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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.
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
61 l-cycle control, progression from G1 through S phase and into mitosis is ordered by thresholds of inc
63 ansmitted via maintenance methylation during S phase and might play a role in the dynamic regulation
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
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
76 between DNA replication in the mother cell (S phase) and equal partitioning of the replicated chromo
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
85 atment suppressed colony formation, elicited S phase arrest during cell cycle progression, and induce
88 ies show that LBH deficiency in FLS leads to S-phase arrest and failure to progress through the cell
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.
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
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
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
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
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
124 the loading onto chromatin of various intra-S-phase checkpoint mediators and found that NONO favours
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
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
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
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
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
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
165 CDK18-depleted cells accumulate in early S-phase, exhibiting retarded replication fork kinetics a
169 cle analysis of HSPCs demonstrated increased S-phase fraction coupled with suppressed G0/G1 entry.
171 chromatin formation, epigenetic silencing of S-phase genes and permanent cell cycle arrest or cellula
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
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
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
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
202 quired for manifestation of this defect, and S phase NER proficiency is correlated with the capacity
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
212 nd break (DSB) repair pathways are active in S phase of the cell cycle; however, DSBs are primarily r
214 whereas CDK4 interacts with p53-RS in the G1/S phase of the cells, phosphorylates it, and enhances it
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
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
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
240 Here, we discovered a fundamental role of S-phase protein kinase 2 (Skp2) in the formation and pro
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
247 rence in the replication profile of an early S phase sample in the mutant, prompting the hypothesis t
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
256 of acetylation: Smc3 acetylation by Eco1 in S phase stabilizes cohesin association with chromosomes,
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
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
267 eins are synthesized in large amounts during S-phase to package the newly replicated DNA, and are amo
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
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
286 at the arrest of KRas-driven cancer cells in S-phase upon Q deprivation is due to the lack of deoxynu
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
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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