ライフサイエンスコーパス: M phase

1 one functional pathway within the T module (M-phase).

2 es simulated HeLa cells to accumulate in the M phase.

3 as evidenced by accumulation of cells in G2/M phase.

4 ncrease in the percentage of cells in the G2/M phase.

5 of their radiation-induced arrest in the G2/M phase.

6 ndocycle is a modified cell cycle that lacks M phase.

7 delays cell cycle progression through the G2/M phase.

8 on during interphase and its reactivation in M phase.

9 TSE1 is expressed exclusively in late G2 and M phase.

10 proliferation and reduced cells in the S+G2/M phase.

11 te, at the ribosomal level, cells entry into M phase.

12 rylated in a CDK1-dependent manner during G2/M phase.

13 etely) explain the full activation of Gwl at M phase.

14 the entire cell cycle length, principally in M phase.

15 tion by arresting the cell cycle at the G(2)-M phase.

16 dk1 as a critical regulator of DSB repair in M phase.

17 tially functional during both S phase and G2/M phase.

18 m it when progesterone-treated oocytes reach M phase.

19 F1 at the G1/S phase and with MyoD at the G2/M phase.

20 migration, and it arrests cancer cells in G2/M phase.

21 ntation of erythroid related genes in the G2/M phase.

22 B2 gene cluster that are expressed during G2/M phase.

23 ed apoptosis and cell cycle arrest at the G2/M phase.

24 linA2-EGFP were expressed from mid-G1 to mid-M phase.

25 resulting in cell-cycle inhibition at the G2-M phase.

26 NA damage and induce growth arrest at the G2/M phase.

27 f Gwl and PP1, Gwl and PPP1R3B dissociate in M phase.

28 terphase cells, and robust clustering during M phase.

29 P(Low) ISCs and percentage of these cells in M-phase.

30 chromosomes to hypercompact when delayed in M-phase.

31 reases the level of CDK1 activity during the M-phase.

32 ase entry and inhibits CDK1 during the whole M-phase.

33 lease from thymidine block, corresponding to M-phase.

34 , leading to the unusual length of the first M-phase.

35 riven cancer cells arrest in either S- or G2/M-phase.

36 and is required for successful completion of M-phase.

37 sume a constant time for traversing the S/G2/M phases.

38 stem cells, which accumulate in the S and G2/M phases.

39 with peak expression in both S phase and G2/M phases.

40 aive pluripotency and by shortening the S-G2/M phases.

41 lling late cell cycle events in the G(2) and M phases.

42 ng cancer cell arrest at both the S and G(2)/M phases.

43 HK2 kinases and cell cycle arrest in S or G2/M phases.

44 rinosomes were also observed in the S and G2/M phases.

45 nt and incomplete DNA decatenation in G2 and M phases.

46 estradiol effects on progression into S and M phases.

47 se (1-fold) and a peak due to cells entering M phase (2-fold).

48 The 12-month (M), phase 3, double-blind, randomised TRANSFORMS study d

49 pid cleavage cycles consisting only of S and M phases, a critical N/C ratio is reached, which causes

50 y where cells were destroyed not by frank G2-M phase abrogation but rather by initiating a cumulative

51 and reduced cell accumulation in S and G(2)/M phases after 24 h of incubation.

52 cle progression showed an accumulation of G2/M phase, altered population in G1 and S phases, and incr

53 of SAS cells via arresting cell cycle at G2/M phase and activating the extrinsic Fas-mediated membra

54 Cell cycle arrest in G2/M phase and an increased DNA repair response were observ

55 noma cell lines by arresting the cells in G2/M phase and caused apoptosis.

56 ART treatment led to cell cycle arrest at G2/M phase and cell accumulation in sub-G1 phase.

57 rmation, induced cell cycle arrest in the G2/M phase and cleavage of caspases 3, 8, and 9 and poly(AD

58 rmore, the delay of the cell cycle in the G2/M phase and decrease in cell proliferation seen upon dep

59 The cells showed a cell-cycle arrest in G2/M phase and defects in plasmid and chromosome segregatio

60 ng the transition from the S phase to the G2/M phase and functions in radiation-induced G2 checkpoint

61 lysing the distribution of cells in S phase, M phase and G2 from the time just prior to the migration

62 ore, CD133(+) cells exhibited an extended G2-M phase and increased polarized asymmetric cell division

63 X-SDT increased the ratio of cells in the G2/M phase and induced 3-4 times more cell apoptosis compar

64 l cycle, Dyrk2 interacts with TERT at the G2/M phase and induces degradation.

65 pound 16c caused cell cycle arrest in the G2/M phase and interacted with the colchicine-binding site

66 tion states, facilitate mitotic functions in M phase and promote chromatin compaction and cell cycle

67 ies, 16a was shown to block cell cycle in G2/M phase and to disrupt microtubule formation and display

68 he inhibition of the cell cycle in G1 and G2/M phases and reduces the cell cycle markers like cyclin

69 es cells to undergo strictly ordered G1/S/G2/M phases and respond adaptively to regulatory signals; h

70 phosphorylated by DNA-PKcs during the G2 and M phases and that DNA-PK-dependent hnRNP-A1 phosphorylat

71 delay or arrest of the cardiac cell cycle in M-phase and a failure of cardiomyocyte progenitors to in

72 ting phosphorylated forms accumulated toward M-phase and disappeared after release from a mitotic blo

73 In zebrafish, both mitosis (M phase) and DNA synthesis (S phase) are clock-controlle

74 but arrested cell cycle (in the S- and G(2)/M-phases) and decreased cyclins A and D1 protein levels.

75 the p53 pathway, cell cycle arrest at the G2/M phase, and caspase-dependent apoptotic cell death.

76 HPS4 primarily affects the cells in the G(2)/M phase, and that the drug has a delayed effect with the

77 ytes, the percentage of cardiomyocytes in G2/M phases, and the number of cardiomyocytes by 10% in cul

78 ed proportion of total division time in S/G2/M phases, and this proportion is correlated between sibl

79 per chromosome segregation, arrests cells at M-phase, and delays overall cell cycle progression.

80 early embryonic cell cycle, not just during M-phase, and how Thr-295 is kept dephosphorylated during

81 exit but also applies to entry into meiotic M-phase, and identify a crucial APC/C-PP6c-Aurora A axis

82 demonstrate that factors controlling the G2/M phase are necessary to block pluripotency upon inducti

83 ious melanoma cell lines and could induce G2/M phase arrest and cell apoptosis.

84 ation of p21 expression and a significant G2/M phase arrest in T24T and HCT116 cells without affectin

85 ination reduced AR degradation and abrogated M phase arrest induced by 2-ME.

86 also increased the G2/S ratio, indicating G2/M phase arrest.

87 epidermal JB6 P+ cells at the level of G(2)-M phase arrest.

88 ions to cell-cycle kinases that mediate G(2)-M phase arrest.

89 ell proliferation, migration, and induced G2/M phase arrest.

90 R is the major DNA repair mechanism after G2/M phase arrest.

91 methyl sulfoxide) platinum(II) 3a induced G2/M phase arrest.

92 M-phase arrest and the consequent induction of apoptosis

93 Q mimicked Q deprivation--causing S- and G2/M-phase arrest in K-Ras mutant cancer cells.

94 Ectopically expressed FBXL2 triggered G2/M-phase arrest, induced chromosomal anomalies and increa

95 that conditional Sp2-null NSCs and NPCs are M phase arrested in vivo.

96 of functional cohesin complexes, at least in M phase-arrested cells.

97 the induction of cell cycle arrest in the G2/M phase as a direct consequence of effective tubulin bin

98 ate the modulation of MT stability in G2 and M phase as a regulatory element in the control of centro

99 splayed a delayed cell cycle entry into G(2)/M phase at 24 h after initiation of adipogenesis.

100 urs only near 4.8 TPa, where the metallic C2/m phase becomes most stable.

101 Moreover, a cell cycle G2/M phase block was observed at high-dose combinations, co

102 linked by catenated strands of DNA) and a G2/M-phase block characteristic of the decatenation checkpo

103 bitor p21(WAF1/CIP1), leading to specific G2/M phase blockade in KRAS-mutant cells.

104 moting homologous recombination repair in G2/M phase but also facilitating fidelity of Ku80-dependent

105 st of the PC3 cell cycle at the G0/G1 and G2/M phases but did not affect the DU145 cell cycle, althou

106 rylation events additively activate CPEB4 in M-phase by maintaining it in its monomeric state.

107 post-mitotic endocycles, as we find only the M-phase-capable polyploid cells of the papillae and fema

108 ionization at the interface of the LC and MS/MS phases, causing under- or overestimation of metabolit

109 mation of multinucleate cells by restraining M phase CDK activity to allow bud formation prior to nuc

110 Once a bud has formed, M phase CDK drives cells through a normal mitotic divisi

111 cytotoxicity for cancer cells by inducing G2/M phase cell cycle arrest and apoptosis.

112 Pharmacologically these compounds lead to G2/M phase cell cycle arrest and induction of cellular apop

113 re, knockdown of FEN1 resulted in G1/S or G2/M phase cell cycle arrest and suppressed in vitro cellul

114 ion also impairs proliferation and causes G2/M phase cell cycle arrest with concurrent down-regulatio

115 cells, A2780/WT and A2780/PTX(R), induced G2/M phase cell cycle arrest, and improved chemo-resistance

116 ell growth was related to an induction of G2/M phase cell cycle blockade.

117 G(1) phase cell population and increased the M phase cell population, while infection with the ORF12

118 ied by cell senescence and let-7 inducing G2-M phase cell-cycle arrest without senescence.

119 diation-induced DNA damage, aneuploidy, G(2)/M phase cell-cycle arrest, and apoptosis.

120 antagonizes the ability of RASSF1A to induce M-phase cell cycle arrest.

121 c kinase Plk1 (Polo-like kinase 1) and other M-phase cell-cycle proteins, which may underlie AI PCa g

122 androgen receptor cofactor to drive G(2) to M-phase cell-cycle transit.

123 d GFAP with significant decreases in both G2/M phase cells and cell number.

124 hases and is displaced from the chromatin of M-phase cells, suggesting that LSD1 or H3K4me2 alternati

125 iferating cells transit from interphase into M-phase, chromatin undergoes extensive reorganization, a

126 M-phase chromosomes are also resected in cell-free extra

127 The M phase clustering of Kv2.1 at PM:ER MCS in COS-1 cells

128 ers of Kv2.1 are localized to PM:ER MCS, and M phase clustering of Kv2.1 induces more extensive PM:ER

129 Six2Cre(+);p53(fl/fl) cells in the S and G2/M phases compared with Six2Cre(+);p53(+/+) cells.

130 stored Cdc20 inhibitor production and normal M phase control.

131 ARPP19 stands at a crossroads in the meiotic M-phase control network by integrating differential effe

132 ln1 and Cln2, and not by Cln3 or later S- or M-phase cyclins, but the responsible cyclin interface wa

133 As expected, MCM-2-7 loading in late M phase depended on the prereplicative complex (pre-RC)

134 activity with LY294002 reduced the G(1) and M phase differences observed in cells infected with wild

135 wer than control cells and accumulated in G2/M phase due to chronic activation of a DNA damage respon

136 Cdk1 promotes S- and M-phases during the cell-cycle but also suppresses endor

137 a microsecond phase, we observe a slower 1.4-ms phase during refolding to the native state.

138 eplicated chromosomes to the daughter cells (M phase) during eukaryotic cell division is governed by

139 During M phase, Endosulfine (Endos) family proteins are phospho

140 t and specific to the cell cycle phase as G2/M phase enriched cells show a 6-fold increase in targeti

141 other dimension to Hec1 function centered on M phase entry and early prometaphase progression and cha

142 ting factor (MPF); Gwl is thus essential for M phase entry and maintenance.

143 Unexpectedly, impaired M phase entry is due to instability of the Cdk1-activati

144 r mechanism whereby FlnA loss impaired G2 to M phase entry, leading to cell cycle prolongation, compr

145 to Xenopus embryo cycling extract delays the M-phase entry and inhibits CDK1 during the whole M-phase

146 ting not only the M-phase exit, but also the M-phase entry and progression via limiting the level of

147 We propose a novel mechanism of M-phase entry controlled by CDC6 and counterbalancing cy

148 ition by CDC6, which tunes the timing of the M-phase entry during the embryonic cell cycle.

149 During M-phase entry in metazoans with open mitosis, the concer

150 egulation of endogenous CDC6 accelerates the M-phase entry, abolishes the initial slow and progressiv

151 cterized by a slowing of S phase, a block to M-phase entry, and the ability to re-enter M phase rapid

152 ng an intact Thr-295 residue further delayed M-phase entry.

153 7 dpi, with the proportion of cells in S and M phase exceeding control levels at 5-6 and 6 dpi, respe

154 observed that cells were arrested at the G2/M phase, exhibiting accumulation of cyclins, shrunken sp

155 ponsible for dephosphorylating pEndos during M phase exit.

156 ing cell-cycle transitions is not limited to M-phase exit but also applies to entry into meiotic M-ph

157 It also regulates M-phase exit by inhibiting the activity of the major M-p

158 tributes to two key events that occur during M-phase exit in metazoans: kinetochore disassembly and n

159 Pnuts destruction during M-phase exit is mediated by the anaphase-promoting compl

160 es as CDK1 inhibitor regulating not only the M-phase exit, but also the M-phase entry and progression

161 wn for its role in the mitotic cell cycle at M-phase exit, in G1, and in maintaining genome integrity

162 Disruption of Pnuts degradation delayed M-phase exit, suggesting it as an important mechanism to

163 At M-phase exit, these major changes in cellular architectu

164 sting it as an important mechanism to permit M-phase exit.

165 Here, we identify M phase GAP (MP-GAP) as the primary GAP targeting RhoA d

166 The cell-cycle G(2)-M phase gene UBE2C is overexpressed in various solid tum

167 hat FOXM1 strongly activates promoters of G2/M phase genes and weakly activates those induced in S ph

168 ing endomitosis, they have low expression of M-phase genes.

169 In M phase, Greatwall phosphorylates endosulfine and relate

170 By late M phase, however, Hec1 and cyclin B2 become uncoupled, a

171 even when chromosomes are fully condensed in M phase implicates genome organization in epigenetic inh

172 les and blocked cell-cycle progression at G2-M phase in hepatoma cells via downregulation of CDK1, in

173 ngth of the cell cycle, particularly for the M phase in NSPCs.

174 s tested induced cell cycle arrest at the G2/M phase in PDFS cells derived from a human NFA.

175 duced apoptosis and in arresting cells at G2/M phase in response to DNA-damaging treatment.

176 , also known as Scant in Drosophila, induces M phase in the absence of progesterone when expressed in

177 ient constitutive kinase activity to promote M phase in Xenopus oocytes.

178 plexes for genes expressed during the G2 and M phases in Arabidopsis that can be temporarily separate

179 but little is known on the coupling of S and M phases in unperturbed conditions.

180 Here, we show that the first M-phase in the mouse embryo is significantly extended du

181 cant changes in gene groups that control the M phase, including anaphase-promoting complex genes, via

182 on intermediates in these cells persist into M phase, increasing the number of abnormal anaphase cell

183 n-proliferative multinuclear cells in the G2/M phase, indicating that these two drugs synergize.

184 Cs in S-phase, but had no effect on G1 or G2/M phases, indicating that alcohol specifically targets S

185 ites in these Cdc25 isoforms increases their M-phase-inducing activities.

186 M phase induction by Scant Greatwall requires protein sy

187 nase has been identified as a key element in M phase initiation and maintenance in Drosophila, Xenopu

188 d irreversible transition from interphase to M phase is essential to separate DNA replication from ch

189 In vertebrates, mitotic and meiotic M phase is facilitated by the kinase Greatwall (Gwl), wh

190 In many species the first embryonic M-phase is significantly prolonged compared to the subse

191 to show that its function during late G2 and M-phase is truly required for shaping mitotic chromosome

192 2 films can be ascribed to the presence of p/m phase junctions at the interface.

193 thesis and inhibitory phosphorylation of the M-phase kinase, Cdk1.

194 hibition caused excessive RhoA activation in M phase, leading to the uncontrolled formation of large

195 ported to exhibit phase-phase coupling, or n:m phase-locking, suggesting an important mechanism of ne

196 equency harmonics may generate artifactual n:m phase-locking.

197 cells also expressed pHistone-H3, a late G2/M phase marker detected in approximately 20% of cells du

198 teasomal or lysosomal degradation in S or G2/M phase MIA PaCa-2 cells, respectively.

199 e gamma-tubulin ring complex, and during the M-phase (mitosis) this complex accumulates at the centro

200 d that it caused accumulation of cells in G2/M phase (mitotic blockade) and depolymerization of tubul

201 biquitination in interphase, whereas in G(2)/M phase, NIPA is inactivated by phosphorylation to allow

202 es showed that 10ae arrested the cells in G2/M phase of cell cycle.

203 e network case studies are related to the G2/M phase of the Ascomycota cell cycle; the third is relat

204 PAF15 protein levels peak in the G2/M phase of the cell cycle and drop rapidly at mitotic ex

205 n up to 30-fold by arresting cells in the G2/M phase of the cell cycle and influencing intracellular

206 over, 5f induced cell cycle arrest in the G2/M phase of the cell cycle in a concentration dependent m

207 ghly significant number of genes from the G2/M phase of the cell cycle, and WT1 knockdown experiments

208 mpounds caused the cells to arrest in the G2/M phase of the cell cycle, as would be expected for inhi

209 O-GlcNAc, hindered the transition from G2 to M phase of the cell cycle, displaying a phenotype simila

210 cle progression by arresting cells in the G2/M phase of the cell cycle, retarding cell growth.

211 and 44 arrested >80% of HeLa cells in the G2/M phase of the cell cycle, with stable arrest of mitotic

212 d activate gene expression during the G2 and M phase of the cell cycle.

213 the hinge domain occurs preferentially at G2/M phase of the cell cycle.

214 e CDK1 at T119, S289, and S367 during the G2-M phase of the cell cycle.

215 mitosis, perhaps to promote transition into M phase of the cell cycle.

216 r (NER) and a reduced dATP level in the G(2)/M phase of the cell cycle.

217 the RNMT regulatory domain on T77 during G2/M phase of the cell cycle.

218 recognition complex to either S phase or G2/M phase of the cell cycle.

219 CDK1) at Ser(119) and Ser(175) during the G2/M phase of the cell cycle.

220 ied ovarian cancer cells to arrest in the G2/M phase of the cell cycle.

221 mark post-replicative chromatin until the G2/M phase of the cell cycle.

222 Geminin is present during the S, G2, and M phases of the cell cycle and is degraded during the me

223 Whi5 is synthesized in S/G2/M phases of the cell cycle in a largely size-independent

224 quitination and degradation during G1 and G2/M phases of the cell cycle, whereas the Dia2 protein is

225 PCTAIRE1 phosphorylates p27 during the S and M phases of the cell cycle.

226 ter transcripts and arrested cells in G2 and M phases of the cell cycle.

227 vated levels of genes associated with the G2-M phases of the cell cycle.

228 ce, showed a peak of expression in the S and M phases of the cell cycle.

229 n ligase complex SCF(cyclin F) during G2 and M phases of the cell cycle.

230 the proportion of NPCs within G1, S, and G2/M phases of the cell cycle.

231 cumulation was observed during the S- and G2/M- phase of cell cycle.

232 rmed sister chromatids) from S-phase through M-phase of the cell cycle, each sister pair becomes teth

233 upied genes control apoptosis and govern the M-phase of the cell cycle.

234 pendent apoptosis and arrest cells in the G2/M-phase of the cell cycle; however, using confocal micro

235 M-phase phosphoprotein 8 (MPP8) harbors an N-terminal ch

236 mutant had a reduced effect on the G(1) and M phase populations.

237 Flubendazole halted support cell division in M-phase, possibly by interfering with normal microtubule

238 As the name suggests, during M phase PP2A-B55's attention is diverted to pEndos, whic

239 High Cdk activity during S-G2-M phases produces high levels of the DNA replication fac

240 Similar to M phase progression in maturing Xenopus oocytes, the des

241 Moreover, HDAC3 controls G2/M phase progression mainly through posttranslational sta

242 strated that FoxM1 was required for the G(2)-M phase progression through regulating Cdc2, Cdc20, and

243 pression of cell-cycle regulators that drive M phase progression.

244 CycC, together with Cdk8, primarily affects M-phase progression but mutations that release Cdk8 from

245 kinase 1 (Plk1) plays a pivotal role during M-phase progression.

246 DG) and UA-4 induced cell cycle arrest in G2/M phase, promoted caspase-dependent cell death, reduced

247 New work reveals that the M-phase promoting kinase is opposed by a phosphatase tha

248 phosphorylations added to target proteins by M phase-promoting factor (MPF); Gwl is thus essential fo

249 exit by inhibiting the activity of the major M-phase protein kinase CDK1.

250 regulation, such as spindle, kinetochore and M phase proteins, which are essential for accurate chrom

251 o M-phase entry, and the ability to re-enter M phase rapidly in response to re-feeding.

252 luding delayed progression from S-phase into M-phase, reduced DNA replication in asynchronous culture

253 ssociated with accumulation of cells in G(2)/M phase; reduced levels of cyclin B1, cyclin A, cyclin d

254 ant for cyclin B2 stabilization during early M phase, required for the initial stages of acentrosomal

255 Despite generation of RPA-ssDNA, M-phase resection does not lead to ATR activation or Rad

256 In contrast to the events in S phase, M-phase resection is solely dependent on MRN-CtIP.

257 In later stages of MS, phase rim lesions continue to smolder, exerting detr

258 Thus, M phase-specific H3T3 phosphorylation is governed by the

259 Here we demonstrate that M phase-specific phosphorylation of the intramolecular i

260 Gwl itself is activated by M phase-specific phosphorylations that are investigated

261 ivates the phosphatase PP2A/B55 to stabilize M-phase-specific phosphorylations added to many proteins

262 The M-phase specificity of NPC contact reflects a regulatory

263 system for microtubule reorganization during M-phase spindle assembly.

264 omyocytes in G0/G1 phase and reduction in G2/M phase, suggesting that ENSMUST00000117266 is involved

265 ons in G1/S transition, and nocodazole, a G2/M phase synchronizer, doubles HDR efficiency to up to 30

266 ocalizes to centrioles primarily in S and G2/M phases, the periods during which centrioles duplicate

267 CIP2A strongly interacts with NEK2 during G2/M phase, thereby enhancing NEK2 kinase activity to facil

268 k1 induces persistent ssDNA-RPA overhangs in M phase, thereby preventing both classical NHEJ and Rad5

269 nuclear assembly during the transition from M phase to interphase.

270 extends the availability of dATP in the G(2)/M phase to promote the repair of NER-mediated single-str

271 induced structure transformation from the C2/m phase to the C2 phase in MgV2O6 was detected above 20

272 response and induce growth arrest at the G2/M phase, to induce senescence, as well as autophagy, res

273 TP, which localizes to the bud tip until the M phase, to the division site at cytokinesis, and then t

274 When Gwl is inactivated during the M phase-to-interphase transition, the dynamic balance ch

275 s G(1) to S-phase transit as well as G(2) to M-phase transit through two distinct mechanisms.

276 cal isolates, we found that the degree of G2/M phase transition delay correlated with PSMalpha1 produ

277 S. aureus MW2 (USA400) bacteria induced a G2/M phase transition delay in HeLa cells.

278 ynthetic PSMalpha1 and PSMalpha3 caused a G2/M phase transition delay.

279 lin A2, which was involved in the S and G(2)/M phase transition during cell cycle progression, was in

280 and antagonizes Chk1 to promote the S-to-G2/M phase transition.

281 ion of the CLB2 cluster of genes at the G(2)/M phase transition.

282 , DAZ1/DAZ2 are sufficient to promote G2- to M-phase transition and germ cell division in the absence

283 heckpoint pathways that prevent the G(2)- to M-phase transition in cells with unreplicated or damaged

284 factor FOXM1 is an essential effector of G2/M-phase transition, mitosis and the DNA damage response.

285 G1 Conversely, cells isolated during S or G2-M phases underwent death following mitotic arrest.

286 sted mouse oocytes do not prevent entry into M phase, unless levels of damage are severe.

287 ession was tightly coupled to S phase and G2/M phase via both transcriptional and post-transcriptiona

288 phases with an accumulation of cells in G(2)/M phase was observed, compared to mock-infected controls

289 HepG2 cells in G0/G1, early S, late S and G2/M phases, we found that DNA methylation may act as the p

290 urveillance mechanisms arose when both S and M phases were coincidently set into motion by a unique a

291 netochore complex are normally restricted to M phase when it exerts a pivotal kinetochore-based role.

292 In M phase, when tRNA synthesis peaks, tDNAs localize at nu

293 r-protein genes results in arrest in the G2/M phase, whereas repression of nine other 60S and 22 40S

294 ors disrupted transitions through G1, G2 and M phases, whereas DNA synthesis appeared intact.

295 cell proliferation and arrests cells at G(2)/M phase, which is accompanied by an increased level of p

296 It also blocks the cell cycle at G2/M phase, which is explained by the fact that it inhibits

297 n mid G1 phase and lower levels during S and M phases, while in smt15-1, glutathione levels remained

298 d in an increase in cells arrested at the G2/M phase with a concurrent decrease in S-phase cells.

299 onsists of a long G1 phase, followed by an S/M phase with multiple rapid, alternating rounds of DNA r

300 he heterotrimeric RCC1/Ran/RanBP1 complex in M phase Xenopus egg extracts controls both RCC1's enzyma