes in general are exempt from Rtt109-depen

153 ost likely via transcriptional repression of cell cycle genes in response to stress.

154 ne expression studies point to regulation of cell cycle genes, muscle myosins, NotchR and Wnt pathway

155 inger (ZF) transcriptional regulator of many cell cycle genes.

156 MOS1 and TCP15 both affect the expression of cell-cycle genes D-type CYCLIN 3;1 (CYCD3;1), which may

157 By mapping the cell cycle in detail, we show that directly after replic

158 ow cytometry indicated that cells exited the cell cycle in the same manner.

159 ssociated with cell death and impacts on the cell cycle in three dinoflagellate species (Prorocentrum

160 nd interferon (IFN) pathways, which enforced cell cycling in quiescent HSPCs, resulting in their apop

161 promoter among G1 and G2/M cells, suggesting cell cycle-independent origin of cell-to-cell variation

162 Using cell cycle indexes that measure changes in cell cycle pr

163 KLF2 transcription factor or the CDKN1B/p27 cell cycle inhibitor are recurrent in 16% of patients wi

164 ssion studies revealed that induction of the cell cycle inhibitor Cdkn1a was responsible for the decr

165 e defects was observed upon depletion of the cell cycle inhibitor p21.

166 FOXP3 is also a cell-cycle inhibitor and onco-suppressor in different ce

167 in Arabidopsis by directly upregulating the cell-cycle inhibitor KRP2 in the underlying rib meristem

168 d show that the response is inhibited by the cell-cycle inhibitor p21(Cip).

169 ized in part by expression of the p16(INK4a) cell-cycle inhibitor.

170 least partially through upregulation of the cell cycle inhibitors Cdkn1a and Cdkn2c.

171 ed by the transcriptional stimulation of the cell-cycle inhibitory protein p21(Waf1/Cip1) Consistentl

172 Early cell cycle initiation in hepatocytes after GSK3 inhibiti

173 for regulating PD-L1 protein stability by a cell cycle kinase and reveals the potential for using co

174 , the total numbers of type 1 node proteins (cell cycle kinases Cdr1p, Cdr2p, Wee1p, and anillin Mid1

175 al, but whereas inhibitors of chaperones and cell cycle kinases induce similar transcriptional change

176 Viability and cell cycle kinetics were measured by using flow cytometr

177 This could be traced back to disrupted cell-cycle kinetics and a premature shift to asymmetric

178 naling genes and down-regulation of the G2/M cell-cycle marker gene, CYCB1;1 TCP20 and NLP6&7 also su

179 by mitogens and accompanied by induction of cell-cycle markers, including phosphorylation of the ret

180 cues, which overall entails a modulation of cell cycle, meiosis-related and nutrient transporter gen

181 ssifier, including those involved in mitotic cell cycle, microtubule organization, and chromosome seg

182 ingle-cell microscopy to parameterize a full cell-cycle model based on independent control of pre- an

183 3;1), which may mediate the MOS1 function in cell-cycle modulation.

184 9f caused arrest of cell cycle of MCF-7 and HL-60 cells at G0/G1 phase.

185 a neural progenitor cell (NPC) reenters the cell cycle or exits and differentiates are pivotal for g

186 y, speed and robustness of the fission yeast cell cycle oscillations.

187 inogenic role of NOTCH in vivo Alteration of cell cycle pathways was seen in murine renal tubular cel

188 ase, vascular endothelial growth factor, and cell cycle pathways, whereas esophageal squamous tumors

189 embryos fail to initiate timely MZT, undergo cell-cycle pause, and remain developmentally delayed thr

190 hile protein levels increased throughout the cell cycle, peaking in mitosis.

191 ndependent regulation of pre- and post-Start cell-cycle periods rather than the consequence of an und

192 n independent control of pre- and post-Start cell-cycle periods.

193 th a high proportion of cells in a quiescent cell cycle phase as assessed in wounds, tumors, and aort

194 us, photosynthetic and respiratory capacity, cell-cycle phase, and environmental condition.

195 In both G1 and G2 cell cycle phases, the 2-4% of alpha-satellite assembled

196 Cdk8 reported here did not cause any obvious cell cycle phenotypes.

197 Cell-cycle phosphorylation is temporally ordered, at lea

198 Unexpectedly, in the rapid cell cycles preceding the midblastula transition, a defi

199 least in part, to reversible pausing of the cell cycle preventing S phase associated DNA damage.

200 throughout life and has downstream impact on cell cycle processes.

201 g cell cycle indexes that measure changes in cell cycle profile patterns upon chemical perturbation,

202 proof-of-principle, we conducted large-scale cell cycle profiling of 884 FDA-approved drugs.

203 l outcomes have been attributed to increased cell cycle progression and the development of genomic in

204 cells from nucleolar stress, thus promoting cell cycle progression and tumorigenesis.

205 Furthermore, we show that growth and cell cycle progression are arrested in cells infected wi

206 cyclin-dependent kinase 2 (CDK2), regulates cell cycle progression as cells exit quiescence and ente

207 the CaMKK-like protein kinase Ssp1 promotes cell cycle progression by activating the ARK Cdr2 accord

208 t kinase (CDK) inhibitor p27, which inhibits cell cycle progression by binding cyclin A- and cyclin E

209 ular phenotype was observed while monitoring cell cycle progression in cells lacking MCPH1 function.

210 Cell cycle progression in mammals is strictly controlled

211 the dynamics of chromosome condensation and cell cycle progression in MCPH1 deficient cells under un

212 This study reveals effects of cell cycle progression on the expression of lineage spec

213 s an indirect regulator of transcription and cell cycle progression through the regulation of specifi

214 GH3 cell proliferation through induction of cell cycle progression via activation of the Akt-GSK-3be

215 that mechanisms regulating mRNA translation, cell cycle progression, and gene expression differ from

216 ny formation, elicited S phase arrest during cell cycle progression, and induced both intrinsic and e

217 scription factor FoxM1 plays a vital role in cell cycle progression, is activated in numerous human m

218 d cilia and is important for cell signaling, cell cycle progression, polarity, and motility.

219 letal metabolism, intracellular trafficking, cell cycle progression, repair/maintenance, bioenergetic

220 cation, telomere maintenance and elongation, cell cycle progression, signal transduction and cell pro

221 s known about how NAP activity is coupled to cell cycle progression.

222 ated by Ipl1/Aurora B phosphorylation during cell cycle progression.

223 s of cancer, and its down-regulation impairs cell cycle progression.

224 ays critical roles in signaling pathways and cell cycle progression.

225 es to transiently suppress DNA synthesis and cell cycle progression.

226 rease in the doubling time and impairment of cell cycle progression.

227 criptional blockade of genes associated with cell cycle progression.

228 , suggesting intrinsic circadian patterns of cell cycle progression.

229 unctions non-cell-autonomously to facilitate cell-cycle progression and stem cell proliferation.

230 tein 3 (IGFBP3), and that this regulates SCC cell-cycle progression and tumor growth in vivo Furtherm

231 prolongs mitotic length and interferes with cell-cycle progression in human cells, and it causes cel

232 Instead, we showed that mycobacterial cell-cycle progression is regulated by an unprecedented

233 to DZ proliferation rather than for allowing cell-cycle progression itself and must be regulated dyna

234 chanisms of PI3Kalpha and CDK4/6 blockade on cell-cycle progression, DNA damage response, and immune-

235 oss of pigmentation, and melanoblasts showed cell-cycle progression, migration, and cytokinesis defec

236 processes, including cytoskeletal dynamics, cell-cycle progression, signal transduction, gene expres

237 king nitrate assimilation and signaling with cell-cycle progression.

238 s are necessary for kinetochore assembly and cell-cycle progression.

239 d reveals insights into the requirements for cell-cycle progression.

240 nal regulation, cellular growth control, and cell-cycle progression.

241 in ligation, and increased the expression of cell cycle-promoting cyclin proteins, without enhancing

242 miRNA family causes derepression of multiple cell cycle-promoting proteins, thereby preventing epithe

243 SP-7, DFF-45, NPM, YWHAZ, Src, PAX2, MAPK8), cell cycle promotion and cancer progression (CDK1, CDK2,

244 a potential pathway involved, expression of cell cycle proteins was assessed.

245 et MDSC population via downstream effects on cell cycle proteins.

246 facilitate robust and long-term depletion of cell-cycle proteins and reveals insights into the requir

247 human microRNAs (miRNAs) directly regulating cell-cycle proteins.

248 ng the signature are likely regulated by the cell cycle rather than by TGFbeta.

249 nduced quiescence but facilitates subsequent cell cycle re-entry.

250 Nuf exhibits a cell cycle-regulated concentration at the centrosome tha

251 Mcl-1 was cell cycle-regulated during HR, with its expression peak

252 ng Xenopus egg extract, we show that direct, cell-cycle-regulated binding of M18BP1 to CENP-A nucleos

253 of Fun30 to DSBs is sufficient to bypass the cell cycle regulation of long-range resection, indicatin

254 onverge on aspects of cell proliferation and cell cycle regulation, including DNA synthesis (NPAT), D

255 Furthermore, one pathway that is involved in cell cycle regulation, REACTOME_CHROMOSOME _MAINTENANCE,

256 y involved in diverse biological signals and cell-cycle regulation although further replication in a

257 Thus, Ki-67 expression varies due to cell-cycle regulation, but it remains a reliable readout

258 ates at specific enhancer regions of the key cell cycle regulator Cdkn1a and the stem cell regulator

259 lerosis through, at least in part, targeting cell cycle regulator cyclin A and connective tissue grow

260 Vasculature proliferation also involves the cell cycle regulator KIP-RELATED PROTEIN2 and ABERRANT L

261 Here we show that CYREN (cell cycle regulator of NHEJ) is a cell-cycle-specific i

262 th an increased expression of p21cip1/waf, a cell cycle regulator that is involved in the differentia

263 Here, we show that the cell cycle regulator, cyclin-dependent kinase 2 (CDK2),

264 KDM5-activated genes include a large set of cell cycle regulators and that the KDM5s are necessary f

265 of the cell cycle and reduced expression of cell cycle regulators during the initiation stage of rep

266 The cell cycle regulators E2F1, MYC, MYBL2 (B-Myb) and FOXM1

267 Z/YAP promote SC proliferation by activating cell cycle regulators, while targeting critical differen

268 Here, we demonstrate the application to cell cycle regulatory network analysis for Saccharomyces

269 resulted in suppression of proapoptotic and cell-cycle-regulatory target genes.

270 le checkpoint under hypoxia and analyzed key cell cycle related proteins for their potential role in

271 ivity, but a specific sensitivity profile to cell cycle-related drugs identified samples with higher

272 eterminacy as well as a general signature of cell cycle-related gene expression.

273 In this study, we determine the functions of cell cycle-related kinase (CDK20) in radiochemoresistanc

274 Our results suggest that overexpression of cell-cycle-related genes are a characteristic of prolife

275 n, the mechanisms that promote cardiomyocyte cell cycle remain incompletely understood.

276 To define variations in cell-cycle requirements between cultured cell lines, we

277 ved proteins that are thought to control the cell cycle, senescence and tumor suppression.

278 During the long G2 phase of the cell cycle, seven different interphase node proteins mai

279 at CYREN (cell cycle regulator of NHEJ) is a cell-cycle-specific inhibitor of cNHEJ.

280 iple types of human tumors regardless of the cell cycle stage.

281 pervised manner and, in classifying discrete cell cycle stages, we reach a sixfold reduction in error

282 i-C data to separate cells by karyotypic and cell-cycle state differences and identify cell-to-cell h

283 Using the device, we obtain cell-cycle statistics for C. elegans vulval development,

284 k signals to the 'mother' cell to modify its cell cycle status.

285 lls treated or untreated with androgen after cell-cycle synchronization.

286 vidence suggests that LBH could modulate the cell cycle, the precise mechanism is unknown and its imp

287 rs have emerged as the most promising of the cell-cycle therapeutics and intense efforts are now unde

288 yeast, we identified the circuit dominating cell cycle timing.

289 nd cyclin A to stage individual cells in the cell cycle to determine the levels of histones or histon

290 aberrant genetic materials often causes the cell cycle to go awry, leading to malignant transformati

291 p21 was up-regulated; proliferation and G1/S cell-cycle transition slowed.

292 d transduces multiple signals to control key cell-cycle transitions during Plasmodium gametogenesis.

293 Flow cytometry analysis indicated the cell cycle was arrested at the G2 phase after FAM83H-AS1

294 le genes involved in maintaining the mitotic cell cycle were rapidly down-regulated and senescence ge

295 knocked down, mushroom body neuroblasts exit cell cycle when nutrients are withdrawn.

296 e defined as a distinct state outside of the cell cycle while displaying a sequential cell order refl

297 rogressing synchronously through the mitotic cell cycle, while preserving the coupling of cell divisi

298 G1 subpopulations that progress through the cell cycle with distinct temporal profiles post-elutriat

299 ells released from senescence re-entered the cell cycle with strongly enhanced and Wnt-dependent clon

300 ate a molecular difference in the control of cell cycle withdrawal in fetal and postnatal myogenic st