ライフサイエンスコーパス: G2 phase

1 Eg5-opposing forces slow down separation in G2 phase.

2 sis and leads to endoreplication of DNA from G2 phase.

3 proliferation, and they are also arrested at G2 phase.

4 loops are generally stable from G1 to S and G2 phase.

5 d Golgi similar to control cells arrested in G2 phase.

6 bilizing factor maintaining Emi1 levels in S/G2 phase.

7 platin and acute cell-cycle arrest in late S-G2 phase.

8 alum to examine the fate of core histones in G2 phase.

9 y restrict DOX-induced apoptosis of cells in G2 phase.

10 itotic cell size through a shortening of the G2 phase.

11 o decondense their chromosomes and return to G2 phase.

12 ative complex (pre-RC) onto origins in S and G2 phase.

13 uster contains genes weakly regulated during G2 phase.

14 azoan development even in cycles that lack a G2 phase.

15 ) by phosphorylating Rad54 at Ser572 in late G2 phase.

16 1) also blocks cellular proliferation at the G2 phase.

17 cell cycle regulated protein that peaks at S/G2 phase.

18 niversal inducer of cell cycle arrest at the G2 phase.

19 damage DNA induce a transient return to late G2 phase.

20 post-translational induction of cyclin D1 in G2 phase.

21 during the synchronous transition from S the G2 phase.

22 RNAs whose upregulation is known to occur in G2 phase.

23 psis ABP1 prematurely advanced nuclei to the G2 phase.

24 ent a second round of initiation during S or G2 phase.

25 ent manner as cells progress from S phase to G2 phase.

26 e accumulation with a concurrent decrease in G2 phase.

27 eparation during cleavage cycles that lack a G2 phase.

28 during HR, with its expression peaking in S/G2 phase.

29 P1-dependent non-homologous end joining in S/G2 phase.

30 ly monitored by a decatenation checkpoint in G2 phase.

31 own-regulated and the cell cycle arrested in G2 phase.

32 ity of BRCA1 to prolong cell cycle arrest in G2 phase.

33 usly described for Cdt1 proteolysis in S and G2 phase.

34 o timely regulate its abundance during S and G2 phase.

35 iptional activation of key G2/M genes during G2 phase.

36 f the noncompact zones of Golgi membranes in G2 phase.

37 to S phase and is degraded before entry into G2 phase.

38 y phosphorylation of Cdc2 during S-phase and G2-phase.

39 e, but both pathways are active in the S and G2 phases.

40 ith Cdk2 reaches a plateau during late S and G2 phases.

41 te homologous recombination during the S and G2 phases.

42 ) (p21-/-) as the cells reach the late-S and G2 phases.

43 clusively to full cycles encompassing G1 and G2 phases.

44 se, but dynein accumulates only during S and G2 phases.

45 r nearly all DSB repair outside of the S and G2 phases.

46 amage sites is antagonized by BRCA1 in S and G2 phases.

47 tivation order of Cdk2 and Cdk1 during S and G2 phases.

48 nd IR-induced 53BP1 foci formation during G1/G2-phases.

49 Surprisingly, we demonstrate that in G2 phase, 53BP1 is required for HR at HC-DSBs with its r

50 In G1-, S-, and G2-phases, a majority of CTCF molecules was bound transi

51 e G2 phase, indicating that the ABP1-induced G2 phase advance is an indirect effect of cell expansion

52 indicated the cell cycle was arrested at the G2 phase after FAM83H-AS1 knockdown.

53 e show that Cyclin B1(-/-) embryos arrest in G2 phase after just two divisions.

54 s to the subsequent accumulation of cells in G2 phase and a prolongation of the cell cycle.

55 We show that CyclinB1-Cdk1 is inactive in G2 phase and activated at a set time before nuclear enve

56 during Drosophila oogenesis--are arrested at G2 phase and can serve as a model cell type for investig

57 l-cycle regulation, driving cells into the S-G2 phase and causing aberrant cytokinesis.

58 Centrosome separation is initiated in G2 phase and completed in M phase.

59 th this, the loss of PHF8 leads to prolonged G2 phase and defective mitosis.

60 ometric reporter of the transition from S to G2 phase and engineered a far-red fluorescent protein, m

61 ched at short telomeres from early S through G2 phase and even into the next cell cycle.

62 cells, continue to incorporate BrdUrd in the G2 phase and exhibit nuclear Cdc6 and MCM5 co-localizati

63 ase, whereas phosphorylation of NIPA in late G2 phase and mitosis inactivates the complex to allow fo

64 t PHF8 protein levels are the highest during G2 phase and mitosis, and we found PHF8 protein stabilit

65 tosis on treatment, PC3 cells accumulated in G2 phase and mitosis, suggesting a weak spindle assembly

66 enriched in the plasma membrane during late G2 phase and mitosis.

67 central regulator that drives cells through G2 phase and mitosis.

68 ulators of the cell cycle, especially in the G2 phase and mitosis.

69 cumulated in synchronized HeLa cells in late G2 phase and mitosis.

70 210 target genes are essential regulators of G2 phase and mitosis.

71 ange at the MBT, including the addition of a G2 phase and onset of late replication.

72 Bora accumulates in the G2 phase and promotes Aur-A-mediated activation of Polo-

73 cycle: Cdc5 is imported into the nucleus in G2 phase and released to the cytoplasm in anaphase, wher

74 pr for the induction of cell cycle arrest in G2 phase and suggest that Vpr may use this complex to pe

75 however, cyclin D1 fails to increase during G2 phase and the cell becomes arrested in the next G1 ph

76 pressing thyroid cells progressed into S and G2 phases and evoked a checkpoint response characterized

77 has the most potent effects during the S and G2 phases and induces E2F transcription factor-dependent

78 turely condense their chromosomes during mid G2-phase and delay decondensation at the completion of m

79 in D-NHEJ or HRR in cells irradiated in the G2-phase and identify B-NHEJ as the main DSB repair path

80 ghout the cell cycle and particularly in the G2-phase and is thought to backup predominantly D-NHEJ.

81 RNA transcription, arresting cells in the S/G2 phase, and are effective against cisplatin-resistant

82 romotes Rad51 chromatin removal during HR in G2 phase, and its absence in S phase is required for rep

83 d XCL100 was phosphorylated on serine during G2 phase, and on serine and threonine in a p42 MAPK-depe

84 , but also causes a cell cycle arrest during G2 phase, and thus prevents cells from entering mitosis.

85 and intrachromosomal breaks during the S and G2 phases, and cells lacking CYREN accumulate chromosoma

86 ine stem cells (GSCs) have short G1 and long G2 phases, and diet-dependent systemic factors often mod

87 ing complex/cyclosome) activity during S and G2 phases, and is believed to be required for proper mit

88 was higher in cells with nuclei at the S and G2 phases, and manipulating the genes whose activation o

89 we show that p53 activation leads to G1 and G2 phase arrest and can protect cells from mitotic block

90 tion of PR-SET7 in mouse embryos resulted in G2 phase arrest followed by massive cell death and defec

91 essed cells but inhibited the maintenance of G2 phase arrest following ionizing radiation (IR), there

92 logical significance of the p42 MAPK-induced G2 phase arrest, using Xenopus egg extracts as a model s

93 ted that T-cadherin reexpression resulted in G2 phase arrest, which was confirmed by mitotic index an

94 but in the absence of ATM elicited a delayed G2 phase arrest.

95 is restored by the artificial induction of a G2-phase arrest even when ATR, BRCA1, or FANCA is absent

96 lex and enabling p53-dependent apoptosis and G2-phase arrest.

97 (Cnp1) to accumulate at centromeres in S and G2 phase-arrested cells in a replication-independent mec

98 ed a greater abrogation of IR-induced S- and G2-phase arrests by caffeine in p53-deficient cells, par

99 reaks (DSB) were preferentially generated in G2 phase as detected by colocalization of H2AX and 53BP1

100 d the gamma-H2AX induction and abrogation of G2 phase as induced by Wee1 inhibition in breast and ova

101 80 ionizing radiation induced foci (IRIF) in G2 phase, as these are factors that restrict resection.

102 oliferation by inducing cell cycle arrest in G2 phase, as well as apoptosis in CTCL cell lines.

103 0.07 microM(IC50) of BNP1350 accumulated in G2 phase at 24 h after drug removal.

104 ly evaluated in FT210 cells, which arrest at G2 phase at the restrictive temperature (39 degrees C),

105 izosaccharomyces pombe (meiotic prophase and G2 phase), budding yeast Saccharomyces cerevisiae (young

106 air of DSBs by homologous recombination in S/G2 phase but also for MMEJ in G1.

107 directly modulate the GSC cell cycle at the G2 phase, but additional unknown dietary mediators contr

108 arly G1 phase of each cell cycle and lost in G2 phase, but it is not known when TAD structure and int

109 cyclin B markers of G1, S, and early to mid G2 phases, but not in RPCs expressing the phosphohistone

110 ma associates with chromosomes in G1, S, and G2 phases, but that association is abolished coincident

111 ght to trigger centrosome separation in late G2 phase by phosphorylating the motor protein Eg5 at Thr

112 e that negatively regulates mitotic entry in G2 phase by suppressing cyclin B-Cdc2 activity, but its

113 Thus, cells trapped in either G1 or G2 phase can apparently still enter and complete the pro

114 hypothesis that GRASP55 is inhibited in late G2 phase, causing unlinking of the Golgi ribbon, we foun

115 During S/G2 phases, CDK1 and CDK2 (CDK1/2) phosphorylate RECQL4 o

116 show that ASF/SF2 inactivation results in a G2-phase cell cycle arrest and subsequent programmed cel

117 iferation, increased apoptosis and increased G2-phase cell cycle arrest) and reduced the in vivo grow

118 21, causing a slowing of proliferation and a G2-phase cell cycle arrest.

119 Prevalent detection of PCNA foci in G2 phase cells after ATAD5 depletion suggests that defec

120 Here, we show that UV irradiation of G2 phase cells causes ATR-dependent but replication-inde

121 rtonic stress triggers a cell cycle delay in G2 phase cells that appears distinct from the morphogene

122 n of inactive HDAC3-H1.3 complexes from late G2 phase cells, and phosphorylation of HDAC3 in the comp

123 In G2 phase cells, DNA double-strand break repair switches

124 In G2 phase cells, where telomerase is active, Cdc13 and Es

125 e replication dependent, and found in G1 and G2 phase cells.

126 ly G1 cycling cells and high levels in S and G2 phase cells.

127 anosome, PPL2 is a nuclear enzyme present in G2 phase cells.

128 st DNA double-strand breaks (DSBs) in S- and G2-phase cells are repaired accurately by Rad51-dependen

129 and G1 contain two p220 foci, whereas S- and G2-phase cells contain primarily four p220 foci.

130 adiation-induced DNA double-strand breaks in G2-phase cells in an ATM-dependent pathway.

131 phase cells and increased numbers of G1- and G2-phase cells indicating reduced DNA synthesis, consist

132 ngly, however, a substantial proportion of S/G2-phase cells transduced by the double-stranded but not

133 ited to sites of X-ray-induced DNA damage in G2-phase cells, but not in G1, and only when DNA damage

134 nant AAV2 vectors preferentially occurs in S/G2-phase cells, suggesting that the preference for S/G2

135 lication takes place almost exclusively in S/G2-phase cells, while HSV-1 DNA replication is restricte

136 However, when PRR is restricted to the G2 phase, cells utilize REV3-dependent translesion synth

137 and hydroxyurea resistance, as well as S and G2 phase checkpoint control.

138 several tissues leads to activation of S- or G2-phase checkpoints resulting in irreversible cell cycl

139 s not directly required for IR-induced S and G2-phase checkpoints, the ATM kinase likely has differen

140 ng and for maintaining both the intra-S- and G2-phase checkpoints.

141 reaks and gaps was found to be applicable to G2-phase Chinese hamster ovary cells irradiated with 10-

142 study, we use this same system to show that G2 phase chromatin lacks determinants of replication tim

143 hed during S phase and maintained throughout G2 phase (cohesion).

144 phosphorylation occurring through G1, S and G2 phases, concomitant with a switch from coactivator to

145 egulation of cell cycle arrest in premeiotic G2 phase coordinates germ cell maturation and meiotic ce

146 rmore, the ability of Vpr to arrest cells in G2 phase correlates with its ability to interact with Cu

147 s specifically phosphorylated in synchronous G2-phase cultures; its cytoplasmic levels increased by C

148 Once induced in G2 phase, cyclin D1 expression becomes Ras independent t

149 ct, inhibiting Cdc2 activation and causing a G2 phase delay or arrest.

150 s way, the expression levels of cyclin D1 in G2 phase determine the fate of the next cell cycle.

151 ll cycle, for example, the introduction of a G2 phase, dictate the response to checkpoint activation,

152 itochondria impose a cell cycle delay at the G2 phase disrupting cell proliferation without affecting

153 ansformed cells that fail to launch a robust G2 phase DNA damage checkpoint and that this renders the

154 wed that despite variability in G1-, S-, and G2 phases, duration of mitosis is short and remarkably c

155 at low levels in G1 and is induced in S and G2 phase, during which point centrioles have already com

156 elevation as the cells progressed from S to G2 phase, even though the inhibitor was able to complete

157 In late S and G2 phases, even though DNA end-joining pathways remain f

158 n osteosarcoma U2OS cells and found that the G2 phase exhibits the highest growth rate, which is mass

159 FA-defective (Fancc(-)) DT40 cells arrest in G2 phase following cross-link damage and trigger apoptos

160 that, despite rapid Cdt1 protein turnover in G2 phase, Geminin promotes Cdt1 accumulation by increasi

161 ent reduced cell proliferation, with induced G2-phase growth arrest (doxorubicin) or G1-phase growth

162 of the cell cycle and showed that ESCs in S/G2 phases have an enhanced capacity to dominantly reprog

163 reciprocal combination, S-phase nuclei in a G2-phase host continued DNA synthesis for several hours

164 associated with a substantial increase in S/G2-phase human HSCs after engraftment into immunodeficie

165 ly cleavage divisions normally but arrest in G2 phase immediately after the midblastula transition.

166 or for the remainder of interphase including G2 phase, implying 3D structure is not sufficient to mai

167 clin D1 protein levels could increase during G2 phase in the absence of new mRNA synthesis.

168 athematical model of the transition from the G2 phase in the cell cycle to mitosis (M) was constructe

169 2-BRCA2 to constrain BRCA2 function to the S/G2 phases in human cells.

170 e effectively abrogates checkpoints in S and G2 phases in XRCC2 mutant cells indicating that checkpoi

171 mulation of rap1GAP-transfected cells in the G2 phase, in comparison to the vector control, indicatin

172 expansion occured before the advance to the G2 phase, indicating that the ABP1-induced G2 phase adva

173 ly compared to G1-phase, but were resumed in G2-phase, indicating that specific interactions need to

174 in a monopolar manner at the old end, and in G2 phase, initiate growth at the previous cell division

175 Furthermore, endoreplication from G2 phase is independent of p53 control.

176 cells, suggesting that the preference for S/G2 phase is independent of the nature of the viral genom

177 ened by the onset of late replication, and a G2 phase is introduced.

178 We show that co-localization of the S/G2 phase kinase, Nek2 and Kif24 triggers Kif24 phosphory

179 ence that HuR phosphorylation at S202 by the G2-phase kinase Cdk1 influences its subcellular distribu

180 Endoreplication from G2 phase lacks all hallmarks of mitosis.

181 airs most DNA double-strand breaks (DSBs) in G2 phase, late repairing DSBs undergo resection and repa

182 not CYCD2;1-expressing) cells show increased G2-phase length and delayed activation of mitotic genes

183 In the intervening G2 phase, mitotic inducers accumulate, which eventually

184 either the numbers of cells in G0-G1, S, and G2 phases nor the rate of [3H]thymidine incorporation, t

185 fined to the apical surface and G1-, S-, and G2-phases occurring at more basal locations.

186 ns lengthened interphase 13 by introducing a G2 phase of a distinct duration.

187 s identified 154 genes that were elevated in G2 phase of cells as compared to early G1 phase includin

188 In G2 phase of cells expressing the HBV X protein (HBx), SU

189 of Cdk1 by Myt1 kinase regulates premeiotic G2 phase of Drosophila male meiosis.

190 ritical role in cyclin D1 suppression during G2 phase of serum-deprived cultures, and therefore in th

191 Cdt1 regulation by FBXO31 is limited to the G2 phase of the cell cycle and is independent of the pat

192 m during fibrotic injury is an arrest in the G2 phase of the cell cycle and lower expression of sever

193 NA leads to the accumulation of cells in the G2 phase of the cell cycle and prevents cells from enter

194 61-overexpressing breast cancer cells in the G2 phase of the cell cycle and the appearance of sub-G1

195 hat a subset of neoblasts is arrested in the G2 phase of the cell cycle by double-labeling with BrdU

196 MKlp2 accumulated in the nucleus during the G2 phase of the cell cycle coincident with the mitotic k

197 recruitment of Axl2p to the bud neck after S/G2 phase of the cell cycle depends on Bud3p and Bud4p.

198 totic genes, (2) delayed progression through G2 phase of the cell cycle due to activation of the G2/M

199 ate firing of replication origins during the G2 phase of the cell cycle is suppressed by cyclin-depen

200 e ubiquitin ligase SCF(beta-TrCP) during the G2 phase of the cell cycle to allow transcriptional dere

201 23::ura4 mutation also causes a delay in the G2 phase of the cell cycle which is corrected when rhp23

202 n Vpr (viral protein R) arrests cells in the G2 phase of the cell cycle, a process that requires acti

203 1 causes cell cycle arrest at mitosis or the G2 phase of the cell cycle, accompanied by endoreduplica

204 cally associate on the centrioles during the G2 phase of the cell cycle, and CP110 is ubiquitylated b

205 ugh Notch-mediated lateral inhibition during G2 phase of the cell cycle, as neighbouring cells physic

206 rrests cells at the DNA damage checkpoint in G2 phase of the cell cycle, but the mechanism underlying

207 and a decrease in the number of cells in the G2 phase of the cell cycle, compared with cells expressi

208 eltarqh1 cells by reducing the length of the G2 phase of the cell cycle, DSB repair continued to be p

209 We show that the COC operates in the G2 phase of the cell cycle, independently of the spindle

210 In G2 phase of the cell cycle, Misu is found in cytoplasmic

211 branches and the proportion of cells in the G2 phase of the cell cycle, retarded plant growth, consi

212 During the long G2 phase of the cell cycle, seven different interphase n

213 ATML1 levels surpass a threshold during the G2 phase of the cell cycle, the cell will likely enter a

214 rtebrates is not fully established until the G2 phase of the cell cycle.

215 ccurs exclusively after DNA replication in S/G2 phase of the cell cycle.

216 t chromosome ends after DNA replication in S/G2 phase of the cell cycle.

217 ak repair in X-irradiated human cells in the G2 phase of the cell cycle.

218 mented nuclei, and they were arrested in the G2 phase of the cell cycle.

219 he G2/M checkpoint, leading to arrest in the G2 phase of the cell cycle.

220 Mre11, phosphorylated NBS1, and ATM in every G2 phase of the cell cycle.

221 zing irradiation in both the S-phase and the G2 phase of the cell cycle.

222 n of topo IIalpha normally occurs during the G2 phase of the cell cycle.

223 romeres are resolved from one another in the G2 phase of the cell cycle.

224 e the sister chromatid and occur during S or G2 phase of the cell cycle.

225 in overall gene expression and arrest in the G2 phase of the cell cycle.

226 We have found that, during the G2 phase of the cell division cycle, TFAP4 is targeted f

227 transcriptional cycling was detected in the G2 phase of the division cycle in fission yeast, consist

228 e report that DILPs specifically control the G2 phase of the GSC cell cycle via phosphoinositide-3 ki

229 ction is a fast process occurring within the G2 phase of the last cell cycle, which is longer than G2

230 Nuclei in G2 phase of the slime mold Physarum polycephalum, when t

231 This gene inventory for G1 and G2 phases of cell cycle will provide the basis for under

232 uction of checkpoint responses in G1, S, and G2 phases of the cell cycle after exposure of cells to i

233 e localized in the nucleus during G1, S, and G2 phases of the cell cycle and are released into the cy

234 , is an SCF(Cyclin F) substrate during S and G2 phases of the cell cycle and is also degraded in resp

235 HR repairs broken DNA during S and G2 phases of the cell cycle but its regulatory mechanism

236 l does not inhibit progression through S and G2 phases of the cell cycle or centrosome duplication.

237 mice revealed that progression through the S/G2 phases of the cell cycle was inefficient.

238 ioresistance is restricted to the late S and G2 phases of the cell cycle, as predicted for genes whos

239 unable to downregulate p27 during the S and G2 phases of the cell cycle, but that this had a surpris

240 duced DSB associates with Sad1 and Kms1 in S/G2 phases of the cell cycle, connecting the DSB to cytop

241 In the S and G2 phases of the cell cycle, DNA double-strand breaks (D

242 phosphorylated by Cdk2/cyclinA in late S and G2 phases of the cell cycle, promoting Pol lambda stabil

243 m apical to basal and back during the G1 and G2 phases of the cell cycle, respectively.

244 ism but is generally restricted to the S and G2 phases of the cell cycle, when DNA has been replicate

245 Treated cells arrested in G1 and G2 phases of the cell cycle, with concomitant reductions

246 tinct Ddc1-mediated mechanisms during G1 and G2 phases of the cell cycle.

247 usly known to repress Cdk1 only during S and G2 phases of the cell cycle.

248 potential of DNA damage arising during S and G2 phases of the cell cycle.

249 of telomere dysfunction in the G0, G1, and S/G2 phases of the cell cycle.

250 air, which occurs predominantly in the S and G2 phases of the cell cycle.

251 e additional functions during the G1, S, and G2 phases of the cell cycle.

252 ted, with maximal levels expressed in late S/G2 phases of the cell cycle.

253 d that blastomeres arrested during the S and G2 phases of the cell cycle.

254 1 and S, whereas geminin is present in S and G2 phases of the cell cycle.

255 covery are fundamentally different in G1 and G2 phases of the cell cycle.

256 EXO1 at four C-terminal S/TP sites during S/G2 phases of the cell cycle.

257 for essential functions of Cdk2 during S and G2 phases of the mammalian cell cycle.

258 allele underwent cell cycle arrest in late S/G2-phase of the cell cycle when shifted to the restricti

259 cling cells) and cyclin B1 (a marker for the G2-phase of the cell cycle).

260 G1, remains in the nucleus throughout S- and G2-phases of the cell cycle and disappears at anaphase.

261 tion of spontaneous DNA damage in the S- and G2-phases of the cell cycle and elevated genomic instabi

262 show that Greatwall binds active PP2A/B55 in G2 phase oocytes but dissociates from it when progestero

263 Late G2 phase phosphorylation between the two elements by MPF

264 Here, we report that in G2 phase polo-like kinase 1 (Plk1) can trigger centrosom

265 ions suggested that the latter cells were in G2 phase, prior to the onset of mitosis: these cells con

266 or arrest, while those treated in late S- or G2-phase progress to mitosis and divide.

267 instability correlated with enhanced S- and G2-phase-specific cell killing, delayed kinetics of gamm

268 cycle, while HR is primarily active in the S/G2 phases suggesting that there are cell cycle-specific

269 age, whereas HR is active primarily in the S/G2 phases suggesting there are cell cycle-specific mecha

270 own led to arrest of cells within the G1 and G2 phases, suggesting blockage of cell cycle progression

271 High Rep protein levels in S/G2 phase support AAV2 replication and inhibit HSV-1 repl

272 e transcription-independent acquisition of a G2 phase that is essential for preventing entry into mit

273 ypertonic stress-induced cell cycle delay in G2 phase that is mediated in a novel way by Swe1p in coo

274 of immediate early (IE) gene expression in S/G2 phase that normally restricts the onset of the HCMV r

275 During S and G2 phases the ubiquitin ligase complex APC/C is inhibite

276 In late S/G2 phase, the DNA damage-responsive E3 ligase RNF8 conju

277 Later and only in S and G2 phase, the homologous recombination machinery assembl

278 levels of Est2p and Est1p binding in late S/G2 phase, the period in the cell cycle when yeast telome

279 tially enriched at short telomeres in late S/G2 phase, the time of telomerase action.

280 DNA synthesis, and induced to high levels in G2 phase through Ras activity to commit the cells to con

281 MHD1 phosphorylation on Thr-592 during S and G2 phases thus interfering with DNA replication and prog

282 etch triggers cells that are paused in early G2 phase to activate calcium-dependent phosphorylation o

283 replication and promote the transition from G2 phase to mitosis, respectively.

284 We show that cells proceed from G2 phase to replicate their DNA in the absence of mitosi

285 totic cyclins drives the transition from the G2 phase to the M phase in embryonic cells, the trigger

286 rated artificially by HO endonuclease in the G2 phase, we show that dna2-defective strains are impair

287 In contrast to this role for 53BP1 in HR in G2 phase, we show that it is dispensable for HR in S pha

288 and that the majority of hepatocytes in S or G2 phase were eliminated by apoptosis.

289 n, we found that cells arrest permanently in G2 phase when Ku expression is turned off.

290 (IR)-induced 53BP1 foci formation during G1/G2-phases when H4K20-2Me levels are low.

291 repair (HRR) is functional during the S- and G2-phases, when a sister chromatid becomes available.

292 precipitate and colocalize to centrosomes in G2 phase, where AurA becomes active.

293 sphorylation of NF-kappaB subunits in G1 and G2 phases, where Chk1 is inactive.

294 to G2/M arrest, characterized by a prolonged G2 phase, which can be rescued by expression of wild typ

295 Growth factors stimulate high levels during G2 phase, which commits the cell to continue through G1

296 tage of these cells are arrested in the late G2 phase, which explains the reduced principal/intercala

297 rillar collagen can also arrest cells at the G2 phase, which is mediated in part by p21(CIP1).

298 15-phosphorylated Cdk1 (pY15-Cdk1) in S and G2 phases, which correlates with an elevated frequency o

299 ate spontaneous DNA damage during the S- and G2-phases, which is indicative of fork damage.

300 to repair DNA double-strand breaks (DSBs) in G2 phase with HR preferentially repairing heterochromati