ライフサイエンスコーパス: S phase

1 /M arrest and reduction in the time spent in S phase.

2 ss and cell cycle delays, foremost in G1 and S phase.

3 om returning to quiescence as cells approach S phase.

4 ing a transcriptional program that initiates S phase.

5 and chromatin of RDH genes primarily in the S phase.

6 ng DNA replication, resulting in a prolonged S phase.

7 s that were actively replicating host DNA in S phase.

8 anscriptional factor for the transition into S phase.

9 eased proliferation and cell accumulation in S phase.

10 intain genome integrity and stability during S phase.

11 spindle that assembles during a HU-extended S phase.

12 long noncoding RNAs (cenRNAs), especially in S phase.

13 ents and promotes nucleosome assembly during S phase.

14 NA, encounters a variety of obstacles during S phase.

15 at anticipate their initiation timing during S phase.

16 tiated well before the entry into G2, during S phase.

17 inactive in late G1/S, promoting entry into S phase.

18 triction point several hours before entering S phase.

19 ed when cells accumulate abasic sites during S phase.

20 osis, and promote faster entry into the next S phase.

21 d R-loop formation around this repeat during S phase.

22 ed by replication origins that fire in early S phase.

23 following the release of HeLa cells from G1/S phase.

24 ycle such that centrosomes duplicate once in S phase.

25 cient for complete genome duplication within S phase.

26 s and preventing cell cycle progression into S phase.

27 sites of ongoing replication throughout the S phase.

28 r require Scc2 to capture sister DNAs during S phase.

29 longation processes that mostly occur during S phase.

30 loci replicating during different stages of S phase.

31 -cycle checkpoint, as some cells reinitiated S phase.

32 all or collapse replication forks during the S phase.

33 tionally active chromatin replicating in mid S phase.

34 eres and localized to sites of DNA damage in S phase.

35 mere cohesion is not resolved prematurely in S phase.

36 the first regions to replicate in very early S phase.

37 t with reduced probability as cells approach S phase.

38 nd the onset of mitosis but does not prevent S phase.

39 his arrangement does not depend on Pol II or S phase.

40 genes, and cell cycle regulators that induce S phase.

41 CDK2 activity and hence succumb to CHK1i in S phase.

42 e-internal DNA replication initiation within S phase.

43 e cell cycle, it only builds cohesion during S phase.

44 plication timing is tightly regulated during S-phase.

45 istone deposition-dependent HR mechanisms in S-phase.

46 cycle arrest and permitting progression into S-phase.

47 sion of CCND2, and continue to cycle through S-phase.

48 generate bi-directional replication forks in S-phase.

49 DNA synthesis, and in DNA repair outside the S-phase.

50 ulation of genotoxic damage, particularly in S-phase.

51 d origins initiating DNA replication late in S-phase.

52 ogression as cells exit quiescence and enter S-phase.

53 vidual DNAs during G1 and sister DNAs during S-phase.

54 aphase-to-metaphase transition and prolonged S-phase.

55 or entered another cell cycle but stalled in S-phase.

56 t takes to duplicate the genome and complete S-phase.

57 alise within the nucleolus from early to mid S-phase.

58 A a cell can synthesise per unit time during S-phase.

59 epression of G1/S target genes in the G1 and S phases.

60 ly occur when cells are transitioning G1 and S phases.

61 e safety and immunogenicity data from this U.S. phase 1 trial of two vaccine candidates in younger an

62 uclear localization and cell cycle arrest in S phase, affecting the viability of different mammalian

63 Restriction of Mus81-Mms4 to M phase but not S phase allows a wildtype response to various forms of r

64 r, DBAN may precipitate cancer by perturbing S phase and by blocking the Chk1-dependent response to r

65 lted in a decrease in the number of cells in S phase and cell proliferation inhibition.

66 tial decrease in p50 chromatin enrichment in S phase and Cycln E is identified as a factor regulated

67 rosis along with cell cycle arrest at the G1-S phase and elicits anti-angiogenic effects.

68 e increase in transcription as cells transit S phase and enter G2, but this response to increased gen

69 We observed that the S phase and G2 phase segments of the nuclear apical move

70 ignificant reduction of replicating cells in S phase and genome-wide impairments of replication origi

71 e of hNPCs by halting DNA replication during S phase and inducing DNA damage.

72 on initiation (IZs) were detected throughout S phase and interacted in 3D space preferentially with o

73 the cell cycle, p50 is mono-ubiquitinated in S phase and loss of this post-translational modification

74 reds of substrates, controlling the onset of S phase and M phase [1-3].

75 found that REC-8 cohesins, which load during S phase and mediate sister-chromatid cohesion, usually o

76 on is needed to duplicate a cell's genome in S phase and segregate it during cell division.

77 ppresses CDK1 kinase activity throughout the S phase and stabilizes an interaction between RIF1 and P

78 yperphosphorylation starting at the onset of S phase and that CDK4/6 activity, but not cyclin E/A-CDK

79 y, ATM was required for efficient entry into S phase and to prevent normal mitotic entry after G(2) p

80 s delayed cell cycle progression through the S-phase and defective response to replication stress.

81 ll-cycle checkpoint kinase 1 (CHK1)-mediated S-phase and G(2)-M-phase cell-cycle checkpoints has been

82 R/CHK1 and GLUT1 arrested sensitive cells in S-phase and led to the accumulation of genotoxic damage,

83 its bypass of DNA lesions encountered during S-phase and may be carried out by translesion DNA synthe

84 in-dependent kinase 1 (CDK1), early onset to S-phase and mitosis, and increased chromosome instabilit

85 n stress, leading to apoptotic cell death in S-phase and mitotic catastrophe.

86 Accordingly, fewer cells in S-phase and reduced proliferation were detected as chara

87 xPhos dysfunction leads to a protracted G(1)/S-phase and results in delayed temporal patterning and r

88 al body in late G1 phase, DNA replication in S phase, and dimethylation of histone H3 in mitosis/cyto

89 M DNA translocase, is more prominent in late S phase, and favors heterochromatin.

90 rticularly at the very beginning and ends of S phase, and identified 5 temporal patterns of replicati

91 hallenged replication forks, averaged across S phase, and model a single species of "stressed" replis

92 ey derive, are often ciliated beyond G1 into S phase, and the presence of the cilium in SMB55 cells d

93 n rate and competence, hardly enter into the S phase, and undergo accelerated senescence.

94 had increased apoptosis, decreased cells in S-phase, and increased cells in G(0)/G(1).

95 hanisms that restrain their formation during S phase are incompletely understood.

96 s early embryonic lethal in mice and induces S phase arrest accompanied by gammaH2AX and DNA damage c

97 ATP depletion and cell death accompanied by S phase arrest and DNA damage only in ADK-expressing cel

98 atment suppressed colony formation, elicited S phase arrest during cell cycle progression, and induce

99 ctase, depleting dNTPs, resulting in durable S phase arrest.

100 Recapitulation of the S-phase arrest state with inhibitors led to an increase

101 milar effects on differentiation markers and S-phase arrest, and genetic or pharmacological Chk1 inac

102 Finally, by mimicking virus-induced S-phase arrest, we show that ZIKV manipulates the cell c

103 ablates the function of CDK4/6 inhibition in S-phase arrested cells when administered contemporaneous

104 (R-loops) that form in infected cells during S-phase as a consequence of beta-ADP-heptose/ ALPK1/TIFA

105 ersible pausing of the cell cycle preventing S phase associated DNA damage.

106 lls sustaining Rb hyperphosphorylation until S phase, at which point cyclin E/A-CDK activity takes ov

107 raneously; although, when cells recover from S-phase block they exhibit sensitivity to CDK4/6 inhibit

108 Additionally, under conditions of S-phase block, p15 and p16 status determined whether cen

109 mCG becomes transiently asymmetric during S phase but is rapidly restored in G2, whereas mCHG rema

110 As result, epithelial cells enter S phase but mitosis is blocked by inhibition of mitotic

111 udy, we show that L. pneumophila avoids host S phase by blocking host DNA synthesis and preventing ce

112 ors such as gemcitabine also arrest cells in S phase by preventing dNTP synthesis.

113 t Ser365 of TRF2, whose dephosphorylation in S phase by the PP6R3 phosphatase provides a narrow windo

114 naturally occurring DNA damage incurred over S-phase causes p53-dependent accumulation of p21 during

115 At the beginning of S-phase, Cdk2 phosphorylated c-Myc at Serine 62, promoti

116 This leads to an S-phase cell cycle arrest in RS4:11 cells corresponding

117 7 induces DNA damage, checkpoint activation, S-phase cell cycle arrest, and cell death in sensitive b

118 cell lines resulted in DNA damage response, S-phase cell cycle arrest, and reduction in cell growth.

119 ock-in mutation in Cul9 (Deltap53) increases S-phase cell population, accumulates DNA damage during D

120 -571 regulated efficient DNA replication and S-phase cell-cycle progression.

121 Consequently, the first S phase cells are hypersensitive to replication stress.

122 al-I expression maintain a greater number of S phase cells compared with low ST6Gal-I expressors, ref

123 t after TBI thereby increasing the number of S phase cells in crypts in wild-type but not Cdkn1a(p21(

124 ugh MRE11 and MUS81-mediated DNA cleavage in S phase cells.

125 arrest with reductions in the proportion of S-phase cells and proliferation index.

126 CDK4 in Ph+ ALL cells, and markedly suppress S-phase cells concomitant with inhibition of CDK6-regula

127 H. pylori resides in close proximity to S-phase cells in the gastric mucosa of gastritis patient

128 ed DNA damage occurs co-transcriptionally in S-phase cells that activate NF-kappaB signaling upon inn

129 t treated with hydroxyurea (HU) activate the S phase checkpoint kinase Rad53, which prevents DNA repl

130 tes, disruption of DNA replication causes an S phase checkpoint response, which regulates multiple pr

131 rapidly signal fork stalling to activate the S phase checkpoint.

132 involved in replication fork stabilization, S-phase checkpoint activation and establishment of siste

133 E-822, to prevent chemotherapy-induced intra-S-phase checkpoint activation and evaluated the antitumo

134 Both S-phase checkpoint activity and H3K4me are crucial for f

135 gradation, thereby preventing attenuation of S-phase checkpoint functions and a compromised capacity

136 ilon (Pol epsilon) was shown to activate the S-phase checkpoint in yeast in response to replicative s

137 s that are stalled by DNA damage activate an S-phase checkpoint that prevents irreversible fork arres

138 larization involves a novel, DDR-independent S-phase checkpoint, triggered by appressorium turgor gen

139 n and a potential role for PP2A in the intra-S-phase checkpoint.

140 In early S phase, cohesin stably binds to cohesin associated regi

141 th the idea that chromatin relocation during S phase contributes to maintenance of epigenetic landsca

142 pose that by restricting E2F activity to the S phase, cyclin F controls one of the main and most crit

143 to a persistent Top1cc-like DPC lesion in an S phase-dependent manner to assist in the eviction of cr

144 chanism might be arresting the cell cycle at S phase, depolarization of mitochondrial membrane potent

145 ow that greigite is a stable phase in the Fe-S phase diagram at ambient temperature.

146 natures that map onto known regions of water's phase diagram.

147 In contrast to conventional S phase DNA synthesis, BIR proceeds by a migrating D-loo

148 anistically, OGG1i and shRNA depletion cause S-phase DNA damage, replication stress and proliferation

149 ition of DNA replication, arrest of cells at S-phase, DNA damage, and finally apoptosis.

150 week after induction, 19% of CMs that enter S-phase do so twice, CM number increases by 40%, and YAP

151 sulted in compromised HR and misrejoining of S-phase DSBs, and increased the sensitivity to DNA-damag

152 icates that Geminin is downregulated in late S-phase due to an unknown mechanism.

153 distances, replication stress, and prolonged S-phase duration.

154 imum required to complete replication within S-phase duration.

155 kup origins that help maintain robustness in S-phase duration.

156 During S-phase, dynamic and stable interactions decreased consi

157 , giving rise to three Commitment Points for S phase entry (CP1-3).

158 rough deleterious TP53 mutations), premature S phase entry (due to CCNE1 amplification, RB1 loss, or

159 tion during the G1-to-S transition initiates S phase entry and cell cycle commitment.

160 However, hyperactive or expedited S phase entry causes replication stress, DNA damage and

161 studies, and propose a unified model for the S phase entry decision.

162 s of post-replicative H3K27me3 or preventing S phase entry inhibited recruitment of new TFs to DNA an

163 Efficient S phase entry is essential for development, tissue repai

164 S phase entry is mitogen-independent in the daughter G1

165 itutes the predominant control mechanism for S phase entry of daughter cells.

166 ring signalling and the Estrogen-mediated G1/S phase entry pathways were found upregulated.

167 rmally ensures sufficient MCM loading before S phase entry.

168 ng retinal neurogenesis results in increased S-phase entry and delayed cell cycle exit.

169 istinct stages of the cell cycle, suppresses S-phase entry and promotes progression into mitosis.

170 It inhibits cell motility and promotes S-phase entry by inhibiting the activity of the master r

171 RB loss promoted S-phase entry in DCX(+) cells and increased apoptosis in

172 ow that the DNA damage checkpoint regulating S-phase entry is controlled by a phosphorylation-depende

173 t to which cyclin E1 overexpression perturbs S-phase entry, DNA replication, and numbers and structur

174 nzyme to link central energy metabolism with S-phase entry.

175 rotein of the SAPS-domain family involved in S-phase entry.

176 of Whi3, an RNA-binding protein controlling S-phase entry.

177 se paralogs cannot replace CitA in promoting S-phase entry.

178 uestions about the fidelity of BrdU to label S-phase, especially during conditions when DNA damage is

179 gative cells caused G1 cell cycle arrest and S phase fork stalling.

180 However, the number of cells in S-phase from 24 h to 72 h was increased significantly by

181 verlap significantly with those bound by the S-phase gene transcription factor E2F1.

182 s suggest that transcription activity during S phase generates R-loops, which contributes to the emer

183 chromatin formation, epigenetic silencing of S-phase genes and permanent cell cycle arrest or cellula

184 Most perturbed genes fall into the class of S-phase genes, which are regulated by pocket proteins.

185 As in S phase, global mobility in G1 phase is controlled by th

186 BrdU, which are incorporated into DNA during S-phase, have been widely used to quantify beta-cell pro

187 During S phase, Hmo1 protects under-wound DNA from Top2, while

188 , individual-level data from GlaxoSmithKline's Phase II and III clinical trials of the monovalent rot

189 eals the average replication dynamics across S phase in an unperturbed cell population; FACS is used

190 s activates the DDR to maintain the cells in S phase in order to promote viral replication and that d

191 During S phase in Saccharomyces cerevisiae, chromosomal loci be

192 at were responsible for there being only one S-phase in each cell cycle, and that ensured that mitosi

193 X9 reduced cell cycle progression from G1 to S-phase in mouse fibroblasts.

194 DNA end resection, which is promoted during S phase, in part by BRCA1.

195 DONSON protein and is more frequent in early S phase, in regions marked by euchromatin.

196 ecreasing E2F-dependent transcription during S-phase increases or decreases replication capacity, and

197 reduce the protein level of Geminin in late S-phase independent of the APC/C.

198 temic dose of methotrexate, a DNA-synthesis (S phase) inhibitor, has been used since 1991 for outpati

199 Xi position in S phase is also corrupted in cells adapted to long-term

200 single DNAs, that acetylation of Smc3 during S phase is associated with J heads, and that sister DNAs

201 However, transition from G(1) to S phase is blocked in the absence of Midkine-a, resultin

202 Accurate copying of DNA during S phase is essential for genome stability and cell viabi

203 phosphorylation of TRF2 at Ser365 outside of S phase is required to release RTEL1 from telomeres, whi

204 eported to be essential for interaction with S phase kinase-associated protein 1 (SKP1) and RNA silen

205 They bind to S-phase kinase-associated protein 1 (SKP1) through the F

206 and TgPhyA) catalyze prolyl-hydroxylation of S-phase kinase-associated protein 1 (Skp1), a reaction e

207 ), damaged DNA-binding protein 1 (DDB1), and S-phase kinase-associated protein 2 (SKP2) as components

208 Here, we identified S-phase kinase-associated protein 2 (SKP2) as E3 ligase

209 s in part by opposing the down-regulation of S-phase kinase-associated protein 2 (SKP2) by the more w

210 The E3 ligase S-phase kinase-associated protein 2(Skp2) is overexpress

211 ng at DNA replication origins to prepare for S phase, known as origin licensing.

212 ls occurs in a defined temporal order during S phase, known as the replication timing (RT) programme.

213 1 inhibition caused DNA damage and arrest in S phase, leading to earlier onset apoptosis.

214 S-phase length is determined by DNA synthesis rate, whic

215 letion leads to decreased number of cells in S phase, likely owing to the function of CDK11 in RDH ge

216 During S-phase, minor DNA damage may be overcome by DNA damage

217 ntracellular hyaluronan synthesis during the S phase of cell division.

218 kinases (CDK4 and CDK6) regulate entry into S phase of the cell cycle and are validated targets for

219 n, induced apoptosis, and accumulated in the S phase of the cell cycle with higher efficacy than eith

220 s cerevisiae, depends on progression through S phase of the cell cycle, but the molecular nature of t

221 f the MCM complex, primarily during the G(1)/S phase of the cell cycle.

222 n showed PACS-1 nuclear localization at G(1)-S phase of the cell cycle.

223 profiles from cells in early, mid, and late S phase of the mitotic cell cycle.

224 es in a rhythmic fashion unique to each gene's phase of transcription.

225 lation can only be initiated at the G1/early S phases of cell cycle upon the treatment onset, resulti

226 n Saccharomyces cerevisiae during the G1 and S phases of the cell cycle.

227 Transcription occurs during the S-phase of increasingly permissive cleavage cycles.

228 nucleus and has a role in the progression of S-phase of the cell cycle, and both these functions requ

229 by inducing rapid entry of B cells into the S-phase of the cell cycle, decreasing expression of cycl

230 d increased the percentage of GSCs in M- and S-phase of the cell cycle.

231 Thus, AEE788 prevents entry into the S-phase of the cell division cycle.

232 l cells because some cells are apoptotic, in S-phase, or otherwise of poor quality.

233 vent cell-cycle entry, thus interfering with S-phase- or mitosis-targeting agents.

234 sable for replication to be completed within S-phase period.

235 is post-translational modification increases S phase progression and chromosomal breakage.

236 BARD1/BRCA1 during the cell cycle regulates S phase progression to maintain genome integrity.

237 for repriming, unrestrained replication, and S phase progression upon limiting nucleotide levels.

238 Restoration of miR-874 expression impeded S phase progression, suppressing aggressive growth pheno

239 HAT1 expression was critical for S-phase progression and maintenance of H3 lysine 9 acety

240 s of recombination, prophase axis length and S-phase progression, in budding yeast.

241 ng initiation of G1/S transition and daytime S-phase progression, overnight increase in G2/M, and cyc

242 eads to replication problems, such as slower S-phase progression, resulting in the accumulation of si

243 og bias for crossover formation and promotes S-phase progression.

244 er, PCNA is also ubiquitinated during normal S-phase progression.

245 Our results identified an essential S-phase promoting factor of the unconventional P. falcip

246 Here, we discovered a fundamental role of S-phase protein kinase 2 (Skp2) in the formation and pro

247 Legionella pneumophila replication, whereas S phase provides a toxic environment for bacterial repli

248 Although pyruvate delays cell entry into S phase, pyruvate represses histone gene expression inde

249 te the restriction of Rad52 mediator foci to S phase, Rad51 foci form at high levels in G1 phase.

250 Although Tceal8 inhibited E2f2-induced S-phase re-entry, Bex1 facilitated DNA synthesis while i

251 Cyclin D1, a G1-S phase regulator, is upregulated in parathyroid adenoma

252 ts 24.84-h rhythm and altering the pacemaker's phase-relationship to sleep in a manner that is known

253 udies implicate the metalloprotease SPRTN in S phase removal of DPCs, but how SPRTN is targeted to DP

254 We identified the cause of the S-phase requirement for silencing establishment: removal

255 cation rates, thus shortening or lengthening S-phase, respectively.

256 ells, high activity can be attained in early S phase, resulting in DNA cleavage and cell death.

257 rimeric PB protein DCP1A rapidly (within ~10 s) phase-separates in mammalian cells during hyperosmoti

258 During S phase, specialized replicative histone variants ensure

259 R2 is S-phase specific and used for DNA replication, whereas p

260 from the original Fucci system to respond to S phase-specific CUL4(Ddb1)-mediated ubiquitylation alon

261 reduction by the designed Cu complexes is an S-phase-specific event that is associated with increased

262 ere duplication is not required to stabilize S phase spindle structure, leading us to propose a model

263 f replication perturbation and DNA damage in S phase, suggesting it acts as a post-replicative resolv

264 Sirt2, which level peak in S phase, sustains RNR activity at or above a threshold l

265 We propose that TRF1 facilitates S-phase telomeric DNA synthesis to prevent illegitimate

266 distinct average time of replication during S phase that depends on the spatial and temporal pattern

267 timulates HDR during a reversible slowing of S-phase that is unexplored for Cas9-induced HDR.

268 limiting for the onset of mitosis and of the S-phase, that were responsible for there being only one

269 o DNA damage has been studied extensively in S phase, the response in interphase has not, and the que

270 In S-phase, the checkpoint inhibits replication initiation,

271 ion impedes the progression of cells through S phase, thereby preventing the completion of host DNA r

272 ccurrence of G4 structures peaks at the late S phase, thus correlating with the accumulation of long

273 FI1 localizes USP9X to the centrosome during S phase to deubiquitylate STIL, a critical regulator of

274 nases promoted and maintained BKPyV-mediated S phase to enhance viral production.

275 ponse in order to keep the infected cells in S phase to replicate the viral DNA.

276 -2'-deoxyuridine (BrdU) incorporation during S-phase to label newly replicated strands, followed by H

277 mologous recombination (HR) cooperate during S-phase to safeguard replication forks integrity.

278 Surprisingly, the shift from 'S-phase' to 'damage-response' dNTP levels only minimally

279 cation initiation, possibly extending beyond S phase, to support predominantly chromosome-internal DN

280 iptome analysis revealed up-regulation of G1/S phase transition genes (myelocytomatosis oncogene cell

281 thelial cell proliferation and cell cycle G1/S phase transition, whereas the upregulated genes were i

282 ion and inducing cell cycle arrest at the G1/S phase transition.

283 CDK2 and thereby contributes to increased G1-S phase transitions and cell proliferation.

284 nonnuclear kinases might be influencing FUS's phase transitions.

285 During S-phase, UNG2 remains associated with the replication fo

286 Arpp19 knockout did not perturb the S phase, unlike Ensa gene ablation.

287 Thus, we demonstrate the role of a S-phase up-regulated lncRNA in cell-cycle progression vi

288 Further, we demonstrate that an S-phase-upregulated lncRNA, SUNO1, facilitates cell-cycl

289 e replication time at specific points during S phase using a synchronized cell population.

290 sent report reveals that cells irradiated in S-phase utilize a different form of wiring between DNA-P

291 at ensured that mitosis only took place when S-phase was properly completed.

292 Stalled cells exhibited prolonged S-phase, were defective in DNA synthesis and had increas

293 synthetized DNA into nucleosomes during the S phase when their expression is highly upregulated.

294 y Polo-like kinase 4 (Plk4) and initiates in S-phase when a daughter centriole grows from the side of

295 t response but also occurs in an unperturbed S-phase when too many origins fire simultaneously.

296 thesis and translocate to the nucleus during S-phase, where they form a multienzyme complex with thym

297 in treatment, resistant cells accumulated in S phase, which partially depended on ZRANB2, SYF2 and th

298 l as in vitro growth by cell cycle arrest at S phase with increased cell size and nuclei.

299 Our model picks P and S phases with precision close to manual picks by human a

300 continuous absence of cohesin, pass through S-phase with typical spatio-temporal patterns of replica