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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

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