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1 ated by cyclin-dependent kinases and the DNA damage checkpoint.
2 ucleosome dynamics is independent of the DNA damage checkpoint.
3 rt of the MBF core, is the target of the DNA damage checkpoint.
4  dimer is essential for establishing the DNA damage checkpoint.
5 le checkpoint but instead depends on the DNA damage checkpoint.
6 agents, even in mutants defective in the DNA damage checkpoint.
7 gonizes the involvement of NOTCH1 in the DNA damage checkpoint.
8 poison acriflavine (ACF), activating the DNA damage checkpoint.
9 uired for replisome assembly and for the DNA damage checkpoint.
10 repair before the execution of an intact DNA damage checkpoint.
11 otic response of the conserved pachytene DNA damage checkpoint.
12  but they are compromised for the G(2)/M DNA damage checkpoint.
13 plication and subsequently arrest at the DNA damage checkpoint.
14 l cycle because of the activation of the DNA damage checkpoint.
15  the G(2) phase, thereby attenuating the DNA damage checkpoint.
16 ia telangiectasia and rad3 related-based DNA damage checkpoint.
17 termines the activation threshold of the DNA damage checkpoint.
18 e-strand breaks (DSBs) that activate the DNA-damage checkpoint.
19 lex, but they maintain an intact S phase DNA damage checkpoint.
20 A lesions and subsequent activation of a DNA-damage checkpoint.
21  that is the effector molecule in the G2 DNA damage checkpoint.
22 in gamma-H2AX induction, or an abrogated DNA damage checkpoint.
23 miR-106b overrides a doxorubicin-induced DNA damage checkpoint.
24  as cells are unable to recover from the DNA damage checkpoint.
25 nd cooperate in ATR activation in the G1 DNA damage checkpoint.
26 tation that prevents induction of the G2 DNA damage checkpoint.
27  persist are therefore eliminated by the DNA-damage checkpoint.
28 d cohesion, and inactivated a third, the DNA damage checkpoint.
29  recovery or when the cells adapt to the DNA damage checkpoint.
30 ks (DSBs), eukaryotic cells activate the DNA damage checkpoint.
31 s and also functions in the ATR-mediated DNA damage checkpoint.
32 tion of the metabolic checkpoint and the DNA damage checkpoint.
33 central anti-tumorigenic function of the DNA damage checkpoints.
34 m DNA double-strand breaks that activate DNA damage checkpoints.
35  agents and play a role in activation of DNA damage checkpoints.
36 dent arrest is genetically distinct from DNA damage checkpoints.
37  to facilitate repair by HR and regulate DNA damage checkpoints.
38 ate DNA damage and to activate host cell DNA damage checkpoints.
39 /Chk1 to promote efficient activation of DNA damage checkpoints.
40 equires interdependence with mediator of DNA damage checkpoint 1 (MDC1) and H2AFX.
41 se (DDR) proteins, including mediator of DNA damage checkpoint 1 (Mdc1) and p53 binding protein 1 (53
42 duced gammaH2AX foci recruit mediator of DNA damage checkpoint 1 (MDC1) and p53 binding protein 1 (53
43 eaks and associates with the mediator of DNA damage checkpoint 1 (MDC1) and the ataxia telangiectasia
44 omplex components (MCMs) and mediator of DNA damage checkpoint 1 (MDC1) expression.
45 inding protein 1 (53BP1) and Mediator of DNA damage checkpoint 1 (MDC1) to endogenous DSBs.
46                 We show that mediator of DNA damage checkpoint 1 (MDC1), a binding partner of phospho
47 together with recruitment of mediator of DNA damage checkpoint 1 (MDC1), and the Mre11-Rad50-Nbs1 (MR
48 ylated H2AX (gammaH2AX), and mediator of DNA damage checkpoint 1 (MDC1), as well as components of pre
49 damage factors such as NBS1, mediator of DNA damage checkpoint 1 (MDC1), RNF8, 53BP1, and BRCA1.
50 X, also known as H2AFX)- and mediator of DNA damage checkpoint 1 (MDC1)-dependent events.
51 cylation of histone H2AX and mediator of DNA damage checkpoint 1 (MDC1).
52  blocks recruitment of MDC1 (mediator of DNA damage checkpoint 1) and 53BP1 (p53 binding protein 1) t
53  by gamma-H2AX and by MDC-1 (mediator of DNA damage checkpoint 1), which binds to gamma-H2AX in chrom
54  phosphorylated histone 2AX, mediator of DNA-damage checkpoint 1, and p53 binding protein 1, at DSBs
55 rand breaks (DSBs) and activation of the DNA damage checkpoint [2-7].
56 ransformation by enabling cells to evade DNA damage checkpoints activated by oncogenic stimuli.
57 s error-prone in this context because of DNA damage checkpoint activation and base pair lesions and u
58 ese data demonstrate that L1CAM augments DNA damage checkpoint activation and radioresistance of GSCs
59  the recruitment of factors critical for DNA damage checkpoint activation and repair by homologous re
60 ing L1CAM by RNA interference attenuated DNA damage checkpoint activation and repair, and sensitized
61 s, we found that H3K14ac is critical for DNA damage checkpoint activation by directly regulating the
62 eoprotein aggregates form in response to DNA damage checkpoint activation in egg chambers of females
63 hase arrest accompanied by gammaH2AX and DNA damage checkpoint activation in mouse embryonic fibrobla
64 eated cells show slower DNA replication, DNA damage checkpoint activation, and an increased apoptotic
65 y passage primary MEFs is antagonized by DNA damage checkpoint activation, consistent with nuclear cy
66 ection, the generation of ssDNA, affects DNA damage checkpoint activation, DNA repair pathway choice,
67 ckdown is independent of p53 activation, DNA damage checkpoint activation, or changes in the AKT path
68  dependent on ATM-, but not ATR-mediated DNA damage checkpoint activation.
69  result from Chk-2 (checkpoint kinase-2) DNA damage checkpoint activation.
70 egulates RAD53 transcription to suppress DNA damage checkpoint activation.
71 he metabolic conversion of ANI-7 induces DNA damage, checkpoint activation, S-phase cell cycle arrest
72 acetylation of the ATM kinase, promoting DNA-damage-checkpoint activation and cell survival.
73 s required for rapid inactivation of the DNA damage checkpoint after DSB repair.
74  exacerbated by Pif1, which triggers the DNA damage checkpoint along a pathway involving Pif1's abili
75 n further genes of the HR pathway or the DNA damage checkpoint also give rise to somatic mutation pat
76 r of Mre11 at DNA ends, shutting off the DNA damage checkpoint and allowing cell cycle progression.
77 Cs) display a preferential activation of DNA damage checkpoint and are relatively resistant to radiat
78 15 ablation potentiated induction of the DNA damage checkpoint and cancer cell death by 6-thioguanine
79 n ART-27 depletion include regulators of DNA damage checkpoint and cell cycle progression, suggesting
80 3 gene is dependent on activation of the DNA damage checkpoint and chromatin remodelling by SWI/SNF.
81 aling abrogates the activation of the G2 DNA damage checkpoint and confers specific sensitization of
82 tants were associated with activation of DNA damage checkpoint and depletion of dNTP concentrations t
83  that is essential for activation of the DNA damage checkpoint and DNA repair by homologous recombina
84 re involved in the maintenance of a G2/M DNA damage checkpoint and DNA repair mediated by the nonhomo
85 A damage by concurrently attenuating the DNA damage checkpoint and DNA repair, resulting in polyploid
86 ivation of these kinases from the G(2)/M DNA damage checkpoint and efficient checkpoint recovery.
87 d by the recombination machinery and the DNA damage checkpoint and is likely an important aspect of h
88                        This sustains the DNA damage checkpoint and is suppressed by Rad53 phosphoryla
89 rol the activity of cyclin A at the G(1) DNA damage checkpoint and may thereby prevent S-phase entry
90 tein complex that impacts mammalian G2/M DNA damage checkpoint and NHEJ.
91        UmuD is implicated in a primitive DNA damage checkpoint and prevents DNA polymerase IV-depende
92                                          DNA damage checkpoint and recombinational repair are both im
93 s loading mechanism and association with DNA damage checkpoint and repair enzymes.
94 ex at DSBs occurs independently of known DNA damage checkpoint and repair proteins.
95       Mec1-Ddc2 (ATR-ATRIP) controls the DNA damage checkpoint and shows differential cell-cycle regu
96 ls that fail to launch a robust G2 phase DNA damage checkpoint and that this renders them sensitive t
97 A turnover through the activation of the DNA-damage checkpoint and the Aft1/Aft2-controlled iron regu
98 obility in G1 phase is controlled by the DNA damage checkpoint and the Rad51 recombinase.
99 s from the age-related activation of the DNA damage checkpoint and the resulting degradation of histo
100               In budding yeast, both the DNA damage checkpoint and the spindle assembly checkpoint (S
101 ls a previously unknown function for the DNA damage checkpoint and the spindle position checkpoint in
102 h well-defined functions in mitosis, the DNA damage checkpoint and the spindle position checkpoint, h
103 n kinase Rad53 is a key regulator of the DNA damage checkpoint and uses its two FHA domains to intera
104 tect telomeres against activation of the DNA damage checkpoints and recombinational repair.
105 n essential factor for the initiation of DNA damage checkpoints and the maintenance of genomic stabil
106 ity to recruit telomerase, activates the DNA damage checkpoint, and loses heterochromatin at telomere
107 ific DSBs, fail to properly activate the DNA-damage checkpoint, and show genetic interactions with DS
108 p21, which promotes cell-cycle arrest at DNA damage checkpoints, and Gadd45 and p53R2, with pivotal r
109 umulated oxidative DNA damage, activated DNA damage checkpoints, and showed G1-phase arrest at atmosp
110 B repair and the deoxyribonucleic acid (DNA) damage checkpoint are unclear.
111                                 Although DNA damage checkpoints are broadly activated in response to
112 late on the lagging strand, resulting in DNA damage-checkpoint arrest and cell death.
113 0 is required to allow the adaptation of DNA damage checkpoint-arrested cells with an unrepaired DSB
114                                     G2/M DNA damage checkpoint, ATM signaling, mitochondrial dysfunct
115 Obfc2b does not affect the initiation of DNA damage checkpoints, Atm activation, or the maintenance o
116         This process is regulated by the DNA damage checkpoint, because RFWD3 is phosphorylated by AT
117 t the requirements for recovery from the DNA damage checkpoint become more stringent with increased l
118 only on Mec1 and other components of the DNA damage checkpoint but also on the presence of the centro
119 hality that is dependent on the upstream DNA damage checkpoint but independent of the downstream core
120 process resulting from activation of the DNA damage checkpoint by an ATR-regulated pathway, which fun
121 r with UmuC, plays a role in a primitive DNA damage checkpoint by decreasing the rate of DNA synthesi
122 s of spindle-class females, an activated DNA damage checkpoint causes inefficient Grk translation and
123 ls compromised in DNA repair pathways or DNA damage checkpoints, cells reliant on homologous recombin
124                                      The DNA damage checkpoint clamp (the 9-1-1 complex) has been rep
125                                The yeast DNA damage checkpoint clamp Ddc1-Mec3-Rad17 (human Rad9-Hus1
126 der, replication factor C (RFC), and the DNA damage checkpoint clamp loader, Rad24-RFC, using two sep
127 progression is reduced in the absence of DNA damage checkpoint components and nonhomologous end-joini
128 ncogenic transformation, and hyperactive DNA damage checkpoints, consistent with upregulated levels a
129 on down-regulation was associated with a DNA damage checkpoint consisting of p53, p21, and endothelia
130                                      The DNA damage checkpoint, consisting of an evolutionarily conse
131 These findings provide new insights into DNA damage checkpoint control and further underscore the cri
132 microcephaly, plays an important role in DNA damage checkpoint control and mitotic entry.
133 ity of HPV-16 E7 involves attenuation of DNA damage checkpoint control by accelerating the proteolyti
134  we show that the CHK2 (CHEK2)-dependent DNA damage checkpoint culls not only recombination-defective
135                                      The DNA damage checkpoint (DDC) is often robustly activated duri
136 se to DNA DSBs, cells activate a complex DNA damage checkpoint (DDC) response that arrests the cell c
137 n cell-cycle progression enforced by the DNA-damage checkpoint (DDC) signalling pathway positively co
138 signal transduction cascade known as the DNA damage checkpoint (DDC).
139                   Despite the underlying DNA damage checkpoint defects, increased DNA damage signalin
140 r of cells after they have experienced a DNA damage checkpoint delay is poorly characterized.
141  we define a role for MRN in the S-phase DNA damage checkpoint-dependent slowing of replication that
142 various cellular processes including the DNA damage checkpoint, DNA repair, and transcription.
143 rc1 experience chronic activation of the DNA damage checkpoint during chromosome replication and do n
144 of signaling complexes that activate the DNA damage checkpoint effector kinase Chk1.
145                    Here we show that the DNA-damage checkpoint eliminates oocytes via the pro-apoptot
146 streplication repair complex, downstream DNA-damage checkpoint factors (Rad53, Chk1, and Dun1), or th
147 rized genes, including mRNA splicing and DNA damage checkpoint factors.
148 ve been known to be downregulated by the DNA damage checkpoint for many years.
149  homologous recombination repair and the DNA damage checkpoint for viability.
150                   Aberrant regulation of DNA damage checkpoint function leads to genome instability t
151     We found that Dss1p and Rae1p have a DNA damage checkpoint function, and upon treatment with UV l
152 7 in either activation or termination of DNA damage checkpoint function.
153 ork metabolism, are required for S-phase DNA damage checkpoint function.
154 ddition to a structural role, Mrc1 has a DNA damage checkpoint function.
155 d increased expression of cell cycle and DNA damage checkpoint genes (false discovery rate <0.25; nor
156 ed by disruption of either MEC1 or RAD53 DNA damage checkpoint genes, as well as the lethality seen w
157 atory step controlling activation of the DNA damage checkpoint in Bacillus subtilis.
158 ress, DNA damage, and abrogates the G(2) DNA damage checkpoint in both normal and malignant cells.
159 AFs), Asf1 and CAF-1, in turning off the DNA damage checkpoint in budding yeast.
160        Finally, we suggest escaping this DNA damage checkpoint in maternal ageing may be one of the c
161                     Previous work on the DNA damage checkpoint in Saccharomyces cerevisiae has shown
162 d4(TopBP1) facilitates activation of the DNA damage checkpoint in Schizosaccharomyces pombe by physic
163 ion DNA repair enzymes and activates the DNA damage checkpoint in the G2 cell cycle phase.
164 eatment, and the noted abrogation of the DNA damage checkpoint in the MTA1-depleted cells may be, at
165 in is also required for the integrity of DNA damage checkpoints in somatic cells, where cohesin loadi
166 ), and leads to frequent mutagenesis and DNA damage checkpoint induction.
167  one example, a pathway-based screen for DNA damage checkpoint inhibitors identified a compound, MARP
168 c genotoxic stress and susceptibility to DNA damage checkpoint inhibitors.
169                                   The G2 DNA damage checkpoint inhibits Cdc2 and mitotic entry throug
170 d conditions and the DNA replication and DNA damage checkpoints into a single transcriptional complex
171      However, it remains unclear how the DNA damage checkpoint is activated by oxidative stress at th
172                This lack of an efficient DNA damage checkpoint is because oocytes fail to effectively
173 nt when a DSB is slowly repaired and the DNA damage checkpoint is fully activated.
174 t mechanism of how an ATR-Chk1-dependent DNA damage checkpoint is mediated by APE2 in the oxidative s
175 ng yeast (Saccharomyces cerevisiae), the DNA damage checkpoint is regulated by a signaling cascade of
176 aintains proliferation despite activated DNA damage checkpoints is incompletely understood.
177                 Thus, SAC, much like the DNA damage checkpoint, is essential for genome stability.
178 t kinase 1 (Chk1), a component of the G2 DNA damage checkpoint, is important in the resistance of nor
179 ing agents is independent of the replication damage checkpoint kinase ataxia telangiectasia-mutated a
180 ed by mutations in the gene encoding the DNA damage checkpoint kinase ATM, is characterized by multis
181 oration causes DNA damage that activates the damage checkpoint kinase Chk1 and sensitizes cells to UV
182 ks the serine 345 phosphorylation of the DNA damage checkpoint kinase Chk1 by Rad3 (ATR) at broken re
183 sitive to single-agent inhibition of the DNA damage checkpoint kinase Chk1, leading us to examine dow
184                                      The DNA damage checkpoint kinase Mec1(ATR) is critical for maint
185 n of the Trp53 tumor suppressor or Chek2 DNA damage checkpoint kinase rescued Smc5 cKO neurodevelopme
186 mour cells to clinical inhibitors of the DNA damage checkpoint kinase, ATR, both in vitro and in vivo
187 nuclear foci and activation of the Rad53 DNA damage checkpoint kinase, indicating that the toxicity i
188 r suppressor genes Egr1 and JunB and the DNA damage checkpoint kinase, polo-like kinase 2 (Plk2) as d
189 ei from syncytial blastoderm embryos via DNA damage checkpoint kinase-mediated retention of specific
190  we show that, in the absence of induced DNA damage, checkpoint kinase-1 (CHK1), an enzyme essential
191 vase complex (BLM-TOP3A-RMI1/2, or BTR), DNA damage checkpoint kinases (ATR and Chk1), HR proteins (B
192 the existing knowledge of the targets of DNA damage checkpoint kinases and provides insights into the
193  core component of NHEJ, partnering with DNA-damage checkpoint kinases ataxia telangiectasia mutated
194 nse to DNA damage is orchestrated by the DNA damage checkpoint kinases ATAXIA TELANGIECTASIA MUTATED
195                                          DNA damage checkpoint kinases ATR and WEE1 are among key reg
196 of the Eya2 phosphatase activity and the DNA damage checkpoint kinases Chk1 and Chk2 in wild-type axo
197     In normal cells, p53 is activated by DNA damage checkpoint kinases to simultaneously control the
198 e phosphorylations were dependent on the DNA damage checkpoint kinases, Mec1/Tel1 and Rad53.
199 DK), Dbf4-dependent kinase (DDK) and the DNA damage checkpoint kinases.
200                        Besides canonical DNA damage checkpoint-mediated phosphorylation, DNA damage-i
201 ains with deletions of both ISC1 and the DNA damage checkpoint mediator gene RAD9 display reduced mor
202 on of the conserved helicase PIF1 and/or DNA damage checkpoint-mediator RAD9.
203                           In the S-phase DNA damage checkpoint, MRN acts both in activation of checkp
204     Novel targeted therapies against the DNA damage checkpoint or stem-cell maintenance pathways may
205  Recently, strategies aimed at targeting DNA damage checkpoints or DNA repair processes have demonstr
206 GR are not achieved by either activating DNA damage checkpoints or regulating the expression of the G
207                      We propose that the DNA damage checkpoint pathway coordinates resection and nucl
208                              We find the DNA damage checkpoint pathway facilitates HR, in part, by pr
209 ear extensions, whereas inactivating the DNA damage checkpoint pathway in a DNA repair mutant reduced
210           Here we identify roles for the DNA damage checkpoint pathway in facilitating homologous rec
211                                      The DNA damage checkpoint pathway is activated in response to DN
212 he Chk2-mediated deoxyribonucleic acid (DNA) damage checkpoint pathway is important for mitochondrial
213 MTA1 also participates in the UV-induced DNA damage checkpoint pathway remains unknown.
214 etermine whether reduced activity in the DNA damage checkpoint pathway would cooperate with MMR defic
215  functions as a mediator in the ATR-Chk1 DNA damage checkpoint pathway.
216 ticipates in the UV-induced ATR-mediated DNA damage checkpoint pathway.
217 a cells and relieves the reliance on the DNA damage checkpoint pathway.
218 , Mitotic Arrest-Deficient 2 [MAD2]) and DNA-damage-checkpoint pathway (e.g., Mitosis Entry Checkpoin
219  gene sets with concurrent activation of DNA damage checkpoint pathways as compared with Mtg16(-/-).
220                                          DNA damage checkpoint pathways operate to prevent cell-cycle
221 ion fork protection, and DNA replication/DNA damage checkpoint pathways.
222 (DSB) repair, meiotic recombination, and DNA damage checkpoint pathways.
223                             Although the DNA damage checkpoint PI3-kinases ATM and ATR localize to te
224                                      The DNA damage checkpoint plays a crucial role in maintaining fu
225 pha mutant activated the ATM/R-dependent DNA damage checkpoint, probably due to reduced catalytic act
226 ere it plays a key role in advancing the DNA damage checkpoint process.
227  docking site to recruit the mediator of DNA damage checkpoint protein 1 (MDC1) and DNA repair protei
228 interact with phosphorylated mediator of DNA damage checkpoint protein 1 (phospho-MDC1) or E3 ubiquit
229 le checkpoint proteins MDC1 (mediator of DNA damage checkpoint protein 1) and BRCA1 (breast cancer pr
230 he DDR factors because MDC1 (mediator of DNA damage checkpoint protein 1), which normally binds to ga
231  have found that TRF2 interacts with the DNA damage checkpoint protein Chk2.
232 shed that Cdc2 kinase phosphorylates the DNA damage checkpoint protein Crb2(53BP1) in mitosis, the fu
233                                      The DNA damage checkpoint protein Hus1 associates with Rad9 and
234             53BP1, first identified as a DNA damage checkpoint protein, and BRCA1, a well-known breas
235 rate that by fusing AtCRY2 to the TopBP1 DNA damage checkpoint protein, light-induced AtCRY2 PBs can
236                              Mediator of DNA Damage Checkpoint protein, MDC1, and H2AX are chromatin
237 A, XPC, TFIIH, XPG, and XPF-ERCC1), core DNA damage checkpoint proteins (ATR-ATRIP, TopBP1, RPA), and
238     Here, we find that within minutes of DNA damage checkpoint proteins are assembled at the kinetoch
239             The requirement for specific DNA-damage checkpoint proteins suggests roles in recruiting
240 ch include mechanisms of RFP regulation, DNA damage checkpoint proteins, as well as kinases that regu
241 omotes DSB processing and recruitment of DNA damage checkpoint proteins, thus implicating cohesin in
242  binding by homologous recombination and DNA damage checkpoint proteins.
243                           In response to DNA damage, checkpoint proteins halt cell cycle progression
244 LK1 at threonine 210, a prerequisite for DNA damage checkpoint recovery, remained detectable followin
245 its degradation plays a critical role in DNA damage checkpoint recovery.
246                    Here we show that the DNA damage checkpoint regulating S-phase entry is controlled
247 ogress has advanced our understanding of DNA damage checkpoint regulations, little is known as to how
248  chromatin remodeling complexes regulate DNA damage checkpoints remain unclear.
249                            Activation of DNA damage checkpoints requires the rapid accumulation of nu
250  damage cause a metabolic checkpoint and DNA damage checkpoint, respectively.
251 berrant replication, and activation of a DNA damage checkpoint response (DDR), rendering therapeutic
252  and Rad5) and in the early steps of the DNA-damage checkpoint response (Rad17, Mec3, Ddc1, Mec1, and
253 itin-ligase CRL4 controls cell cycle and DNA damage checkpoint response and ensures genomic integrity
254 e signal that activates the ATR-mediated DNA damage checkpoint response and that the signal is enhanc
255 etic agent to analyze the basic steps of DNA damage checkpoint response in a biochemically defined sy
256 s genetically interact with genes in the DNA damage checkpoint response pathway and in the insulin si
257 es signaling through the Chk1 arm of the DNA damage checkpoint response via recruitment and stimulati
258              However, no deficiencies in DNA damage checkpoint response were detected in Cdc14b mutan
259 ion for IKK and NF-kappaB modulating the DNA-damage checkpoint response, allowing the cell to integra
260 hesin is involved in both DSB repair and the damage checkpoint response, although the relationship be
261 tide damage repair, mismatch repair, and DNA damage checkpoint response, but its function in DNA doub
262 se many activated oncoproteins trigger a DNA damage checkpoint response, which serves as a barrier to
263 ssential set of factors for ATR-mediated DNA damage checkpoint response.
264  9-1-1 checkpoint complex to enhance the DNA damage checkpoint response.
265 otein that coordinates activation of the DNA-damage-checkpoint response by coupling binding of the 9-
266 rigins become active despite an elevated DNA damage-checkpoint response.
267               Chk1 is a key regulator of DNA damage checkpoint responses and genome stability in euka
268 amage through preferential activation of DNA damage checkpoint responses and increased capacity for D
269 hat the HPV-16 E7 oncoprotein alleviates DNA damage checkpoint responses and promotes mitotic entry b
270 re, we show that L1CAM (CD171) regulates DNA damage checkpoint responses and radiosensitivity of GSCs
271 yclin D1b was not sufficient to abrogate DNA damage checkpoint responses, it did efficiently overcome
272 t L1CAM signals through NBS1 to regulate DNA damage checkpoint responses.
273  (MRN), thereby repressing ATM-dependent DNA damage checkpoint responses.
274 to dissect MRN's ATM-independent S-phase DNA damage checkpoint roles from its role in ATM activation.
275 s that are essential for the assembly of DNA damage checkpoint signaling and DNA repair protein compl
276 tical feature of the human ATR-initiated DNA damage checkpoint signaling has not been demonstrated in
277 osphorylation of Rad53 when the upstream DNA damage checkpoint signaling is turned off.
278  form bulky lesions on DNA that activate DNA damage checkpoint signaling pathways in human cells.
279                        In fission yeast, DNA damage checkpoint signaling requires Rad3, the homolog o
280 s that promitotic activity must override DNA damage checkpoint signaling to drive proliferation.
281  mutated and Rad3-related (Atr)-mediated DNA damage checkpoint signaling, including activation of the
282 duced foci (TIFs), indicating defects in DNA damage checkpoint signaling.
283 strand breaks (DSBs), and by attenuating DNA damage checkpoint signaling.
284 s the processing and repair of DSBs with DNA damage checkpoint signalling, preserving genome integrit
285                           In response to DNA damage, checkpoint signalling protects genome integrity
286 ein kinase is an important transducer of DNA damage checkpoint signals, and its mutation contributes
287          Here we show that the conserved DNA damage checkpoint sliding clamp (the 9-1-1 complex) play
288                                              Damage checkpoint systems cause cell cycle arrest, promo
289 o damaged DNA, leading to both premature DNA damage checkpoint termination and inhibition of DNA repa
290 ein kinase that is a key mediator of the DNA damage checkpoint that responds to DNA double-strand bre
291 ed and damaged DNA, these cells evade the G2 damage checkpoint to form ultrafine bridges, fragmented
292 criptase activity and the Chk2-dependent DNA damage checkpoint to prevent FOA.
293 processes that include activation of the DNA damage checkpoint, transient cell cycle arrest, DNA dama
294 3 and Rad3-mediated phospho-signaling in DNA damage checkpoint were moderately reduced in the tel2 mu
295 ks (DSBs), eukaryotic cells activate the DNA damage checkpoint, which is orchestrated by the PI3 kina
296 was associated with activation of a G2/M DNA damage checkpoint, which prevented activation of the cyc
297         In Saccharomyces cerevisiae, the DNA damage checkpoint, which responds to lesions such as dou
298 -strand breaks (DSBs), and activation of DNA damage checkpoints, which in primary human cells leads t
299                           DNA repair and DNA damage checkpoints work in concert to help maintain geno
300 , cells with DNA damage that override the G2 damage checkpoint would precociously enter mitosis and u

 
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