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1 detection at sites of replication (i.e. the replisome).
2 rases function independently within a single replisome.
3 ntering a Tus-ter roadblock on an individual replisome.
4 advances in the structure of the eukaryotic replisome.
5 t connects multiple accessory factors to the replisome.
6 only capable of binding mismatches near the replisome.
7 uced by mutations that displace Pol from the replisome.
8 , triggered an interest in the dynamics of a replisome.
9 lation machinery, metabolic enzymes, and the replisome.
10 are concentrated and assembled into the HSV replisome.
11 how replication proteins enter and leave the replisome.
12 bonucleoside 5'-triphosphates (dNTPs) at the replisome.
13 echanisms to facilitate lesion bypass by the replisome.
14 n integral part of the minimal mitochondrial replisome.
15 DNA polymerase alpha (Pol alpha) within the replisome.
16 human polymerase and other components of the replisome.
17 s simply less processive in the context of a replisome.
18 oenzyme remains stably associated within the replisome.
19 the occupancy of polymerases within a moving replisome.
20 on of the leading-strand polymerase from the replisome.
21 hat keeps primase tethered to the eukaryotic replisome.
22 o coordinate enzymatic activities within the replisome.
23 he rate and fidelity of the Escherichia coli replisome.
24 contrast, RecA severely inhibits the Pol III replisome.
25 se to the Cdc45-MCM-GINS helicase within the replisome.
26 inds mismatches without associating with the replisome.
27 helicase, primase, and sliding clamp in the replisome.
28 ex forms an essential part of the eukaryotic replisome.
29 signed to either identical polymerase in the replisome.
30 in the same direction of replication by the replisome.
31 synthesis by the fully reconstituted Pol III replisome.
32 he conserved core of the archaeal/eukaryotic replisome.
33 ncounters a Tus-ter barrier before the other replisome.
34 ntifies a process unprecedented in bacterial replisomes.
35 nitiation and the overall functioning of DNA replisomes.
36 LS) is used to rescue progression of stalled replisomes.
37 , and processively as constituents of active replisomes.
38 plicative helicase is a crucial component of replisomes.
39 found in the Escherichia coli and eukaryotic replisomes.
40 sub-cellular localization of nascent DNA and replisomes.
41 e collisions of transcription complexes with replisomes.
42 their interaction with active leading-strand replisomes.
43 Duplication is concerted by replisomes.
45 nome instability, because any loss of paused replisome activity creates a requirement for reloading o
50 polymerases that are proximally bound to the replisome and continuously replenished from solution.
51 he organization of the catalytic core of the replisome and form an important step towards determining
53 4 histone chaperone that associates with the replisome and orchestrates chromatin assembly following
54 r data provide a quantitative picture of the replisome and replication stress response proteomes in 3
57 ress the stalled fork in the presence of the replisome and SSB; however, RuvAB generates a completely
58 elated with its separation distance from the replisome and that MutS motion slows when it enters the
59 45 clamp is continuously associated with the replisome and that no additional clamps accumulate on th
60 ecruitment and retention of Tof1-Csm3 by the replisome and that this complex antagonizes the Rrm3 hel
61 sites of collision between components of the replisome and the transcription apparatus and that it is
63 rrest is manifested by a failure to assemble replisomes and by decreased rates of cell growth and rRN
64 system to comprehensively study thermophilic replisomes and evolutionary links between archaeal, euka
65 by checkpoint proteins that protect arrested replisomes and inhibit new initiation when replication i
66 ollisions between DNA replication complexes (replisomes) and barriers such as damaged DNA or tightly
67 between cellular DNA replication machinery (replisomes) and damaged DNA or immovable protein complex
68 between cellular DNA replication complexes (replisomes) and obstacles such as damaged DNA or frozen
70 d events that impart negative effects on the replisome are counterbalanced by the positive effects of
74 and the proteins that work at the fork (the replisome) are known targets for the signaling pathways
78 ication initiates where forks meet through a replisome assembly mechanism normally associated with fo
84 protein complexes and place newly identified replisome-associated proteins into functional pathways.
87 of a DNA replication complex (break-induced replisome) at telomeres or elsewhere in the mammalian ge
88 polymerase does not result in loss from the replisome because of its contact with the leading-strand
89 tion fork progression is slowed down and the replisome becomes unstable in the presence of hydroxyure
90 that MutS dynamically moves to and from the replisome before mismatch binding to scan for errors.
92 ing replication fork stalling stabilizes the replisome, but how these modifications safeguard the for
93 strand template only transiently stalls the replisome, but it too is degraded, allowing Okazaki frag
95 ze this coordination in the bacteriophage T7 replisome by simultaneously monitoring the kinetics of l
97 lymerase III holoenzyme in a stalled E. coli replisome can directly bypass a single cyclobutane pyrim
98 ding the molecular basis for how the E. coli replisome can maintain high processivity and yet possess
100 es, and assembly in vitro and in vivo into a replisome capable of coordinated leading/lagging strand
105 t with the idea that polyubiquitylation of a replisome component (Mcm7) leads to its disassembly at t
107 at replication protein A (RPA), an essential replisome component that binds single-stranded DNA, has
110 We conclude that the stochastic behavior of replisome components ensures complete DNA duplication wi
113 provide evidence that Rtt107 associates with replisome components, and both itself and its associated
114 axis, but is independent of other canonical replisome components, ATM and ATR, or the homologous rec
117 searched for functional interactions in the replisome context by subjecting HSV-1 UL8 protein to ext
119 tivation, but how specific components of the replisome coordinate with ATR to activate Chk1 in human
120 , Polzeta-dependent mutagenesis triggered by replisome defects or UV irradiation in vivo was not decr
121 vation occurs in strains, in which intrinsic replisome defects promote the participation of error-pro
123 r data provide insight into the mechanism of replisome disassembly during eukaryotic DNA replication
124 identify CRL2(Lrr1) as a master regulator of replisome disassembly during vertebrate DNA replication
125 ve short lifetimes (<8 min), suggesting that replisome disassembly is quite prevalent, possibly occur
126 be rescued in a manner that does not involve replisome disassembly or reassembly, albeit with loss of
130 nd helicase stay together at the lesion, the replisome does not dissociate and the helicase does not
133 * subassembly frequently disengages from the replisome during DNA synthesis and exchanges with free c
135 proteins form a stable complex, known as the replisome, enabling them to act together in a highly coo
138 that is positioned such that one of the two replisomes encounters a Tus-ter barrier before the other
139 that aid resumption of replication by paused replisomes, especially those halted by protein-DNA barri
143 Our investigations revealed that in E. coli, replisome formation at the plasmid origin involves inter
145 coli sliding clamp is a protein mediator of replisome formation, which uses a common surface pocket
147 Eukaryotic DNA replication terminates when replisomes from adjacent replication origins converge.
149 ibition is a multistep process that disrupts replisome function and permits cleavage of the replicati
151 pancy of multiple DNA polymerases within the replisome has been observed primarily in bacteria and is
154 In vitro studies of reconstituted E. coli replisomes have attributed this remarkable processivity
156 colocalizes with the DNA polymerase complex (replisome) immediately following DNA damage or damage-in
157 sistent with the presence of only one active replisome in a significant fraction of cells (>40%).
159 H3/H4 tetramer suggest a direct role of the replisome in handling nucleosomes, which are important t
161 terized the dynamic movement of MutS and the replisome in real time using superresolution microscopy
162 ndicates that the protein accumulates at the replisome in sporulating cells, likely through a direct
168 ese findings reveal the hidden potential for replisome inactivation, and hence genome instability, in
169 rate that most pausing events do not lead to replisome inactivation, that transcription complexes are
171 ading strand lesion skipping activity of the replisome, indicating that they are competing reactions.
173 e inherent risk of genome instability, since replisomes invariably encounter DNA lesions or other str
177 ds, we demonstrate that the bacteriophage T7 replisome is able to directly replicate through a leadin
180 uced rate after replisome stalling, that one replisome is capable of skipping multiple lesions, and t
187 rks, but perhaps surprisingly, the resulting replisome is liable to intrastrand and interstrand switc
188 he SSB-dependent recruitment of RecOR to the replisome is necessary for loading and organizing RecA i
190 constituted DNA replication system where the replisome is stalled by collision with leading-strand te
191 constituted DNA replication system where the replisome is stalled by collision with leading-strand te
192 n of alpha, beta, or tau subunits within the replisome is sufficient to signal and induce the RecF-me
193 ial component of the human mitochondrial DNA replisome is the ring-shaped helicase TWINKLE-a phage T7
196 ex acts in a dynamic fashion with the moving replisome, leading to alternating phases of slow and fas
198 ng proteins associated with helicases in the replisome may have coevolved with helicases to increase
199 d single-molecule methods, and show that the replisome may solve the topological problem independent
203 ading- and lagging-strand polymerases in the replisome must be coordinated to avoid the formation of
205 chinery responsible for DNA replication, the replisome, must efficiently coordinate DNA unwinding wit
206 Ctf4 trimer hub and the first look at a core replisome of 20 different proteins containing the helica
207 ture of the approximately 650-kDa functional replisome of bacteriophage T7 assembled on DNA resemblin
213 mere damage recognition by the break-induced replisome orchestrates homology-directed telomere mainte
217 plicative helicases are the motor engines of replisomes powered by the conversion of chemical energy
218 These collisions can lead to the ejection of replisomes prior to completion of replication, which, if
221 merases can alleviate potential obstacles to replisome progression by facilitating DNA lesion bypass,
222 Instead, the tethering of SCF(Dia2) to the replisome progression complex increases the efficiency o
223 racts with the Ctf4 and Mrc1 subunits of the replisome progression complex, which assembles around th
225 in the context of chromatin, but subsequent replisome progression requires the histone chaperone FAC
226 e data suggest that PolY1 promotes efficient replisome progression through lagging-strand genes, ther
231 inhibits Twinkle unwinding, suggesting other replisome proteins may be required for efficient removal
232 rating cell nuclear antigen (PCNA) and other replisome proteins on the chromatin during and even afte
234 of Pol alpha to one CMG helicase within the replisome, providing a new model for lagging-strand synt
235 ted to and released from a centrally located replisome, providing, to our knowledge, new insight into
239 ation moves to and transiently dwells at the replisome region, even in the absence of appreciable mis
241 tion and reveal a novel mechanism of how the replisome regulates the replication checkpoint and genom
242 PriA helicase catalyzes the initial steps of replisome reloading onto repaired DNA replication forks
243 owever, the fate and behavior of the stalled replisome remains a central uncharacterized question.
246 hese pathways include lesion skipping by the replisome, replication fork regression followed by eithe
247 The minimal reconstituted leading-strand replisome requires 24 proteins, forming the CMG helicase
248 use thermosensitive mutants to show that the replisome's polymerases uncouple and transiently dissoci
249 capable of dynamic movement to and from the replisome, showing that proper nucleotide binding is cri
251 for the TPR domain of Dia2, either mediating replisome-specific degradation of Mrc1 and Ctf4 or else
252 ere, we show that SCF(Dia2) does not mediate replisome-specific degradation of Mrc1 and Ctf4, either
254 stream of the lesion at a reduced rate after replisome stalling, that one replisome is capable of ski
259 ed, and a large subcomplex of the vertebrate replisome that includes DNA Pol epsilon is retained on D
262 RecD2 helicase inactivates Escherichia coli replisomes that are paused but still functional in vitro
264 otic cells, the assembly of the multi-enzyme replisomes that perform replication is divided into stag
266 y another key component of the mitochondrial replisome, the mitochondrial single-stranded DNA-binding
269 richia coli, the proofreading subunit of the replisome, the varepsilon exonuclease, is essential for
271 ablished that RTEL1 also associates with the replisome through binding to proliferating cell nuclear
272 hat are crucial for unimpeded passage of the replisome through various barriers and difficult to repl
273 ks and resumption of replication by the same replisome thus circumventing the need for replication re
274 ost significantly, Mcm10 enables CMG and the replisome to bypass blocks on the non-tracking DNA stran
275 ngage productively with the Escherichia coli replisome to bypass leading strand template damage, desp
276 in principle, allow DnaB and the associated replisome to continue DNA synthesis without impediment,
277 a2) (SCF [Skp1/cullin/F-box protein]) to the replisome to increase its local concentration at replica
278 enome integrity relies on the ability of the replisome to navigate ubiquitous DNA damage during DNA r
281 hat it is a constituent of the mitochondrial replisome, to which it provides an additional exonucleas
282 junction with immunolocalization analyses of replisomes, to investigate the sub-cellular localization
285 examine the dynamics of the Escherichia coli replisome, using ensemble and single-molecule methods, a
286 that Ctf4 recruits the Chl1 helicase to the replisome via a conserved interaction motif that Chl1 sh
288 lC proteins within each cell and within each replisome, we elucidate the diffusion characteristics of
289 opposite effects of RecA on Pol III and TLS replisomes, we propose that RecA acts as a switch to reg
290 crofuidics, we investigate the effect on the replisome when encountering these barriers in live Esche
291 The details concerning the dynamics of the replisome when encountering these Tus-ter barriers in th
292 Mec1 and Rad53 might prevent collapse of the replisome when nucleotide concentrations are limiting, t
293 A) is situated at the core of the eukaryotic replisome, where it acts as an interaction scaffold for
294 dent Cdc7 kinase (DDK) and recruit it to the replisome, where it phosphorylates the DSB-promoting fac
295 d demonstrate that it utilizes a specialized replisome, which underlies ALT telomere maintenance.
296 bacteriophage T7 DNA polymerases within the replisome while we simultaneously observe the kinetics o
297 tudies imply a highly dynamic picture of the replisome with lagging-strand DNA polymerases residing a
298 rcome these challenges, we paused converging replisomes with a site-specific barrier in Xenopus egg e
299 conclude with a brief comparison with other replisomes with emphasis on how coordinated DNA replicat
300 ation fork can be replicated directly by the replisome without the need to activate error-prone pathw
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