ライフサイエンスコーパス: G1 phase

1 ble for targeting cell cycle proteins during G1 phase.

2 ion but blocked cell cycle progression in G0/G1 phase.

3 5 concentrations that extend their pre-Start G1 phase.

4 by gradual removal from chromatin during the G1 phase.

5 in D:Cdk4/6, is the only Rb isoform in early G1 phase.

6 mating pheromones arrests the cell cycle in G1 phase.

7 low the recruitment of 53BP1 to chromatin in G1 phase.

8 specifically suppress the HR-pathway in the G1 phase.

9 dramatically shortening the duration of the G1 phase.

10 RCA1 to damage sites is inhibited by RIF1 in G1 phase.

11 ke state with permanent cell cycle arrest in G1 phase.

12 e ability to arrest cancer cell cycle in the G1 phase.

13 sis, and then to the distal pole in the next G1 phase.

14 nonhomologous end-joining (NHEJ) pathway in G1 phase.

15 cycle mutant that reversibly arrests in the G1 phase.

16 2 expression and results in growth arrest in G1 phase.

17 converted to stable interactions from early G1 phase.

18 in D1/Cdk4 exerts its function mainly in the G1 phase.

19 e Scc2-Scc4 cohesin loader to centromeres in G1 phase.

20 22 40S r-protein genes causes arrest in the G1 phase.

21 ntry until sufficient growth has occurred in G1 phase.

22 ly rarely active in unperturbed cells during G1 phase.

23 tch on a transcriptional program during late G1 phase.

24 ss U:G base pairs at all in Ig genes outside G1 phase.

25 ylation, leading to cell cycle arrest in the G1 phase.

26 apoptosis induction and cell cycle arrest at G1 phase.

27 while HSV-1 DNA replication is restricted to G1 phase.

28 proteins at mitotic exit and throughout the G1 phase.

29 urring most proficiently by parasites in the G1 phase.

30 CM binding, and a subsequent accumulation in G1 phase.

31 zed by a high proliferation rate and a short G1 phase.

32 nd an increased accumulation of cells in the G1 phase.

33 t at G2/M phase and cell accumulation in sub-G1 phase.

34 n damage induction, specifically outside the G1 phase.

35 ipotency is linked to lineage priming in the G1 phase.

36 rigins of DNA replication exclusively during G1 phase.

37 tial to reprogram replication timing late in G1 phase.

38 but not APC/C(C)(dc20), in late mitosis and G1 phase.

39 accessibility that is especially dynamic in G1 phase.

40 cription, exceeding levels observed later in G1 phase.

41 in targeting efficiency compared to cells in G1 phase.

42 tain clusters of cancer cells that arrest in G1 phase.

43 tive capacity due to "contact-inhibition" at G1 phase.

44 me segregation in mitosis and entry into the G1 phase.

45 of cell cycle of MCF-7 and HL-60 cells at G0/G1 phase.

46 uole and a specific arrest of cells in early G1 phase.

47 te replicating regions of the genome in late G1 phase.

48 ) function and the presence of RNA in the G0/G1 phase.

49 nd-joining (MMEJ), a subtype of alt-NHEJ, in G1-phase.

50 sions also die or arrest, mostly in the next G1-phase.

51 rigins in vivo but cells remained blocked in G1-phase.

52 D1 down-regulation and cell cycle arrest in G1-phase.

53 ies were necessary for cells to re-enter the G1-phase.

54 p<0.003) induced cell cycle arrest in the G0/G1 phases.

55 ogenic differentiated counterparts with long G1 phases.

56 lation of p21 during mother G2- and daughter G1-phases.

57 The typical pattern is two EGJ in G1 phase (1 kinetoplast/1 nucleus, 1K1N) through S-phase

58 a population peak due to cells at the end of G1 phase (1-fold) and a peak due to cells entering M pha

59 In late G1 phase, a large fraction of MCM proteins are loaded on

60 ones is a main component of this abbreviated G1 phase, although the details of this mechanism are not

61 t there is a lower frequency of cells in the G1 phase among old compared with young long-term HSCs, s

62 with SsnB showed an increase of cells in the G1 phase and a decrease of cells in the S phase.

63 ndrial membrane potential, cell arrest in G0/G1 phase and apoptosis/necrosis in a dose-dependent mann

64 excluded from the nucleus during part of the G1 phase and at the transition from G0 to G1.

65 n during mitosis; CDK6 remains SUMOylated in G1 phase and drives the cell cycle through G1/S transiti

66 tering of a subset of replication origins in G1 phase and for the early initiation of these origins i

67 n, resulting in cell cycle inhibition at the G1 phase and increased caspase 3 activity and apoptosis.

68 ing that the unique relationship between the G1 phase and invasion effectively synchronizes short-ter

69 proteins for degradation in mitosis and the G1 phase and is an important component of the eukaryotic

70 xameric MCM2-7 complex onto chromatin during G1 phase and is dependent on the licensing factor Cdt1.

71 eted to centromeres exclusively during early G1 phase and is subsequently maintained across mitotic d

72 g the cell cycle, with highest levels in mid G1 phase and lower levels during S and M phases, while i

73 ignaling to arrest cell cycle progression in G1 phase and promoted sexual differentiation.

74 rease of neonatal mouse cardiomyocytes in G0/G1 phase and reduction in G2/M phase, suggesting that EN

75 y, we found that the cell cycle arrest at G0/G1 phase and the alterations of CDK4/6 and Cyclin D1 tri

76 cycle, increasing first transiently in late G1 phase and then again later in G2/M.

77 M) proteins are loaded onto chromatin during G1-phase and define potential locations of DNA replicati

78 selinexor treatment occurs from a protracted G1-phase and early S-phase.

79 at excess MCM2-7 complexes are loaded during G1 phase, and are required during S phase to overcome re

80 n of p21, p27, and p53, cell cycle arrest at G1 phase, and cell apoptosis.

81 that proper levels of p27 accumulate during G1 phase, and defects in its activation accelerate the t

82 cl-XL, an arrest of the cell cycle at the G0/G1 phase, and eventually apoptosis.

83 53BP1 nuclear body formation in the ensuing G1 phase, and G1 arrest.

84 that the bulk of the variation occurs in the G1 phase, and many mathematical models assume a constant

85 s first loaded at replication origins during G1 phase, and then converted to the active CMG (Cdc45-MC

86 cell growth, to delay the cell cycle in the G1 phase, and to strain or even destroy the microenviron

87 h cells in S phase than with cells in G2 and G1 phases, and S-phase cells contained 10 times more bac

88 sion through the cell cycle and a very short G1 phase are defining characteristics of embryonic stem

89 transcriptionally active sites during the G0/G1 phase are largely unknown.

90 ar apoptosis induction was accompanied by G0/G1 phase arrest and DNA fragmentation.

91 Depletion of TOB1 selectively promoted G1 phase arrest and sensitivity to AKT and mammalian tar

92 d impaired [(3)H]thymidine incorporation and G1 phase arrest as compared with wild type (P4WT).

93 em cell tumorigenicity by enhancing multiple G1 phase arrest pathways rather than by silencing p21Cip

94 cle alteration with S phase reduction and G0/G1 phase arrest, induce cell apoptosis via the activatio

95 e) resulted in decreased cell viability with G1-phase arrest and disruption of Wnt/beta-catenin signa

96 activated DNA damage checkpoints, and showed G1-phase arrest at atmospheric oxygen levels (21%).

97 nsistently, the mutant cardiomyocytes showed G1-phase arrest due to activation of the p53-mediated DN

98 in levels of p16(INK4a) and p21(Waf1); (iii) G1-phase arrest of the cell cycle; and (iv) decreases in

99 n of cell viability was associated with: (i) G1-phase arrest, (ii) inhibition of expressions of cycli

100 licase complex at replication origins during G1 phase as an inactive double hexamer.

101 d also restored DSB-repair proficiency in G0/G1 phase as measured by pulsed-field gel electrophoresis

102 haromyces cerevisiae, size control occurs in G1 phase before Start, the point of irreversible commitm

103 Initiation of HR in the G1 phase blocks non-homologous end joining (NHEJ) impair

104 During the G1 phase, both CDK and DDK are downregulated, which allo

105 Mcm2-7 loads onto chromatin during early G1 phase but is not converted into an active helicase un

106 eractions decreased considerably compared to G1-phase, but were resumed in G2-phase, indicating that

107 s license each DNA replication origin during G1 phase by assembling a prereplication complex that con

108 is exclusively mono-phosphorylated in early G1 phase by cyclin D:Cdk4/6.

109 of AIB1 inhibited cell cycle progression at G1 phase by decreasing the mRNA levels of cyclin A2, cyc

110 tivates the Rb tumor suppressor during early G1 phase by progressive multi-phosphorylation, termed hy

111 We show that both 1 and 3 cause G1 phase cell cycle arrest at lower concentrations, foll

112 -transactivated p21 expression and abolished G1 phase cell cycle arrest in stomach cancer.

113 Induction of a G1 phase cell cycle arrest, caused primarily by the inhi

114 prostate cancer cells, with miR-34a inducing G1 phase cell-cycle arrest accompanied by cell senescenc

115 d miR-149* blocked cell growth leading to G0-G1 phase cell-cycle arrest and apoptosis in colorectal c

116 oduced dose-dependent cytotoxicity, caused a G1 phase cell-cycle arrest and induced apoptosis.

117 evels) decreased proliferation and induced a G1 phase cell-cycle arrest.

118 SGK3 attenuated melanoma growth by inducing G1 phase cell-cycle arrest.

119 ual inhibitors demonstrated that they induce G1-phase cell cycle arrest in breast cancer cells and tr

120 yclohexylmethoxy)-9H-purin-2-amine] leads to G1-phase cell cycle arrest in the marine diatom, Phaeoda

121 ic studies showed that ailanthone induced G0/G1-phase cell cycle arrest, as indicated by decreased ex

122 ntration (0.1-0.5 muM), pevonedistat induced G1-phase cell cycle arrest, downregulation of Bcl-xL lev

123 for podocyte hypertrophy that relies on post-G1-phase cell cycle arrest.

124 ocess, intimately linking AhR biology to the G1-phase cell cycle program.

125 aryl hydrocarbon receptor (AhR) can disrupt G1-phase cell cycle progression following exposure to pe

126 ely regulates nuclear CKI-1 levels to ensure G1-phase cell cycle progression in germ cells.

127 rns transcription of AP-1-element containing G1-phase cell cycle regulators such as Myc and Ccnd1 to

128 nificantly inhibited cell growth by inducing G1-phase cell-cycle arrest in pre-LSCs, reduced LSC freq

129 ive CDK4/6 inhibitors that induce reversible G1-phase cell-cycle arrest in retinoblastoma-positive tu

130 9.66 x 10(-6) and 68.8%, respectively, in a G1-phase cell.

131 ndent growth arrest occurs in stable diploid G1 phase cells before genome instability can occur.

132 no discernible V(D)J recombination defect in G1 phase cells beyond that observed in Atm-deficient cel

133 Analysis of G1 phase cells deficient in H2AX or 53BP1 reveals DNA en

134 We show that ATR kinase activity in G1 phase cells is important for survival after IR and th

135 s is associated with a novel role for ATR in G1 phase cells.

136 of the machinery that can resect DNA ends in G1-phase cells and suggest that there may be species-spe

137 Interestingly, promotion of MMEJ by 53BP1 in G1-phase cells is only observed in the presence of funct

138 triction factor that prevents capsulation in G1-phase cells.

139 ining (NHEJ), the main DSB repair pathway in G1-phase cells.

140 c-NHEJ-proficient but also -deficient human G1-phase cells.

141 Among all G1 phase checkpoint regulators, human p21Cip1 was found

142 the presence of high Cdk activity during the G1 phase, chromatin can be effectively licensed for DNA

143 thyltransferase activity at the beginning of G1 phase, coordinating mRNA capping with the burst of tr

144 rowth, loss of pluripotency and a lengthened G1 phase, correlating with increased polyadenylation of

145 two genes on ChrI-CLN3 and CCR4, encoding a G1-phase cyclin and a subunit of the Ccr4-Not deadenylas

146 rowth arrest was attributed to inhibition of G1-phase cyclin-dependent kinase 2 (CDK2) activity.

147 iescent (G0) rat myoblasts transiting to the G1 phase, cyclin D1 (Ccnd1) mRNA was associated with two

148 RAG DSBs are generated in G1-phase developing lymphocytes, where they activate the

149 ion of a second flagellar basal body in late G1 phase, DNA replication in S phase, and dimethylation

150 Their depletion causes G1-phase dormancy and reversible initiation of the slend

151 y rescuing LNCaP cells from growth arrest at G1 phase due to the lack of androgen.

152 d accelerated hepatocyte progression through G1 phase during the regenerative process.

153 Whereas p110alpha is activated at G1-phase entry and promotes protein synthesis and gene e

154 Chlamydomonas cell cycle consists of a long G1 phase, followed by an S/M phase with multiple rapid,

155 DNA-damage response and cell cycle arrest in G1 phase, followed by apoptosis.

156 uced G2-phase growth arrest (doxorubicin) or G1-phase growth arrest (5-FU).

157 oreover, ectopic CELF1 overexpression caused G1-phase growth arrest, whereas CELF1 silencing promoted

158 ted the greatest purinosome formation in the G1 phase; however, elevated levels of purinosomes were a

159 fter genome replication in S phase occurs in G1 phase; however, how new CENP-A is loaded and stabiliz

160 study, we show that uracils generated in the G1 phase in B cells can generate equal proportions of A-

161 RuphenImH mediates cell cycle arrest in the G1 phase in both cells and is more prominent in p53(+/+)

162 dependent kinase inhibitors that control the G1 phase in cell cycle, only p18 and p27 can negatively

163 They arrest cell growth in G1 phase in contrast to cisplatin (S phase) with a high

164 loss of Pin1 causes cell cycle arrest in the G1 phase in CPCs, concomitantly associated with decrease

165 oride currents, and arrested cells at the G0/G1 phase in nasopharyngeal carcinoma CNE-2Z cells.

166 ggest that, although BLM is downregulated in G1 phase in order to promote NHEJ-mediated DNA repair, i

167 iates at late telophase and continues during G1 phase in somatic tissues in the organism, later than

168 ansfection with Ad VP16hLXRalpha blocked the G1 phase, increased caspase-dependent apoptosis, and slo

169 rochromatic domains, was established in late G1 phase, indicating that origin timing can be reset sub

170 an increase in the percentage of cell in G0/G1 phase induced by RV metabolite treatments, as well as

171 nduced U by UNG2 occurs predominantly during G1 phase, inducing faithful repair, mutagenic processing

172 in which the transition through mitosis and G1 phase is crucial for establishing a window of opportu

173 r cells of these mutants, likely because the G1 phase is shorter and a new bud site is established pr

174 2) interaction of heparin with RMCs in early G1 phase is sufficient to induce signaling pathway(s) fo

175 atory circuitry directing HvyA expression to G1-phase is conserved during evolution, and HvyA ortholo

176 ion of BRCA1/BRCA2/RAD51 specifically in the G1-phase leading to impaired DSB repair.

177 rine diatom, and that arresting cells in the G1 phase leads to remodeling of intermediate metabolism

178 pluripotent stem cells with naturally short G1 phases load MCM much faster than their isogenic diffe

179 that proliferating B cells had a very short G1 phase (<3.5 h), a total cell cycle time of approximat

180 s through DNA DSB intermediates generated in G1-phase lymphocytes by the RAG endonuclease.

181 In G1-phase lymphocytes, DNA ends that are processed by CtI

182 Here, we show that in murine G1-phase lymphocytes, KAP-1 promotes resection of DSBs t

183 e structural integrity of broken DNA ends in G1-phase lymphocytes, thereby preventing these DNA ends

184 (ESCs), where a rapid cell cycle and a short G1 phase maintain the pluripotent state, evidence has be

185 In the G1-phase, MBD3, in the context of the Mi-2/NuRD (nucleos

186 In fact, a shortened G1 phase might protect ES cells from external signals in

187 ble concentrations, by arresting cells at G0/G1 phase of cell cycle and without any induction of KSHV

188 ntrol values without stress induction in the G1 phase of cell cycle.

189 ming program are re-established during early G1 phase of each cell cycle and lost in G2 phase, but it

190 Here we show that geminin is present in G1 phase of mouse pluripotent cells in contrast to somat

191 applications included tracking the transient G1 phase of rapidly dividing mouse embryonic stem cells

192 plication timing is established during early G1 phase of the cell cycle (timing decision point [TDP])

193 strated that cells were markedly arrested in G1 phase of the cell cycle after CDK11(p110) downregulat

194 During CSR, DSBs are produced in the G1 phase of the cell cycle and are repaired by the class

195 Primary cilia start forming within the G1 phase of the cell cycle and continue to grow as cells

196 DNA cleavage by RAG occurs only at the G1 phase of the cell cycle and generates two hairpin-sea

197 The SMuSh pathway delays cells in the G1 phase of the cell cycle and improves cell survival in

198 lecule inhibitor led to cell accumulation in G1 phase of the cell cycle and reduced expression of cel

199 Trim71 knockdown prolongs the G1 phase of the cell cycle and slows embryonic stem cell

200 cation processivity factor PCNA primarily in G1 phase of the cell cycle and, directly, in vitro.

201 creases the proportion of cells in the early G1 phase of the cell cycle and, in more than 25 embryoni

202 -null uterus are able to proceed through the G1 phase of the cell cycle before getting arrested in th

203 prolonging the time that cells spend at the G1 phase of the cell cycle due to an increase in cyclin

204 censing of origins of replication during the G1 phase of the cell cycle has been implicated in Meier-

205 ity led to failure of cells to arrest in the G1 phase of the cell cycle in response to DNA damage.

206 n of critical cellular regulators during the G1 phase of the cell cycle is achieved by anaphase-promo

207 In somatic cells, the length of the G1 phase of the cell cycle is tightly linked to differen

208 kpoints that exist in the latter part of the G1 phase of the cell cycle that are dependent upon essen

209 ration of external growth signals during the G1 phase of the cell cycle to initiate DNA replication.

210 argets on PTEC cell growth (cell size during G1 phase of the cell cycle).

211 This was due to a prolonged G1 phase of the cell cycle, a significant increase in th

212 glucose stimulation require 8 h to enter the G1 phase of the cell cycle, and this time is prolonged i

213 logous recombination is inhibited during the G1 phase of the cell cycle, but both pathways are active

214 Licensing is restricted to G1 phase of the cell cycle, but G1 length varies widely

215 ramatically, and the cells accumulate in the G1 phase of the cell cycle, leading to almost complete p

216 duced accumulation of cyclin D1 shortens the G1 phase of the cell cycle, promotes mitotic replication

217 (NHEJ), a repair process predominant in the G1 phase of the cell cycle, rejoins DSBs either accurate

218 no acids are limiting, T cells arrest in the G1 phase of the cell cycle, suggesting that they have sp

219 During the G1 phase of the cell cycle, they remain loaded on DNA bu

220 11A caused CDKN1B/p27-mediated arrest in the G1 phase of the cell cycle, whereas depletion of RacGAP1

221 ing is the predominant mechanism used in the G1 phase of the cell cycle, while homologous recombinati

222 th stable loss of SOX10 were arrested in the G1 phase of the cell cycle, with reduced expression of t

223 NA damage by restricting RAG activity to the G1 phase of the cell cycle.

224 tion Complex (ORC) onto the chromatin during G1 phase of the cell cycle.

225 ng keratins, where it bound p27(KIP1) during G1 phase of the cell cycle.

226 re-RCs) at origins of replication during the G1 phase of the cell cycle.

227 nd 1 blocks the growth of cancer cells at G0/G1 phase of the cell cycle.

228 on, cytokinesis and the establishment of the G1 phase of the cell cycle.

229 le in maintaining the proper duration of the G1 phase of the cell cycle.

230 ) governs the transition from mitosis to the G1 phase of the cell cycle.

231 Mis18beta, limiting complex formation to the G1 phase of the cell cycle.

232 trates as cells exit mitosis and reenter the G1 phase of the cell cycle.

233 ewal by sustaining rapid transit through the G1 phase of the cell cycle.

234 tivation events and arrested cells in the G0/G1 phase of the cell cycle.

235 from proliferation to differentiation in the G1 phase of the cell cycle.

236 hase restricts V(D)J recombination to the G0-G1 phase of the cell cycle.

237 lasts and arrested both cell lines at the G0/G1 phase of the cell cycle.

238 s uncoupled from limiting amino acids in the G1 phase of the cell cycle.

239 eliminating cum1(+) sense transcript in the G1 phase of the cell cycle.

240 pression of RPL23a resulted in arrest at the G1 phase of the cell cycle.

241 metabolic cycling is associated with the G0/G1 phase of the cell division cycle of slowly growing bu

242 development, we show that lengthening of the G1 phase of the pancreatic progenitor cell cycle is esse

243 Bivalency of developmental genes during the G1 phase of the pluripotent stem cell cycle contributes

244 ure populations of hESCs in G2, mitotic, and G1 phases of the cell cycle, we found striking variation

245 lex that is loaded onto chromatin during the G1-phase of the cell cycle and required for initiation o

246 During G1-phase of the cell cycle, normal cells respond first t

247 During G1-phase of the cell-cycle the replicative MCM2-7 helica

248 Conversely, low Rep protein levels in G1 phase permit HSV-1 replication but are insufficient f

249 The dose- and time-dependent increase of G1 phase population was observed by treatment of 3d alon

250 the mitotic cycle itself, arresting cells in G1 phase prior to the S-phase transition.

251 of MCM-chromatin interactions that differ as G1 phase progresses and do not colocalize with sites of

252 holipase activity, is a critical effector of G1 phase progression through the cell cycle and suggest

253 eine-induced death by methods that inhibited G1 phase progression, including down-regulation of cycli

254 distinct from that of Spt16, which promotes G1 phase progression.

255 cells promotes cell growth arrest at the G0/G1 phase, reduces cell proliferation and delays tumor gr

256 dation during interphase prevents the normal G1 phase regrowth of mitochondrial networks following ce

257 alization patterns at different times during G1 phase, remaining associated with late replicating reg

258 oaded onto chromatin cumulatively throughout G1 phase, showing no detectable exchange with a graduall

259 Analysis of cells in S, G2/M, and G1 phases shows that H4K20me1 increases after S phase an

260 f RB, P107, and P130 in 2i ESCs results in a G1-phase similar to that of serum ESCs.

261 led, which is primarily achieved by the late G1 phase-specific activation of cyclin-dependent kinase

262 istance to radiation-induced DNA damage in a G1 phase-specific manner.

263 equired for joining DSB intermediates of the G1 phase-specific V(D)J recombination reaction in progen

264 ed ubiquitin chains to tankyrase 1, while in G1 phase such ubiquitin chains are removed by BRISC, an

265 simvastatin induced cell cycle arrest at G0/G1 phase, suggested by downregulation of CDK4/6 and Cycl

266 ted SMC growth by arresting cell cycle in G0/G1 phase, suggesting that ablation of YAP-induced impair

267 tion with the key initiation factor Cdc45 in G1 phase, suggesting that Fkh1 and Fkh2 selectively recr

268 e fraction of MCM2 and MCM4 increases during G1 phase, suggestive of reiterative licensing.

269 ecture occurs during a brief period in early G1 phase termed the replication timing decision point (T

270 nd a concomitant cell cycle delay during the G1 phase that enables more efficient clearance of misfol

271 exhibit a unique cell cycle with a shortened G1 phase that supports their pluripotency, while apparen

272 We found that during G1 phase, the APC(Cdh1)-mediated degradation of Clb5 was

273 show that, analogous to the situation in the G1 phase, the Saccharomyces cerevisiae checkpoint kinase

274 In G1 phase, the yeast's 32 telomeres are clustered into 6-

275 42 is activated in two temporal steps in the G1 phase: the first depends on Bud3, whereas subsequent

276 FGF-2 induced both KIS and Cdc25A during the G1 phase; the maximum KIS expression was observed 4 hour

277 cle arrest of the cells, specifically in the G1 phase thereby preventing their progression to the S-p

278 etween replication-timing domains during the G1 phase, thereby revealing a function of Rif1 as organi

279 em cell types display cell cycles with short G1 phases, thought to minimize susceptibility to differe

280 ly of centromeric chromatin is restricted to G1 phase through inhibitory action of Cdk1/2 kinases in

281 HN3 action may involve cell-cycle arrest at G1 phase through Yes-associated protein signaling.

282 leading to the arrest of cell growth in the G1 phase to prepare cells for mating.

283 presses its activity at the beginning of the G1 phase to prevent early activation.

284 3 siRNA inhibited cells to progress from the G1 phase to the S phase, but pretreatments of cells with

285 y delaying the G1/S-phase and the mitosis to G1-phase transitions.

286 n maintaining Gps1 at the bud neck from late G1 phase until midanaphase.

287 r (CKI) p57(KIP2), an important regulator of G1 phase, using deletion mutant mice.

288 , mating pheromones arrest the cell cycle in G1 phase via a pheromone-activated Cdk-inhibitor (CKI) p

289 howed that the proportion of cells in the G0/G1-phase was lower and that of cells in the S-phase was

290 MCF-7 cells concentrated in S-phase or G0/G1-phase were treated for 24 h with short or long multiw

291 therefore, does not efficiently occur during G1 phase when CDK is inactive.

292 ion, we show that DNA synthesis can occur in G1 phase when CDKs and DDK are limited.

293 , and catabolism by SAMHD1 is maximal during G1 phase when large dNTP pools would prevent cells from

294 arrested the cell cycle of melanoma cells in G1 phase, whereas cis-dichlorido[(1,3-dibenzyl)imidazol-

295 1 stably associating with heterochromatin in G1 phase, whereas other ORC subunits have transient inte

296 correlates with cell cycle arrest in the G0/G1 phase, which is mediated by increased expression of p

297 gher number of cells with purinosomes in the G1 phase, which was further confirmed by cell synchroniz

298 lls lacking RABL6A predominantly arrested in G1 phase with a moderate mitotic block.

299 Cells accumulated in G1 phase with oversized pools and stopped growing.

300 -molecule inhibitors (2i ESCs) have a longer G1-phase with hypo-phosphorylated RB, implying that they