ライフサイエンスコーパス: S phase

1 ifying a window for UV-irradiation damage in S phase.

2 poptosis and arresting the cell cycle at the S phase.

3 ation signals during G1, that is, before the S phase.

4 hibition occurred preferentially in mid/late-S phase.

5 ar localization of E2(Y131A) occurred in mid-S phase.

6 de reductase and reversibly arrests cells in S phase.

7 required for expression of histone genes in S phase.

8 loci replicating during different stages of S phase.

9 but are higher in regions replicated late in S phase.

10 degradation of stalled replication forks in S phase.

11 igins in a temporally specific manner during S phase.

12 t to the Mcm2-7 complex in vivo during early S phase.

13 athways to coordinate DNA replication during S phase.

14 ing pro-centriole assembly in the subsequent S phase.

15 significantly abrogates NER uniquely during S phase.

16 r total level of origin initiations in early S phase.

17 18 depletion caused cell cycle arrest before S phase.

18 -cycle checkpoint, as some cells reinitiated S phase.

19 ore bacteria than did cells that were not in S phase.

20 in DNA end resection and HR, specifically in S phase.

21 rofound inhibition of NER exclusively during S phase.

22 all or collapse replication forks during the S phase.

23 Mcm2 in vivo under normal conditions during S phase.

24 replication and progression of cells through S phase.

25 ferentially occurred in the late G1 or early S phase.

26 re, on average, more likely to fire early in S phase.

27 tionally active chromatin replicating in mid S phase.

28 eres and localized to sites of DNA damage in S phase.

29 mere cohesion is not resolved prematurely in S phase.

30 of DDK at unfired replication origins during S phase.

31 longation processes that mostly occur during S phase.

32 ring time and frequency of activation within S phase.

33 to allow replication past damaged lesions in S phase.

34 meres and knobs, which replicate during late S phase.

35 ycC control also affect timing of entry into S phase.

36 yclin A/Cdk2 complex, arrested cell cycle at S phase.

37 ding the ICRs of the imprinted allele during S phase.

38 nd release" protocol to stage entry into the S-phase.

39 nd DNA polymerase epsilon 255 kDa subunit in S-phase.

40 d origins initiating DNA replication late in S-phase.

41 ss the G1 checkpoint, and instead, arrest in S-phase.

42 d DNA damage pathway, which arrests cells in S-phase.

43 resolved down to single replicons throughout S-phase.

44 which was ATR-independent and restricted to S-phase.

45 complete genome duplication within a single S-phase.

46 ogression as cells exit quiescence and enter S-phase.

47 e immune responses and force host cells into S-phase.

48 gnificantly associate with each other during S-phase.

49 es decreases as the cells progressed towards S-phase.

50 ly occur when cells are transitioning G1 and S phases.

51 e Eco1 to trigger its degradation until late S phase [8].

52 tem-zone loss is attributed to shortening of S phase and acceleration of cell cycle exit and neurogen

53 s establish sister chromatid cohesion during S phase and are removed when cohesin Scc1 is cleaved by

54 e loaded helicases are then activated during S phase and associate with the replicative DNA polymeras

55 r, DBAN may precipitate cancer by perturbing S phase and by blocking the Chk1-dependent response to r

56 d primary fibroblast cells slowed entry into S phase and coordinately downregulated genes related to

57 enous RNF157 in melanoma cells leads to late S phase and G2/M arrest and induces apoptosis, the latte

58 omerase II expression was tightly coupled to S phase and G2/M phase via both transcriptional and post

59 f late origin firing, both in an unperturbed S phase and in dNTP limitation.

60 endent kinase (CDK) inhibitor p21 are low in S phase and insufficient to inhibit CDKs.

61 l-cycle control, progression from G1 through S phase and into mitosis is ordered by thresholds of inc

62 process or protein that acts at the start of S phase and is required for Chk1 phosphorylation.

63 ansmitted via maintenance methylation during S phase and might play a role in the dynamic regulation

64 specificity, drive the temporal ordering of S phase and mitosis.

65 S phase and mitotic onset are brought about by the actio

66 on (R = 0.98) between the number of cells in S phase and P. gingivalis invasion, the organism was mor

67 s DNA ends, allowing the initiation of HR in S phase and providing a mechanism of DSB repair pathway

68 promoting the cell cycle transition through S phase and therefore cell proliferation.

69 referentially associates with E2F1 at the G1/S phase and with MyoD at the G2/M phase.

70 human cell forms around 3200 clusters at mid S-phase and fires approximately 100,000 origins to compl

71 nts express high levels of genes controlling S-phase and have many more cells undergoing DNA replicat

72 rosome, which coordinates the nuclear cycle (S-phase and mitosis) and budding cycle (cytokinesis) of

73 trolling both the timely progression through S-phase and mitotic entry, suggesting that CYB-3 is both

74 Schwann cells (SCs) require YAP/TAZ to enter S-phase and, without them, fail to generate sufficient S

75 ev1 (Polzeta5) complexes in vitro at 'normal S-phase' and 'damage-response' dNTP concentrations.

76 between DNA replication in the mother cell (S phase) and equal partitioning of the replicated chromo

77 l proliferation, led to cell cycle arrest at S phase, and decreased colony formation rate.

78 al body in late G1 phase, DNA replication in S phase, and dimethylation of histone H3 in mitosis/cyto

79 at phosphorylate replication proteins during S phase, and Dpb11, Sld2, Sld3, Pol , and Mcm10 are fact

80 y of the undifferentiated spermatogonia into S phase; and (3) retinoid signaling regulated spermatogo

81 main family 1, isoform A) are involved in G1-S phase arrest and act as potential tumor suppressor gen

82 ATP depletion and cell death accompanied by S phase arrest and DNA damage only in ADK-expressing cel

83 NLS induced cell apoptosis and cell cycle G1/S phase arrest by inactivating Akt signaling pathway, wh

84 Knockdown of MUCL1 induced a G1/S phase arrest concomitant with decreased cyclin D and i

85 atment suppressed colony formation, elicited S phase arrest during cell cycle progression, and induce

86 e induction of ROS by RSV was independent of S-phase arrest and actually reinforced the latter.

87 RSV induced S-phase arrest and cellular senescence in a dose-depende

88 ies show that LBH deficiency in FLS leads to S-phase arrest and failure to progress through the cell

89 Hypersensitive cells underwent early S-phase arrest at drug doses sufficient to inhibit great

90 study identifies the molecular basis for the S-phase arrest caused by Q deprivation in KRas-driven ca

91 studies indicate that LBH deficiency induces S-phase arrest that, in turn, exacerbates inflammation.

92 in RRM2 reduction, critical dNTP depletion, S-phase arrest, and apoptosis.

93 disturbed iron metabolism, archazolid caused S-phase arrest, double-stranded DNA breaks, and p53 stab

94 GTP and dATP levels in the dNTP pool causing S-phase arrest, providing evidence for RR inhibition in

95 o-senescent effect of RSV, it occurred after S-phase arrest.

96 s believed to bind randomly to DNA and cause S-phase arrest.

97 than the cell panel median and lacked early S-phase arrest.

98 ersible pausing of the cell cycle preventing S phase associated DNA damage.

99 has explored the relationship between water's phase behavior in hydrophobic confinement and the mech

100 robing each telomere thousands of times each S-phase but only rarely forming a stable association.

101 d cells to progress from the G1 phase to the S phase, but pretreatments of cells with p21 and p27 siR

102 late cell cycle transition between G0/G1 and S phases by up-regulation of the expression of CDK4 and

103 methylation patterns are transmitted through S-phase by the maintenance methyltransferase Dnmt1.

104 , and daughter centrioles (which assemble in S phase) cannot themselves duplicate or organize centros

105 naturally occurring DNA damage incurred over S-phase causes p53-dependent accumulation of p21 during

106 emonstrate a fundamental distinction between S phase Cdk1 waves, which propagate as active trigger wa

107 fficient hepatocyte proliferation due to G1 /S-phase cell cycle arrest with overexpression of p27 and

108 7 induces DNA damage, checkpoint activation, S-phase cell cycle arrest, and cell death in sensitive b

109 ressor retinoblastoma protein (RB) regulates S-phase cell cycle entry via E2F transcription factors.

110 ock-in mutation in Cul9 (Deltap53) increases S-phase cell population, accumulates DNA damage during D

111 ection by M. oryzae requires two independent S-phase cell-cycle checkpoints.

112 al-I expression maintain a greater number of S phase cells compared with low ST6Gal-I expressors, ref

113 t after TBI thereby increasing the number of S phase cells in crypts in wild-type but not Cdkn1a(p21(

114 ase than with cells in G2 and G1 phases, and S-phase cells contained 10 times more bacteria than did

115 racterized molecularly by an accumulation of S-phase cells with high levels of hyperphosphorylated RP

116 In other S-phase cells, however, ATRi induces moderate ssDNA and

117 This RR-22Rv1 cell line was enriched in S-phase cells, less susceptible to DNA damage, radiation

118 eplication stress and activation of an intra-S phase checkpoint, and suppressed the growth of VHL-/-

119 involved in replication fork stabilization, S-phase checkpoint activation and establishment of siste

120 cell cycle re-entry after DNA damage-induced S-phase checkpoint activation.

121 re equally important for triggering of intra-S-phase checkpoint and ATM signaling promoted recovery o

122 ilon (Pol epsilon) was shown to activate the S-phase checkpoint in yeast in response to replicative s

123 Recovery from the S-phase checkpoint includes inactivation of checkpoint s

124 the loading onto chromatin of various intra-S-phase checkpoint mediators and found that NONO favours

125 The DNA replication or S-phase checkpoint monitors the integrity of DNA synthes

126 rity of the Pol binding module and block the S-phase checkpoint pathway, downstream of the Mec1 kinas

127 essoria on the rice leaf surface requires an S-phase checkpoint that acts through the DNA damage resp

128 larization involves a novel, DDR-independent S-phase checkpoint, triggered by appressorium turgor gen

129 V-induced DNA damage by activating the intra-S-phase checkpoint, which prevents replication fork coll

130 ion forks is a key step in activation of the S-phase checkpoint.

131 nto how cells recover from activation of the S-phase checkpoint.

132 vities and higher proliferation rates in the S-phase compared with Pin1-null fibroblasts or PIN1-depl

133 lator sororin and causes cohesion defects in S phase, consistent with a role of Naa50 in cohesion est

134 e view that specific mechanisms dedicated to S-phase control are at work in stem cells to protect the

135 om this model and our in vivo data that endo S phase-coupled destruction of Dap reduces the threshold

136 ere that miR-874 down-regulates the major G1/S phase cyclin, cyclin E1 (CCNE1), during serum starvati

137 Dbf4-dependent kinase (DDK) and S-phase cyclin-dependent kinase (S-CDK) are two S phase-

138 Following replication stress in S phase, Dbf4 and Sld3, an initiation factor and essenti

139 harboring such a mutant also display severe S-phase defects.

140 DDK, despite being activated in early S phase, does not phosphorylate Eco1 to trigger its degr

141 sulted in compromised HR and misrejoining of S-phase DSBs, and increased the sensitivity to DNA-damag

142 1-deficient T cells exited G0 but stalled in S phase, due to both bioenergetic and biosynthetic defec

143 Hence, S-phase duration emerges as major target of cell cycle r

144 During S-phase, dynamic and stable interactions decreased consi

145 size measurements, comprehensive analysis of S-phase dynamics and quantification of replication fork

146 is required in neural progenitors for proper S-phase dynamics, as part of its well-established role i

147 ependent (RD)-histone mRNAs expressed during S-phase end in a conserved stem-loop rather than a polyA

148 neurogenic niches in the phase and degree of S-phase entrainment to the clock suggest additional role

149 was accompanied by a transient induction of S-phase entrance by quiescent hepatocytes, indicating th

150 s of post-replicative H3K27me3 or preventing S phase entry inhibited recruitment of new TFs to DNA an

151 ring signalling and the Estrogen-mediated G1/S phase entry pathways were found upregulated.

152 ciation of CDC6 and cyclin E, and a delay in S phase entry.

153 ically, ATX-LPA1 signaling acts by promoting S-phase entry and cell proliferation of chondrocytes bot

154 created by CRL4(Cdt2), promotes irreversible S-phase entry by keeping p21 levels low, preventing prem

155 ction is required for Rb phosphorylation and S-phase entry in cancer cells.

156 RB loss promoted S-phase entry in DCX(+) cells and increased apoptosis in

157 transcription factors triggers irreversible S-phase entry in yeast and metazoans, but why this occur

158 ich leads to early G1 arrest and synchronous S-phase entry upon release of the G1 block, we have deve

159 /6 inhibitors that enable alternate means of S-phase entry, highlighting strategies to prevent the ac

160 f mitosis coupled with aberrant licensing of S-phase entry.

161 rotein of the SAPS-domain family involved in S-phase entry.

162 rt, via noncanonical cyclin D1-CDK2-mediated S-phase entry.

163 of Whi3, an RNA-binding protein controlling S-phase entry.

164 osis, while wave propagation is regulated by S phase events.

165 CDK18-depleted cells accumulate in early S-phase, exhibiting retarded replication fork kinetics a

166 keeping p21 levels low, preventing premature S-phase exit upon DNA damage.

167 osis, and in this study, we describe G2- and S phase-expressed protein 1 (GTSE1).

168 gative cells caused G1 cell cycle arrest and S phase fork stalling.

169 cle analysis of HSPCs demonstrated increased S-phase fraction coupled with suppressed G0/G1 entry.

170 verlap significantly with those bound by the S-phase gene transcription factor E2F1.

171 chromatin formation, epigenetic silencing of S-phase genes and permanent cell cycle arrest or cellula

172 icellular zygotes, including upregulation of S-phase genes, a characteristic of ZGA.

173 tivation of the DNA damage response and a G1/S-phase growth arrest.

174 At the onset of endocycle S (endo-S) phase, H1 is heavily and specifically loaded into lat

175 The enrichment of S-phase histone gamma-H2AX foci and a striking loss of t

176 and Mcm10 genes inhibited the progression of S phase in Drosophila eye imaginal discs.

177 soft agar growth by prolonging cell cycle in S phase in multiple lung cell lines, including the immor

178 opposite of the pattern usually seen across S-phase in human cells, when a single genome is replicat

179 n in KRas-driven cancer cells that arrest in S-phase in response to Q deprivation.

180 imal phosphorylation of H2AX and RPA2 during S-phase in response to ultraviolet (UV) irradiation, as

181 nct E2 nuclear foci, which peaked during mid-S phase, indicating that the recruitment of Rint1 to E2

182 l cancer cells arrested the cell cycle in G1/S phase, inhibited constitutive expression of E6, Cyclin

183 DNA replication during S phase is accompanied by establishment of sister chroma

184 tion of shelterin component Ccq1 during late S phase is involved in telomerase recruitment through pr

185 mbly of the replication fork helicase during S phase is key to the initiation of DNA replication in e

186 al during HR in G2 phase, and its absence in S phase is required for replication fork stability.

187 canonical H3.1 protein, incorporated during S-phase, is maintained at high levels in cells dividing

188 igin firing and ongoing DNA synthesis during S-phase itself, respectively, and hence is functionally

189 n of p27 associated with decreased levels of S-phase kinase-associated protein (Skp)-2, a ubiquitin l

190 ding experiments indicate that neither SKP1 (S-phase kinase-associated protein 1) nor CCNB1 binding w

191 including hepatic induction of cyclin D1 and S-phase kinase-associated protein 2 expression and suppr

192 the expression of the ubiquitin ligase SKP2 (S-phase kinase-associated protein 2), which targets p27

193 KC1 Inhibition of the ubiquitin ligase SKP2 (S-phase kinase-associated protein 2), which targets the

194 (an F-box protein) and the associated Skp1 (S-phase kinase-associated protein-1)-Cullin1 complex, le

195 n CORONATINE INSENSITIVE1 (COI1), part of an S-phase kinase-associated protein1/Cullin1/F-box protein

196 tein, suggesting a simple mechanism by which S-phase length is controlled.

197 the magnitude of circadian variation in CDC, S-phase length, phase angle of entrainment to light or c

198 by loading MCM2-7 double hexamers and during S phase licensed replication origins activate to initiat

199 recruitment when CMG assembly takes place ("S-phase-like").

200 During S-phase, minor DNA damage may be overcome by DNA damage

201 Prior to S phase, multiple origins are poised to initiate replica

202 quired for manifestation of this defect, and S phase NER proficiency is correlated with the capacity

203 In both early and middle S phase nuclei, flow-sorted on the basis of DNA content,

204 pigenetic marker after genome replication in S phase occurs in G1 phase; however, how new CENP-A is l

205 kinases (CDK4 and CDK6) regulate entry into S phase of the cell cycle and are validated targets for

206 HR was harmonized to S phase of the cell cycle to repair broken chromatids an

207 Canonical histones are made in the S phase of the cell cycle.

208 aster regulator that controls entry into the S phase of the cell cycle.

209 ts cooperatively promote transition into the S phase of the cell cycle.

210 lly associates with and invades cells in the S phase of the cell cycle.

211 regulated throughout prolonged late-G1/early-S phase of the cell cycle.

212 nd break (DSB) repair pathways are active in S phase of the cell cycle; however, DSBs are primarily r

213 T187) within the p27 IDR controls entry into S phase of the cell division cycle.

214 whereas CDK4 interacts with p53-RS in the G1/S phase of the cells, phosphorylates it, and enhances it

215 profiles from cells in early, mid, and late S phase of the mitotic cell cycle.

216 is characterized by increased population in S-phase of cell cycle, elevation of Cylin E and Cyclin-d

217 hat the compounds have a clear effect on the S-phase of T. brucei cell cycle by inflicting specific d

218 human telomerase to telomeres occurs during S-phase of the cell cycle, but the molecular mechanism o

219 d that catastrophic DNA damage occurs during S-phase of the cell cycle, with long-term consequences i

220 Thus, AEE788 prevents entry into the S-phase of the cell division cycle.

221 A nontrivial Berry's phase offset to these values gives evidence for axion

222 Instead, the early versus middle S phase patterns in maize could be distinguished cytolog

223 induce phase shift under Pancharatnum-Berry's phase principle.

224 we identify Ubp7 as a novel factor affecting S phase progression after hydroxyurea treatment and demo

225 tion in mammalian cells results in defective S phase progression and the accumulation of DNA damage,

226 our results suggest that Ubp7 contributes to S phase progression by affecting the chromatin state at

227 Furthermore, ubp7Delta cells exhibit an S phase progression defect upon checkpoint activation by

228 mTOR kinase resulted in defects in the slow S phase progression following DNA damage.

229 en for genes whose depletion inhibited G1 to S phase progression when oncogenic cyclin E was overexpr

230 negative regulator that restricts the G1 to S phase progression, is diminished in human psoriatic ep

231 Restoration of miR-874 expression impeded S phase progression, suppressing aggressive growth pheno

232 We found that depletion of Rad51 impairs S-phase progression and increases cell death after UV ir

233 the pyrimidine to purine ratio, compromises S-phase progression and induces DNA-polymerase stalling

234 leaves various DNA binding substrates during S-phase progression and thus protects proliferative cell

235 esults indicate that Ki-67 integrates normal S-phase progression and Xi heterochromatin maintenance i

236 ng initiation of G1/S transition and daytime S-phase progression, overnight increase in G2/M, and cyc

237 in, a tumor suppressor that restrains G1- to S-phase progression.

238 Our results identified an essential S-phase promoting factor of the unconventional P. falcip

239 otic entry, suggesting that CYB-3 is both an S-phase-promoting and mitosis-promoting factor.

240 Here, we discovered a fundamental role of S-phase protein kinase 2 (Skp2) in the formation and pro

241 Cyclin D1, a G1-S phase regulator, is upregulated in parathyroid adenoma

242 kly coupled oscillators influence each other's phase relations.

243 ts 24.84-h rhythm and altering the pacemaker's phase-relationship to sleep in a manner that is known

244 not a static constituent of ORC but displays S-phase restricted nuclear localization and expression,

245 recruitment of 53BP1 to nuclear foci in the S phase, resulting in impaired HR and the accumulation o

246 In addition, during the S phase, Rif1 ensures that replication of interacting do

247 rence in the replication profile of an early S phase sample in the mutant, prompting the hypothesis t

248 Given that arresting cells in S-phase sensitizes cells to apoptotic insult, this study

249 Consistent with the role of RAD6/TLS in late-S phase, SMI#9-induced DNA replication inhibition occurr

250 from the original Fucci system to respond to S phase-specific CUL4(Ddb1)-mediated ubiquitylation alon

251 hase cyclin-dependent kinase (S-CDK) are two S phase-specific kinases that phosphorylate replication

252 al depletion of Rfa1 recapitulates defective S phase-specific NER in wild type yeast; moreover, ectop

253 ing NF-kappaB Overexpressed HOXC10 increases S-phase-specific DNA damage repair by homologous recombi

254 DDK is an S-phase-specific kinase required for replication initiat

255 he expression and stability of CLASPIN in an S-phase-specific manner.

256 of acetylation: Smc3 acetylation by Eco1 in S phase stabilizes cohesin association with chromosomes,

257 Although both G0 and S phase subpopulations were increased in LTHSCs with hig

258 find that RA190 treatment leads to a loss of S phase, suggesting a block of DNA replication, and G2 a

259 y initiation of these origins in the ensuing S phase, suggesting a mechanistic role linking the spati

260 between Chl1 and the cohesin complex during S phase suggests that Chl1 contacts cohesin to facilitat

261 ism was more highly associated with cells in S phase than with cells in G2 and G1 phases, and S-phase

262 In S-phase, the NF-kappaB response was delayed or repressed

263 subunit of cohesin is acetylated (ac) during S phase to establish cohesion between replicated chromos

264 protein Rad50 during the transition from the S phase to the G2/M phase and functions in radiation-ind

265 sion tethers sister chromatids together from S phase to the metaphase-anaphase transition and ensures

266 FANCD2 acts independently of previous S phases to promote alignment and segregation of acentri

267 eins are synthesized in large amounts during S-phase to package the newly replicated DNA, and are amo

268 Surprisingly, the shift from 'S-phase' to 'damage-response' dNTP levels only minimally

269 phosphorylation, and inhibited activation of S-phase transcriptional programs.

270 -dependent kinase 2 (p-CDK2), regulate G1 to S phase transition and their deregulation induces oncoge

271 show that depletion of EZH2 suppresses G1 to S phase transition of GC B cells in a Cdkn1a-dependent m

272 inhibited cell proliferation, cell cycle G1/S phase transition, cell migration and invasion, indicat

273 tion by inducing growth arrest during the G1/S phase transition, promoted apoptosis, and reduced inva

274 E2F1 target genes required to promote G1 to S phase transition.

275 that encode proteins critical for the G1-to-S phase transition.

276 protein, suggesting inhibition of the G1-to-S phase transition.

277 p27(kip1) is a critical regulator of the G1/S-phase transition of the cell cycle and also regulates

278 ntifies a regulatory axis controlling the G1/S-phase transition, relying on the regulation of MT stab

279 scriptional activity that accelerates G1- to S-phase transition.

280 CDK2 and thereby contributes to increased G1-S phase transitions and cell proliferation.

281 thereby preventing their progression to the S-phase, typical of the action of MEK inhibitors.

282 During S-phase, UNG2 remains associated with the replication fo

283 dk2 and is expressed at elevated levels from S phase until early mitosis.

284 ly holds together the sister chromatids from S phase until mitosis.

285 lizes to the spindle pole bodies (SPBs) from S phase until the end of mitosis.

286 at the arrest of KRas-driven cancer cells in S-phase upon Q deprivation is due to the lack of deoxynu

287 Translesion DNA synthesis (TLS) during S-phase uses specialized TLS DNA polymerases to replicat

288 phA2 impaired cell cycle progression through S-phase via downregulation of c-Myc and stabilization of

289 lightwaves can interact, changing each other's phase, wavelength, waveform shape, or other properties

290 u70/80 (Ku), is quickly recruited to DSBs in S phase, we hypothesized that an orchestrated mechanism

291 thesis and translocate to the nucleus during S-phase, where they form a multienzyme complex with thym

292 PAR, was positively correlated with cells in S phase, which is consistent with previous reports indic

293 protein TRF2 recruits RTEL1 to telomeres in S phase, which is required to prevent catastrophic t-loo

294 meiotic recombination 11 (Mre11) nuclease in S phase, which leads to impaired resolution of stalled r

295 DNA double-strand breaks (DSBs) by BRCA1 in S phase, which requires the BRCT domain of BRCA1 and pho

296 various progenitor types was the duration of S-phase, which became shorter as progenitors progressive

297 t species was an organic and/or amorphous Ag-S phase whose proportion slightly varied (from 24% to 36

298 l as in vitro growth by cell cycle arrest at S phase with increased cell size and nuclei.

299 ssociations occur to the least degree during S phase, with the chromosomal overlap becoming largest.

300 sion, thereby maintaining a normal length of S phase without causing detectable Rad53 checkpoint kina