ライフサイエンスコーパス: G1 phase

1 of clusters increased as cells grew through G1 phase.

2 accessibility that is especially dynamic in G1 phase.

3 cription, exceeding levels observed later in G1 phase.

4 in targeting efficiency compared to cells in G1 phase.

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

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

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

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

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

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

11 lume without diminishing size control in the G1 phase.

12 ble for targeting cell cycle proteins during G1 phase.

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

14 5 concentrations that extend their pre-Start G1 phase.

15 by gradual removal from chromatin during the G1 phase.

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

17 mating pheromones arrests the cell cycle in G1 phase.

18 rom the nuclear periphery to the interior in G1 phase.

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

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

21 dramatically shortening the duration of the G1 phase.

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

23 until repair is reactivated in the following G1 phase.

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

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

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

27 we find that global mobility is triggered in G1 phase.

28 cycle mutant that reversibly arrests in the G1 phase.

29 2 expression and results in growth arrest in G1 phase.

30 converted to stable interactions from early G1 phase.

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

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

33 22 40S r-protein genes causes arrest in the G1 phase.

34 ly rarely active in unperturbed cells during G1 phase.

35 tch on a transcriptional program during late G1 phase.

36 t, a specific growth site is selected in the G1 phase.

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

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

39 mosome segregation, and transition from M to G1 phase.

40 required to hyperphosphorylate Rb throughout G1 phase.

41 o S phase, Rad51 foci form at high levels in G1 phase.

42 ithout indication of cell cycle arrest in G0/G1 phase.

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

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

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

46 ntry until sufficient growth has occurred in G1 phase.

47 apoptosis induction and cell cycle arrest at G1 phase.

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

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

50 n damage induction, specifically outside the G1 phase.

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

52 osphorylate MYBL2, and arrest tumor cells in G1 phase.

53 rigins of DNA replication exclusively during G1 phase.

54 tial to reprogram replication timing late in G1 phase.

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

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

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

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

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

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

61 ogenic differentiated counterparts with long G1 phases.

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

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

64 from low copy numbers of transcripts in the G1 phase, 2) identifies the size and time regulation mod

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

66 is rates for E2F8 at different points within G1 phase, accounting for its accumulation in late G1 whi

67 ative helicase that is assembled onto DNA in G1-phase (also known as origin licensing).

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

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

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

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

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

73 on of ABHD5 induces cell cycle arrest at the G1 phase and causes growth retardation in a panel of pro

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

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

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

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

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

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

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

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

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

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

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

85 that recapitulate distinct inter-mitotic and G1 phases and a continuous transition from prometaphase

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

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

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

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

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

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

92 53BP1 nuclear body formation in the ensuing G1 phase, and G1 arrest.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

110 storation of AKT phosphorylation rescued the G1 phase block triggered by RABL6A silencing.

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

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

113 entry is mitogen-independent in the daughter G1 phase, but remains sensitive to DNA damage, such as s

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

131 HRF1 degradation at mitotic exit accelerates G1-phase cell cycle progression and perturbs global DNA

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

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

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

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

136 9.66 x 10(-6) and 68.8%, respectively, in a G1-phase cell.

137 ng with respect to target promoters in small G1 phase cells and accumulate as cells grow, raising the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

159 ted subtelomeric DNA replication in G2/M and G1-phase-enriched cells.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

174 rst G1 upon cell cycle entry and the shorter G1 phases in the second and subsequent cycles.

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

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

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

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

179 As in S phase, global mobility in G1 phase is controlled by the DNA damage checkpoint and

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

181 ate and that transitioning from mitosis into G1 phase is delayed in galectin-8-knockout HaCaT cells a

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

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

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

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

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

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

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

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

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

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

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

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

194 glutathione (GSH) level and inhibition at G0/G1 phase of cell cycle, leading to apoptosis.

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

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

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

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

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

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

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

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

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

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

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

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

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

208 croH2A is incorporated into chromatin in the G1 phase of the cell cycle following DNA replication.

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

210 of the G2/M phase and a reduction of the G0/G1 phase of the cell cycle in both cell lines.

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

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

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

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

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

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

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

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

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

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

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

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

223 11A caused CDKN1B/p27-mediated arrest in the G1 phase of the cell cycle, whereas depletion of RacGAP1

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

241 ion through a sizer operating largely in the G1 phase of the cell cycle.

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

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

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

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

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

247 s of synchronized BY2 cells at S, G2, M, and G1 phases of the cell cycle.

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

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

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

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

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

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

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

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

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

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

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

259 gous recombination proceeds to completion in G1 phase remains controversial.

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

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

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 point machineries promote global mobility in G1 phase, supporting the notion that recombination can o

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

271 e a large program of gene expression in late G1 phase that underlies commitment to cell division, ter

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

273 We discovered that despite the longer G1 phase, the first G1 after cell cycle re-entry is sign

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 In G1-phase, there are ~250,000 nuclear cohesin complexes,

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

283 3 siRNA inhibited cells to progress from the G1 phase to the S phase, but pretreatments of cells with

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

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

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

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

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

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

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

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

292 more [(18)F]FDG in S, G2 or M phases than in G1 phase, which confirms the association between FDG upt

293 the centromere-specific histone dCENP-A in M/G1 phase, which depends on the eviction of previously de

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

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

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

297 link localization of replication origins in G1 phase with Fkh1 activity, which is required for their

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

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

300 ifs are recognized by Cln1/2 cyclins in late G1 phase, yet the key sequence features of these motifs