ライフサイエンスコーパス: S phase entry

1 ge) and two phases of the cell cycle (G1 and S phase entry).

2 ssion, down-regulating p130/Rb2 and inducing S phase entry.

3 ly of MAP kinases is a critical regulator of S phase entry.

4 rmally ensures sufficient MCM loading before S phase entry.

5 c fibroblasts (MEF) accelerates G(0)/G(1) to S phase entry.

6 of cell cycle due to its ability to promote S phase entry.

7 effect of cicaprost on p27(Kip1) levels and S phase entry.

8 osis but does not inhibit E2F activation and S phase entry.

9 ts, whereas in cells lacking p53 it promotes S phase entry.

10 int, which allows time for DNA repair before S phase entry.

11 zoans a role for Cdc6 has only been shown in S phase entry.

12 gradation by the proteasome was required for S phase entry.

13 n and was linked to Rap's ability to promote S phase entry.

14 s suggest that HDHB function is required for S phase entry.

15 D1, that may underlie its role in promoting S phase entry.

16 inactivation of Rb-dependent repression and S phase entry.

17 is insufficient to enable K cyclin-mediated S phase entry.

18 as a second independent function that limits S phase entry.

19 ng to its inactivation and thereby promoting S phase entry.

20 during transition of G1, and higher rates of S phase entry.

21 and continued to require c-myc function for S phase entry.

22 caused an even more dramatic advancement of S phase entry.

23 ciation of CDC6 and cyclin E, and a delay in S phase entry.

24 brogation of the 1,25D3-induced block to the S phase entry.

25 are essential for cyclin E-CDK2 activity and S phase entry.

26 ion of any vector alone had little effect on S phase entry.

27 finity threshold for triggering human B cell S phase entry.

28 all cell cycle phases, and caused premature S phase entry.

29 -induced immediate early gene expression and S phase entry.

30 monoubiquitination and UV DNA repair before S phase entry.

31 iting roles in restriction point passage and S phase entry.

32 m-1 is able to cooperate with Skp2 to signal S phase entry.

33 phase induction of cyclin D1 associated with S phase entry.

34 nding site, thereby inhibiting serum-induced S phase entry.

35 Cdh1 has been implicated in regulating S phase entry.

36 tracellular tension, Rb phosphorylation, and S phase entry.

37 yclin B degradation to allow MI exit without S phase entry.

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

39 es so that specific activator E2Fs can drive S-phase entry.

40 RB hyperphosphorylation and delay premature S-phase entry.

41 n in pre-BII cells associated with decreased S-phase entry.

42 progressed rapidly through G1 with premature S-phase entry.

43 cell cycle progression, including premature S-phase entry.

44 in-null cells with wild-type menin represses S-phase entry.

45 mechanisms of immune activation, leading to S-phase entry.

46 ene results in upregulation of cyclin D1 and S-phase entry.

47 several years to be important regulators of S-phase entry.

48 nduces sustained ERK activation and promotes S-phase entry.

49 2F-dependent acetylation, transcription, and S-phase entry.

50 was followed by expression of cyclin D1 and S-phase entry.

51 INK4a-induced cell cycle arrest and induces S-phase entry.

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

53 ieved to have an essential role in promoting S-phase entry.

54 s the opposite effects by promoting G(1)- to S-phase entry.

55 D1(-/-) cells showed reduced PI3K-dependent S-phase entry.

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

57 cant enhancement of SMC growth via increased S-phase entry.

58 CDK2 by Notch(ic) result in the promotion of S-phase entry.

59 chimeric embryos exhibited extensive ectopic S-phase entry.

60 an E2F-dependent transcriptional program and S-phase entry.

61 repair the damaged DNA upon injury, prior to S-phase entry.

62 tion of Cdk2 and the subsequent induction of S-phase entry.

63 and the pRb pocket-protein family, suppress S-phase entry.

64 ufficient to drive cyclin D1 accumulation or S-phase entry.

65 0 ng/mL IL3 or SCF prevented such a block in S-phase entry.

66 ry required to ensure the irreversibility of S-phase entry.

67 f mitosis coupled with aberrant licensing of S-phase entry.

68 (PSM)-RB, but not wild-type RB, can inhibit S-phase entry.

69 rt, via noncanonical cyclin D1-CDK2-mediated S-phase entry.

70 bstrate of cyclin E-CDK2 and plays a role in S-phase entry.

71 f purified cyclin-Cdks during G1 accelerates S-phase entry.

72 s itself a transcription factor required for S-phase entry.

73 nfirmed the involvement of E2F in IR-induced S-phase entry.

74 distribution of the Mcm2-7 helicase prior to S-phase entry.

75 cell proliferation as shown by inhibition of S-phase entry.

76 erative effect of the S10A mutant to promote S-phase entry.

77 es plant organs by releasing a constraint on S-phase entry.

78 JAK2(V617F) has been shown to promote S-phase entry.

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

80 exhibit an enhanced proliferation and early S-phase entry.

81 led with the onset of DNA replication during S-phase entry.

82 mediated c-Myc expression and DNA synthetic (S) phase entry.

83 quent release of active E2F, is required for S-phase entry [1-3].

84 n and that this modification correlates with S-phase entry [6-8].

85 esulted in a modest decrease in IL-4-induced S phase entry, a further decrease in cell-cycle completi

86 defective p53/Rb pathways, led to premature S phase entry, acute depletion of Cdh1 in primary human

87 of p27Kip1 by small interfering RNA promoted S phase entry after IL-7 withdrawal.

88 a substantial ( approximately 6-h) delay in S-phase entry after serum stimulation.

89 Both S phase entry and activation of cyclin/CDKs were inhibit

90 S phase entry and cell cycle commitment in peripheral T

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

92 2 RNAi seems to protect cells from premature S phase entry and crisis in DNA replication.

93 al role for these regulators in GPC1-induced S phase entry and DNA rereplication.

94 80 alone and observed a significant delay in S phase entry and fork progression but little effect on

95 imultaneous loss of Mcm10 and p180 inhibited S phase entry and led to an accumulation of already repl

96 ates at the G1/S boundary, where it promotes S phase entry and progression by activating Cdk2.

97 combine with and activate cdk2 to facilitate S phase entry and progression.

98 iploid cells, particularly those involved in S phase entry and progression.

99 Even so, S phase entry and proliferation are not increased in Cas

100 ncing cyclin D3 by RNA interference inhibits S phase entry and sensitizes breast cancer cells to TRAI

101 suggest that DMP1 induces genes that inhibit S phase entry and that D-type cyclins can override DMP1-

102 gen synthase kinase-3beta (GSK3beta) induces S phase entry and thereby mitotic clonal expansion (MCE)

103 MP is mitogenic leads to an increase in G(1)/S phase entry and tumor formation.

104 hibit a 70-80% reduction in IGF-1-stimulated S-phase entry and a parallel decrease in the induction o

105 The inhibition of S-phase entry and activity of the cyclin D1-dependent se

106 ce lacking p57(Kip2) exhibited inappropriate S-phase entry and apoptotic nuclei were found in the reg

107 ion of all three proteins resulted in forced S-phase entry and attenuation of checkpoint activation,

108 ugh G1 cyclin-Cdk complexes are required for S-phase entry and can shorten G1 phase when overexpresse

109 ponsible for a major G1 checkpoint, blocking S-phase entry and cell growth.

110 ically, ATX-LPA1 signaling acts by promoting S-phase entry and cell proliferation of chondrocytes bot

111 The transcription factor E2F-1 promotes S-phase entry and death in transformed cells and primary

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

113 his lowers the level of cyclin E1 needed for S-phase entry and delays cyclin E1 proteolysis during S-

114 Cdc25A is required for S-phase entry and dephosphorylates tyrosine-15 phosphory

115 replication-coupled destruction during both S-phase entry and DNA repair; Cdt1 is destroyed first, w

116 ol expression of several genes essential for S-phase entry and DNA replication.

117 acute effect of Men1 mutation is accelerated S-phase entry and enhanced cell proliferation in pancrea

118 p21 deletion also accelerated S-phase entry and enhanced transformation rates in tripl

119 Cyclin E is a G(1) cyclin essential for S-phase entry and has a profound role in oncogenesis.

120 s (K-rasV12) into quiescent PDECs stimulates S-phase entry and induces a pronounced increase in cell

121 s smooth muscle cell (SMC) proliferation and S-phase entry and inhibits transcription of the cell-cyc

122 revious observations, NICD(OE) also inhibits S-phase entry and Ki67 expression and thus reduces the p

123 defects in cell-cycle progression (delays in S-phase entry and metaphase exit) and chromosome condens

124 r studies have suggested that CDK2 regulates S-phase entry and progression, and frequently shows incr

125 e and became immortal but displayed enhanced S-phase entry and proliferation rates similar to wild ty

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

127 ORC1 deficiency perturbs S-phase entry and S-phase progression.

128 e precise timing of E2F1 expression dictates S-phase entry and that accurate timing of E2F1 accumulat

129 th Swi4-t and found that there is precocious S-phase entry and that the length of S phase is extended

130 gion on Cdc34p; this region is essential for S-phase entry and thus the association of these three pr

131 Cyclin A is required for cell cycle S phase entry, and its overexpression contributes to tum

132 by a decreased proliferation rate, impaired S phase entry, and premature senescence.

133 or STAT5 phosphorylation, mediated efficient S phase entry, and promoted cell-cycle progression.

134 uding transcriptional activity, induction of S-phase entry, and apoptosis.

135 LR gene products inhibit S-phase entry, and binding of the LR protein (LRP) to cy

136 cleus in the presence of high serum, impeded S-phase entry, and induced apoptosis in a dose-dependent

137 as stimulated G1 cyclin mRNAs and proteins, S-phase entry, and proliferation without affecting cell

138 that G1 Cdk activation is rate-limiting for S-phase entry, and that Cdk activation is likely to be t

139 Overexpression of NPAT accelerates S-phase entry, and this effect is enhanced by coexpressi

140 ls, roughly corresponding to the time before S-phase entry, and was poorly induced in T cells express

141 e induction of cyclin A is also required for S-phase entry, and we now report that distinct effects o

142 ation of the G(1)/S checkpoint and increased S phase entry, apparently by activating the mitogen-inde

143 the ultimate downstream target as related to S-phase entry appears to be pRb.

144 th arrest and disables checkpoints governing S-phase entry as well as apoptosis in HMECs immortalized

145 n conjunction with cyclin E, participates in S-phase entry as well.

146 yc)D2, a G(1) cyclin implicated in mediating S phase entry, as a potential regulator of hypertrophic

147 U20S cells rescued G1 arrest and resulted in S-phase entry, as measured by the ability to incorporate

148 sed clonogenicity and viability, facilitated S-phase entry, attenuation of apoptosis, formation of tr

149 ed in only a modest decrease in IL-4-induced S phase entry, but a total block of cell-cycle completio

150 ntry is regulated in an analogous fashion to S phase entry, but involves a distinct cyclin/cdk combin

151 th this hypothesis, pRB's ability to prevent S phase entry, but not its ability to inhibit S phase co

152 CSF-1R (Y809F) rescued c-Myc expression and S phase entry, but only in the presence of CSF-1-induced

153 Cdh1 ablation promotes precocious S-phase entry, but it was unclear how this affects DNA r

154 p21(cip1) inhibits S phase entry by binding to cyclin-cdk2 (cyclin-dependen

155 SBF is inactivated upon S-phase entry by Clb/CDK whereas MBF targets are repress

156 n vestibular epithelia elevated cAMP induces S-phase entry by increasing the number of growth factor

157 -beta1 treatment in late G(1) acutely blocks S-phase entry by inhibiting activation of fully assemble

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

159 created by CRL4(Cdt2), promotes irreversible S-phase entry by keeping p21 levels low, preventing prem

160 Accelerated S-phase entry by proliferating R2LivKO hepatocytes coinc

161 an induce the DDR by promoting inappropriate S phase entry, by modifying cellular DDR factors directl

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

163 defects in mitotic chromosome alignment and S-phase entry characteristic of cyclin E overexpression.

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

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

166 transcription-coupled export do not exhibit S phase entry defects or sensitivity to DIA2 expression

167 c HCT116p53(-/-) cells, including unhindered S-phase entry despite DNA damage.

168 Deletion of PrdxII increased ROI, S phase entry, division, and death during in vitro divis

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

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

171 localized to the centrosome and accelerated S phase entry even with mutations that abolish Cdk2 bind

172 NA damage checkpoint and may thereby prevent S-phase entry even when cyclin E-CDK2 activity is deregu

173 ng 4pX-1 cells display pX-dependent G(1) and S phase entry, followed by S phase pause and absence of

174 (U73122) also block cyclin D2 expression and S phase entry following BCR stimulation, as well as trig

175 ls by expression of antisense p27 allows for S-phase entry from quiescence in NIH 3T3 cells expressin

176 p53-deficient cultures exhibiting increased S-phase entry, giant nuclei, multinucleation, multipolar

177 Prior to S-phase entry, glucose metabolism shifts from primarily

178 /6 inhibitors that enable alternate means of S-phase entry, highlighting strategies to prevent the ac

179 NPAT) in these domains occurs at the time of S-phase entry, histone locus bodies are formed approxima

180 In addition, AML1 induces S phase entry in 32Dcl3 myeloid or Ba/F3 lymphoid cells

181 mal-targeting domain essential for promoting S phase entry in a Cdk2-independent manner.

182 rcumventing host cell cycle control to force S phase entry in an otherwise quiescent cell.

183 Neither BCL-x(L) nor BCL2 delayed S phase entry in cells deficient in p27, thus p27 is req

184 F or the E2F-regulated cyclin E gene promote S phase entry in cells expressing phosphorylation-defect

185 ate substantial re-replication within 1 h of S phase entry in cells overproducing the replication fac

186 ate significant suppression of apoptosis and S phase entry in certain tissues compared to Rb mutants,

187 BRLF1 expression induced S phase entry in contact-inhibited fibroblasts and in th

188 mutant can partially restore MCM loading and S phase entry in cyclin E-null cells.

189 differentiation was insufficient to promote S phase entry in either of the situations where ebi muta

190 fundamental role in promoting Ras-dependent S phase entry in mammary epithelial cells, whether in re

191 clin D1 levels by RNA interference inhibited S phase entry in melanoma cells.

192 We show that S phase entry in NHEM requires both adhesion and growth

193 Skp2 knock down inhibits S phase entry in nontransformed mouse embryonic fibrobla

194 p16(INK4a) and resulted in the inhibition of S phase entry in p21/p27-null MEFs.

195 ne expression but are insufficient to induce S phase entry in primary T cells.

196 K/ERK pathway to induce c-Myc expression and S phase entry in response to CSF-1 stimulation.

197 sion of D1/T286A in B lymphocytes results in S phase entry in resting lymphocytes and increased apopt

198 ation of lin-35 Rb, efl-1, or lin-36 allowed S phase entry in the absence of cyd-1/cdk-4 and increase

199 G1 progression and enables cells to sustain S phase entry in the absence of serum growth factors.

200 xpression of proteins that control the G1 to S phase entry in the cell cycle.

201 biting extensive apoptosis and inappropriate S phase entry in the central and peripheral nervous syst

202 more effective in suppressing the premature S phase entry in the MF, reducing the dosage of stg is m

203 IgM:ligand affinity threshold for eliciting S phase entry in the presence of IL-4.

204 in, can prevent DNA replication in vitro and S phase entry in vivo.

205 ction is required for Rb phosphorylation and S-phase entry in cancer cells.

206 show that the expression of NPAT accelerates S-phase entry in cells released from quiescence.

207 eta2 and TGF-beta2 in aqueous humor suppress S-phase entry in cultured rat corneal endothelial cells,

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

209 The p16 peptide inhibited S-phase entry in five cell lines tested, varying between

210 OG, a master transcription factor, regulates S-phase entry in human embryonic stem cells (hESCs) via

211 evels of asbestos (<0.5 microg/cm2) promoted S-phase entry in low (2%) serum through an epidermal gro

212 es during the G(1)/S-phase transition and in S-phase entry in mammalian cells.

213 The p16 peptide blocks S-phase entry in non-synchronized human HaCaT cells by a

214 her Rb phosphorylation is a prerequisite for S-phase entry in Rb-deficient SAOS-2 osteosarcoma cells,

215 gous-targeted disruption leads to a delay in S-phase entry in serum-stimulated mouse embryo fibroblas

216 and birds, the loss of hair cells can evoke S-phase entry in supporting cells and the production of

217 s believed to be the principal constraint on S-phase entry in T cells.

218 a T-cell transcription factor that regulates S-phase entry in T-cells.

219 e CNS, PNS, and lens underwent inappropriate S-phase entry in the conditional mutants at E13.5.

220 cle arrest of specified cells and antagonize S-phase entry in the SMW.

221 binding to CD44 antagonizes mitogen-induced S-phase entry in vascular smooth muscle cells; we now ch

222 on with a GATA-6 expression vector inhibited S-phase entry in VSMCs and in mouse embryonic fibroblast

223 transcription factors triggers irreversible S-phase entry in yeast and metazoans, but why this occur

224 d early G(1) cell-cycle progression, but not S-phase entry, in opposition to the cyclin-dependent kin

225 r in RING finger domain, promotes cell cycle S phase entry independent of p53.

226 WAF1/Cip1-dependent pathway but may control S-phase entry independent of p21.

227 ate E2F transactivation activity and promote S-phase entry independent of p53, yet the mechanism of w

228 p220NPAT, and in addition, p220 can promote S-phase entry independently of histone transcriptional a

229 at mTOR activation is required for efficient S-phase entry, independently of E2F activation, in adeno

230 The S-phase entry induced by forskolin was blocked by monens

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

232 and p130, much of E2F-mediated repression of S phase entry is dependent upon Rb.

233 t of cicaprost on cyclin E-Cdk2 activity and S phase entry is eliminated by deleting p27(Kip1).

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

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

236 This accelerated S-phase entry is accompanied by increased cyclin-depende

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

238 Cdk2 is a major regulator of S phase entry, is activated by mitogenic cytokines, and

239 nged and continuous PDGF exposure results in S-phase entry many hours after the initial burst of acti

240 how that codepletion of FoxM1 inhibits early S phase entry observed in Cdh1-depleted cells.

241 eriments, BrdU incorporation as a marker for S-phase entry occurs at a higher level in transiently tr

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

243 ponsive reporter, a 42% decrease in the mean S phase entry of growth-arrested (G[0]) cells after seru

244 In the postnatal subventricular zone (SVZ), S phase entry of neural progenitor cells (NPCs) correlat

245 YC-ERTM in WI38 cells is sufficient to cause S phase entry of quiescent cells, which is preceded by p

246 with the progression factor A-Myb to promote S phase entry of quiescent smooth muscle cells.

247 b abolished growth of KS cells by preventing S phase entry of the cell cycle, even in the presence of

248 fact that A1, unlike Bcl-2, did not inhibit S-phase entry of activated cells.

249 Interestingly, Kv1.3 block inhibited S-phase entry of both purified OPs in culture and in tis

250 Engagement of beta1-integrins blocked S-phase entry of CD34(+) cells in the absence of IL3 or

251 es unscheduled origin firing and accelerates S-phase entry of cells in the absence of p53.

252 es expression of cyclin D2 and A and hastens S-phase entry of cells.

253 t functions, or, alternatively, they control S-phase entry of different cell types in a tissue-specif

254 miR-221 overexpression leads to rapid S-phase entry of hepatocytes during liver regeneration.

255 HDL and its associated apo, APOE, inhibit S-phase entry of murine aortic smooth muscle cells.

256 Thus, the inappropriate S-phase entry of p300 down-regulated cells is likely to

257 eta2 and TGF-beta2 in aqueous humor suppress S-phase entry of rat corneal endothelial cells.

258 e protein activated by cAMP (EPAC), enhances S-phase entry of SCs by synergistically enhancing the li

259 Strikingly, the timing of S-phase entry or exit is not delayed in dDP mutant clone

260 have asked whether Cdc7 is only required for S-phase entry or if it plays a role during S phase in or

261 tivation of PKA was not sufficient to induce S-phase entry or the activation of either ErbB2 or ErbB3

262 ermore, Id3a fails to promote SMC growth and S-phase entry or to inhibit p21(Cip1) promoter transacti

263 Upon S phase entry, Orc1 is ubiquitinated and targeted for de

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

265 h and parallel decreases in IGF-1-stimulated S-phase entry, PI 3-kinase activity, and induction of th

266 is regulated by inputs that normally control S phase entry, possibly as a quality control mechanism t

267 -ER in NIH-3T3 cells resulted in accelerated S phase entry, proliferation in low serum, morphological

268 Cdk2AF caused premature S-phase entry, rapid cyclin E degradation, abnormal DNA

269 ivation caused only a transient delay in the S phase entry rather than a sustained G1 arrest.

270 al. show that E2F1, a positive regulator of S phase entry, recruits cofactor HCF-1 and associated hS

271 ent kinase (CDK) inhibitor roscovitine after S-phase entry reduced MVM replication, suggesting that C

272 n CRE occupancy, cyclin E-cdk2 activity, and S phase entry, suggesting the involvement of Gi signalin

273 escue the impact of NANOG down-regulation on S-phase entry, suggesting that CDK6 and CDC25A are downs

274 nt, D1-T156A, to inhibit Wnt1/MEK1-dependent S-phase entry suggests that cyclin D1 is a critical down

275 those produced by E2F-1 alone and can drive S-phase entry that is resistant to p21 and independent o

276 wth factor deprivation and induce precocious S-phase entry, thereby triggering cell death.

277 by inhibiting CDK2 activity and forestalling S phase entry through retinoblastoma protein hypophospho

278 inant for this activity and induces aberrant S-phase entry through the inactivation of the retinoblas

279 estriction point but does not interfere with S phase entry under continuous serum stimulation.

280 ich leads to early G1 arrest and synchronous S-phase entry upon release of the G1 block, we have deve

281 Strikingly, blockade of S phase entry using the phosphatidylinositol 3-kinase in

282 Blockade of Ras-induced CDK-2 activity and S phase entry via overexpression of p27 inhibited apopto

283 The E7-induced S phase entry was accompanied by an increase in the acti

284 activation of the G1 cell cycle proteins and S phase entry was linked with apoptosis, we examined hom

285 U incorporation was robust but the timing of S-phase entry was delayed.

286 was induced in these cells, serum-stimulated S-phase entry was significantly inhibited.

287 to the cytoplasm and arresting cells before S-phase entry, we hypothesized that ARF might also inhib

288 Target gene activation and S-phase entry were also blocked by DN E2F1.

289 ellular signaling pathways that underlie the S-phase entry were surveyed by culturing epithelia in th

290 re, nor mechanical tension had any effect on S phase entry when added at later times.

291 ication complexes (pre-RCs) to acutely block S-phase entry when added to cells in late G(1), after mo

292 that Rb phosphorylation is not essential for S-phase entry when G1 cyclin-Cdks are overexpressed, and

293 did not require serum for cdk2 activation or S phase entry whereas loss of the related cdk2 inhibitor

294 d with enhanced signaling and more efficient S phase entry, whereas accelerating receptor degradation

295 erexpression of wild-type PKD3 also promoted S phase entry, whereas depletion of endogenous PKD3 resu

296 cyclin A accumulation in G1 and accelerated S phase entry, whereas USP37 knockdown delayed these eve

297 of the G1 phase of the cell cycle and early S phase entry, which leads to hyperproliferation.

298 t centrosomal duplication is an indicator of S phase entry while centrosome migration marks mitotic e

299 ssion accelerates G(1) phase progression and S phase entry with concomitant DNA replication.

300 iod, to increase the probability that cancer S-phase entries would coincide with drug exposure, which