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 isiveness of the transitions into and out of M phase.

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

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

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

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

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

8 terphase cells, and robust clustering during M phase.

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

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

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

12 in an increased accumulation of cells in G2/M phase.

13 on during interphase and its reactivation in M phase.

14 e majority of the cells found in the S to G2/M phase.

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

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

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

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

19 ession of cellular transcription during G(2)/M phase.

20 s and led to accumulation of cells in the G2/M phase.

21 characterized by arrest of cells in the G(2)-M phase.

22 ession of cellular transcription during G(2)/M phase.

23 restricted to its functions during the G(2)/M phase.

24 rs progenitors to re-enter the cell cycle at M phase.

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

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

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

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

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

30 ve response with cell cycle arrest at the G2/M phase.

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

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

33 tion is cell cycle dependent, peaking in the M phase.

34 F1 at the G1/S phase and with MyoD at the G2/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 g a lesser proportion of their cell cycle in M-phase.

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

39 chromosomes to hypercompact when delayed in M-phase.

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

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

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

43 concentration around spindle poles in early M-phase.

44 isplayed reduced proliferation and prolonged M-phase.

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

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

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

48 estradiol effects on progression into S and M phases.

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

50 x (PI) - the proportion of cells in S, G2 or M phases.

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

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

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

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

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

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

57 trates, controlling the onset of S phase and M phase [1-3].

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

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

60 e vast majority of treated cells in the G(2)/M phase (89%); 2) induces cell death in PC3 cells even a

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

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

63 The Plk1-null MuSCs are arrested at the M-phase, accumulate DNA damage, and apoptose.

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

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

66 ony formation, causing an increase of the G2/M phase and a reduction of the G0/G1 phase of the cell c

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

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

69 ced the arrest of MDR cancer cells at the G2/M phase and caspase-8-related early apoptosis.

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

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

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

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

74 l cycle-dependent; it was higher in the G(2)-M phase and diminished upon G(1) entry.

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

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

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

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

79 nd 7h can induce cell cycle arrest in the G2/M phase and inhibit proliferation and viability in human

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

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

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

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

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

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

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

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

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

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

90 cell migration, arrests cell cycle at the G2/M phase, and induces expression of p(21CIP1) (cyclin-dep

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

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

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

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

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

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

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

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

99 human epidermal keratinocytes (NHEK) from G2/M phase arrest under high-dose X-ray irradiation.

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

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

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

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

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

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

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

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

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

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

110 ruses can be strongly stimulated during G(2)/M phase as a result of inhibition of antiviral gene expr

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

112 The Fd[Formula: see text]m phase at 500 GPa forms buckled honeycomb layers that g

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

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

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

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

117 Restriction of Mus81-Mms4 to M phase but not S phase allows a wildtype response to va

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

119 ion from occurring during S, G(2), and early M phases by preventing MCM helicases from forming prerep

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

121 ests that high [(18)F]FDG uptake in S, G2 or M phases can be largely attributed to increased dry mass

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

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

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

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

126 using microscopy, root growth kinematics, G2/M phase cell count, ploidy levels and ribosome polysome

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

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

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

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

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

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

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

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

135 nt kinase 1 (CHK1)-mediated S-phase and G(2)-M-phase cell-cycle checkpoints has been a promising ther

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

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

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

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

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

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

142 stored Cdc20 inhibitor production and normal M phase control.

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

144 Our data suggest that the G(2)/M phase could represent an "Achilles' heel" of the infec

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

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

147 on the capillary number (Ca)-viscosity ratio(M) phase diagram.

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

149 n heart chamber, we found that CMs in the G2/M phase downregulated sarcomeric and cytoskeletal marker

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

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

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

153 d using proliferative (P)- and midsecretory (MS)-phase endometrium and integrated with the transcript

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

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

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

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

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

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

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

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

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

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

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

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

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

167 7 dpi, with the proportion of cells in S and M phase exceeding control levels at 5-6 and 6 dpi, respe

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

169 ponsible for dephosphorylating pEndos during M phase exit.

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

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

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

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

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

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

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

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

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

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

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

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

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

183 ort from the 2-cohort-locally advanced and R/M-phase II KEYNOTE-629 study.

184 , fully grown G2-stage oocytes readily enter M phase immediately following chemical induction of DNA

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

186 new [1,2]oxazoles to arrest cells in the G2/M phase in a concentration dependent manner and to induc

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

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

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

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

191 DUBs specifically in respective G1/S and G2/M phases in synchronized HeLa cells.

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

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

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

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

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

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

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

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

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

201 2 films can be ascribed to the presence of p/m phase junctions at the interface.

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

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

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

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

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

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

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

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

210 The Im 3 m phase of D(3) S samples exhibits a T(c) significantly

211 ghly efficient synchronization method for G2/M phase of sheep fibroblasts, which was successfully app

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

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

214 tubular epithelial cells arrested at the G2/M phase of the cell cycle and suppressed phosphorylation

215 ubiquitylation and degradation during the G2/M phase of the cell cycle and upon challenging cells wit

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

237 usly, we demonstrated that the G(1) and G(2)/M phases of the host cell cycle are permissive for Legio

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

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

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

241 During late M-phase of the cell-cycle, Cdc6 binds to ORC and the ORC

242 ves the progression of cells into the S- and M-phases of the cell cycle.

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

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

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

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

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

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

249 sing Lmnb2 expression promoted cardiomyocyte M-phase progression and cytokinesis and improved indicat

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

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

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

253 ne/threonine kinase 1 (CDK1) to generate the M phase-promoting factor (MPF) activity essential for pr

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

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

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

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

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

259 lectively, our results suggest that a novel, M-phase specific mechanism of ER-MT association that is

260 ynein RNAi cells, revealing activation of an M-phase specific mechanism of ER-MT association.

261 The induced leaf cells expressed M phase-specific genes of Arabidopsis encoding the mitot

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

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

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

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

266 compounds inducing cell cycle arrest in G(2)/M phase strongly enhanced the replication of VSV-DeltaM5

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

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

269 ls take up twice more [(18)F]FDG in S, G2 or M phases than in G1 phase, which confirms the associatio

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

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

272 The G(2)/M phase thus could represent an "Achilles' heel" of the

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

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

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

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

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

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

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

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

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

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

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

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

285 , arresting cell cycle progression at the G2/M phase, triggering apoptosis, and inhibiting vascular e

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

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

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

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