ライフサイエンスコーパス: replication fork

1 itment of error-prone DNA polymerases to the replication fork.

2 , Ctf4, and the fork protection complex at a replication fork.

3 al nucleosomes are disrupted in front of the replication fork.

4 e two known stabilizers that travel with the replication fork.

5 ly threatened by problems encountered by the replication fork.

6 and then reassembled in the wake of the DNA replication fork.

7 ny time, with ~12 enzymes enriched near each replication fork.

8 rk for understanding DNA transactions at the replication fork.

9 g of the overhang to SSB-coated ssDNA at the replication fork.

10 he DNA crosslink or to stabilize the stalled replication fork.

11 ase RECQ1, which promotes restart of stalled replication forks.

12 that coordinates the enzymatic activities at replication forks.

13 tion of RAD51 nucleofilaments at damaged DNA replication forks.

14 RPi involving MRE11-dependent degradation of replication forks.

15 itigating the effect of protein obstacles on replication forks.

16 stion triggers CMG ubiquitylation at stalled replication forks.

17 (MMC), agents that hinder the progression of replication forks.

18 and tight nucleoprotein complexes, can block replication forks.

19 talling chemotherapeutics causes reversal of replication forks.

20 al for the functional maintenance of stalled replication forks.

21 bes a new role for TIM in protecting stalled replication forks.

22 n kinetics by leading to the collapse of DNA replication forks.

23 tes joining of the strands of the convergent replication forks.

24 PCNA, a DNA clamp and processivity factor at replication forks.

25 bilizes the RPA-ATR-ATRIP complex at stalled replication forks.

26 ses that mediate the repair of collapsed DNA replication forks.

27 dent resection of regressed arms at reversed replication forks.

28 catalytic activity and symmetric movement of replication forks.

29 d Rad5 causes aberrant template switching at replication forks.

30 initiation at oriC and re-start of collapsed replication forks.

31 joining factor XLF promotes the stability of replication forks.

32 ase of the cell cycle and is associated with replication forks.

33 ed to and responsible for protecting stalled replication forks.

34 rotein that stabilizes telomeres and stalled replication forks.

35 hought to be required for progression of the replication forks.

36 ligase activity of the complex by collapsed replication forks.

37 DNA double-strand breaks (DSBs) and stalled replication forks.

38 component of the replisome; and is found at replication forks.

39 f genome duplication by restarting collapsed replication forks.

40 ls' ability to stabilize and restart stalled replication forks.

41 dback loop that fine-tunes MUS81 activity at replication forks.

42 progression and restart of stalled telomere replication forks.

43 olytic degradation of nascent DNA at stalled replication forks.

44 s may encounter DNA lesions, which can stall replication forks.

45 oncomitant loss of cohesion, possibly at DNA replication forks.

46 cated in the resection of HU-induced stalled replication forks.

47 lexes may bind both NER bubble junctions and replication forks.

48 instability caused by unrepaired DNA gaps at replication forks.

49 elongation by the Y-shaped DNA structure of replication forks.

50 hway is activated by R loop-induced reversed replication forks.

51 rm non-B DNA secondary structures that stall replication forks, activate the ATR checkpoint kinase, a

52 combination and also to protect stressed DNA replication forks against spurious nucleolytic attrition

53 tected up to 75 kb downstream of a collapsed replication fork and can be triggered by head-on collisi

54 he replisome is a protein complex on the DNA replication fork and functions in a dynamic environment

55 to defective gap-filling in the wake of the replication fork and incomplete Okazaki fragment maturat

56 esolution of G4 structures both ahead of the replication fork and on the lagging strand template.

57 44 bound H3K9me3-modified nucleosomes at the replication fork and recruited SUV39H1, CRL4, and Mi-2/N

58 structures that can lead to the stalling of replication forks and cause genomic instability.

59 ions in parallel to Chl1 and Mrc1 to protect replication forks and cell viability.

60 function mutant 273H and PARP1 interact with replication forks and could serve as potential biomarker

61 ation of these foci is independent of active replication forks and dependent on the presence of the c

62 Through these versatile activities at replication forks and DNA damage sites, DNA2 functions a

63 of proteins that protect or repair stressed replication forks and due to the continuous proliferativ

64 ly, BRUCE deficiency resulted in stalled DNA replication forks and increased firing of new replicatio

65 n stress response functions to stabilize DNA replication forks and inhibits genome instability and tu

66 pathway protein, FANCD2, locates to stalled replication forks and recruits homologous recombination

67 ding the lagging-strand arm of abandoned DNA replication forks and reloading the replicative helicase

68 iously found that LSD1 associates with HSV-1 replication forks and replicating viral DNA, suggesting

69 tability, thereby aiding TIM localization to replication forks and the coordination of replisome prog

70 rate, which depends on the number of active replication forks and their velocity.

71 evolved several mechanisms that protect DNA replication forks and thus maintain genome integrity and

72 o the nuclear periphery, associates with DNA replication forks, and counteracts TOP1ccs during DNA re

73 of the DNA double helix, restart broken DNA replication forks, and cross over chromatids during meio

74 cation origin firing, of the architecture of replication forks, and of the functional organization of

75 m aborted topoisomerase reactions, collapsed replication forks, and other stressors.

76 cBCD- and RuvAB-dependent reestablishment of replication fork; and efficiencies of degradosome machin

77 In this Review, we discuss how replication forks are actively stalled, remodelled, proc

78 Degradation and collapse of stalled replication forks are main sources of genomic instabilit

79 Without this response, stalled replication forks are not stabilized, and new origin fir

80 a key factor in promoting cell survival when replication forks are stalled or collapsed.

81 DNA repair and the protection of stalled DNA replication forks are thought to underlie the chemosensi

82 broad utility of this tool by demonstrating replication fork arrest by the specifically bound dCas9-

83 Upon replication fork arrest, the replication checkpoint kina

84 ngagement of homologous recombination at DNA-replication-fork associated single-ended double-strand b

85 Several replication-fork-associated "cohesion establishment fact

86 dly reduced in patient cells, accompanied by replication fork asymmetry, increased interorigin distan

87 been reported for replicative helicases at a replication fork at atomic resolution, a prerequisite to

88 ination-initiated pathway that initiates DNA replication forks at late times of T4 bacteriophage infe

89 d populations of challenged and unchallenged replication forks, averaged across S phase, and model a

90 Using replication fork barriers in fission yeast, we report th

91 requencies of Top1-dependent DSBs at natural replication fork barriers.

92 he literature: cooperative origin firing and replication fork barriers.

93 hly transcribed by pol III in vivo are known replication fork barriers.

94 the existence of a 'battleground' at the DNA replication fork between homologous recombination (HR) f

95 RFC enriches and balances PCNA levels at the replication fork, beyond the needs of DNA replication, t

96 HMCES acts at replication forks, binds PCNA and single-stranded DNA, a

97 Instead of utilizing a canonical replication fork, BIR is driven by a migrating D-loop an

98 Instead of a replication fork, BIR is driven by a migration bubble wh

99 must faithfully replicate DNA and cope with replication fork blocks and stalling, while simultaneous

100 kinase restricts excessive DNA unwinding at replication forks by limiting CMG helicase activity, sug

101 2 prevents excessive degradation of reversed replication forks by MRE11.

102 Abnormal processing of stressed replication forks by nucleases can cause fork collapse,

103 Stalled replication forks can be restarted and repaired by RAD51

104 HU-treated rad53 mutants is a consequence of replication fork catastrophes at centromeres.

105 results support a model wherein slow-moving replication forks caused by the lack of Pol e's catalyti

106 lobal replisome disassembly that can trigger replication fork collapse and DNA rearrangements.

107 the polymerization of DNA or RNA, leading to replication fork collapse or transcription arrest, or ca

108 mplexes can impede DNA replication and cause replication fork collapse.

109 opus egg extracts, we previously showed that replication fork collision with DPCs causes their proteo

110 junction of the lagging strand in a PriA-DNA replication fork complex.

111 Over-replication is completely abolished if replication fork complexes are prevented from fusing by

112 me duplication initiates via the assembly of replication fork complexes at defined origins, from wher

113 by the GRF-ZF motifs helps recruit NEIL3 to replication forks converged at an ICL, but the nature of

114 The second repair mechanism requires replication fork convergence, but does not involve DNA i

115 ermination of DNA replication when an active replication fork converges on a collapsed fork (Morrow e

116 The convergence of two DNA replication forks creates unique problems during DNA rep

117 f the leading-strand DNA polymerase from the replication fork DNA helicase, and 2) on the damaged tem

118 Single-molecule assessment of replication fork dynamics in BRG1-deficient cells reveal

119 ion during double-strand break repair and in replication fork dynamics.

120 DNA replication is a stochastic process with replication forks emanating from multiple replication or

121 When replication forks encounter G-quadruplexes, EXO1 resects

122 When replication forks encounter template DNA lesions, the le

123 citate this ligase for DNA repair at stalled replication forks, facilitating mitotic progression.

124 ng to DNA replication stress and stabilizing replication forks following Myc overexpression.See relat

125 DNA replication, thereby providing access to replication forks for other factors.

126 g times lead to origin interference, where a replication fork from an origin can replicate through an

127 by homologous recombination and protects DNA replication forks from attrition.

128 of Fanconi anaemia proteins protect stalled replication forks from degradation by nucleases, through

129 s lacking RAD51's enzymatic activity protect replication forks from MRE11-dependent degradation, as e

130 nctions are also required to protect stalled replication forks from nucleolytic degradation during re

131 FAM111A, but not SPRTN, protects replication forks from stalling at poly(ADP-ribose) poly

132 checkpoint kinase Rad53, which prevents DNA replication forks from undergoing aberrant structural tr

133 These results suggest that HAT1 links replication fork function to the proper processing and a

134 lomere maintenance and resolution of stalled replication forks genome-wide.

135 ading- and lagging-DNA strand synthesis at a replication fork has not been reported.

136 eleasin complex perturbs cohesin dynamics on replication forks, hindering fork progression and promot

137 ryotic CMG helicase with template DNA at the replication fork impairs its helicase activity, which is

138 ss of lesions, pol IV is rarely found at the replication fork in vivo.

139 rious nucleolytic degradation of stalled DNA replication forks in a manner similar to that of cells l

140 in response to circumstances that stall DNA replication forks in both yeast and mammalian cells.

141 Timeless increase RS tolerance by protecting replication forks in cancer cells.

142 ction, processing, and remodeling of stalled replication forks in mammalian cells.

143 origins in order to generate bi-directional replication forks in S-phase.

144 pression on hydroxyurea (HU)-induced stalled replication forks in the setting of BRCA1 deficiency.

145 ex to arrest viral, bacterial and eukaryotic replication forks in vitro.

146 The direct effect of Rad5 on replication forks in vivo, increased recombination, and

147 emerged as being responsible for remodeling replication forks in vivo.

148 Here, we show that ISG15 localizes at the replication forks, in complex with PCNA and the nascent

149 endonuclease Mus81 from cleaving the stalled replication fork inappropriately.

150 ligase UBR5 interacts with components of the replication fork, including the translesion synthesis (T

151 paired replication resulted in a collapse of replication forks, inducing dsDNA breaks, homologous rec

152 Protecting replication fork integrity during DNA replication is ess

153 entifies CtIP as a critical regulator of DNA replication fork integrity, which, when compromised, may

154 tress response, working together to preserve replication fork integrity.

155 n (HR) cooperate during S-phase to safeguard replication forks integrity.

156 associated with un-replicated DNAs ahead of replication forks into cohesive structures behind them,

157 Stabilization of stalled replication forks is a prominent mechanism of PARP (Poly

158 oading of Pds5 and other cohesion factors on replication forks is not affected by the BRCA2 status.

159 on a complex mechanism, where dysfunctional replication forks lead to recruitment of error-prone pol

160 lymerase backtracking, which interferes with replication forks, leading to DNA double-stranded breaks

161 DNA replication stress can stall replication forks, leading to genome instability.

162 y which BRCA1-BARD1 functions in DNA repair, replication fork maintenance and tumour suppression, and

163 sence of RNaseH, which were enriched for DNA replication fork maintenance factors including the MRE11

164 isregulation of chromosome damage repair and replication fork maintenance.

165 This remarkable plasticity of the replication fork may determine the outcome of replicatio

166 Hence, a reduction in single-stranded DNA at replication forks may explain the inability of PMA-induc

167 ccurately reconstruct movement of individual replication forks, measured by DNA combing.

168 When converging replication forks meet during replication termination, t

169 It has been proposed that at stalled replication forks, monoubiquitinated-FANCD2 serves to re

170 t a sequencing method for the measurement of replication fork movement on single molecules by detecti

171 etween two major mechanisms rescuing stalled replication forks - mtDNA degradation and homology-depen

172 complex powers DNA strand separation of the replication forks of eukaryotes and archaea.

173 nd breaks, such as those formed at collapsed replication forks or eroded telomeres.

174 d DNA breaks, such as those formed at broken replication forks or uncapped telomeres.

175 nscription that occurs immediately following replication fork passage, in this case by promoting effi

176 work of interactions important for efficient replication fork pausing.

177 fere with the correct metabolism of arrested replication forks, phenotype reminiscent of defective ho

178 interesting recent data on the relevance of replication fork plasticity to human health, covering it

179 Stabilisation of stalled replication forks prevents excessive fork reversal and t

180 Stabilization of stalled replication forks prevents excessive fork reversal or de

181 bination enzyme RAD51 has been implicated in replication fork processing and restart in response to r

182 plicate' DNA regions, end resection, stalled replication fork processing, and mitochondrial genome ma

183 tudies identify a critical role for STAG2 in replication fork procession and elucidate a potential th

184 rases to sites of DNA damage and impairs DNA replication forks processivity after UV irradiation, lea

185 XLF deficiency leads to defects in replication fork progression and an increase in fork rev

186 ith MCM8-9 and RPA facilitate HR and promote replication fork progression and cellular viability in r

187 ment to chromatin to promote unperturbed DNA replication fork progression and DPC repair.

188 f these positive supercoils is essential for replication fork progression and for the overall unlinki

189 to radiation-induced DNA damage, suppresses replication fork progression and impedes cancer cell sur

190 unctionally relevant, as HAT1 loss decreased replication fork progression and increased replication f

191 lication stress response, promoting telomere replication fork progression and restart of stalled telo

192 valent DNA-protein cross-links (DPCs) impede replication fork progression and threaten genome integri

193 frequently encounters impediments that slow replication fork progression and threaten timely and err

194 Mdm4 in p53-deficient cells compromises DNA replication fork progression as well.

195 with CTNAs and exhibit significant delays in replication fork progression during exposure to CTNAs.

196 nd primase activities that are important for replication fork progression in vitro and in cellulo.

197 ased growth rate can be explained by laggard replication fork progression near the terminus region of

198 A moderate dependence on ATAD2 for replication fork progression was noted only for hdac2 ce

199 nterestingly, no substantial perturbation of replication fork progression was observed, but rather mi

200 A1 and SA2 to 3D chromatin organization, DNA replication fork progression, and DNA double-strand brea

201 se helicase-polymerase uncoupling and impede replication fork progression, but the details of how unc

202 en left unresolved, RNA-DNA hybrids can slow replication fork progression, cause DNA breaks, and incr

203 r induced by interferon-beta, accelerate DNA replication fork progression, resulting in extensive DNA

204 nly full-length Mdm4 was able to support DNA replication fork progression.

205 nd polymerase stalling at DNA damage impairs replication fork progression.

206 mpacts RNR activity, dNTP synthesis, and DNA replication fork progression.

207 es, which reduces the pol III barrier to the replication fork progression.

208 y increased origin firing and retardation of replication fork progression.

209 plate R-loops (head-on) had little impact on replication fork progression.

210 ordination of DNA unwinding and synthesis at replication forks promotes efficient and faithful replic

211 Mechanistically, RAD52 binds to the stalled replication fork, promotes its occlusion and counteracts

212 tic basis of BRCAness, to include defects in replication fork protection (RFP).

213 s indicate that PDS5 proteins participate in replication fork protection and also provide insights in

214 racting replication stress by regulating the replication fork protection complex (FPC).

215 The contribution and regulation of BRCA1 in replication fork protection, and how this role relates t

216 reveal a BRCA1-mediated pathway that governs replication fork protection.

217 h reduced sensitivity to PARPi by overcoming replication fork protection.

218 Cohesin down-regulation restored normal replication fork rates in PDS5-deficient cells, suggesti

219 'on the fly' to promote resumption of rapid replication fork rates, despite lesion bypass occurring

220 f magnitude slower compared to their in vivo replication fork rates.

221 revealing this as a crucial driver of normal replication fork rates.

222 nscription-replication collisions, promoting replication fork recovery, and enforcing a G2/M cell-cyc

223 ntriguingly, ATRX was recently implicated in replication fork recovery; however, the underlying mecha

224 eplication stalling in mitochondria leads to replication fork regression and mtDNA double-strand brea

225 h conversion was shown previously to require replication fork regression, supporting a model in which

226 rase without compromising the advance of the replication fork remains unresolved.

227 rt that Smarcal1 and Zranb3, closely related replication fork-remodeling proteins, have nonredundant

228 of cells with micronuclei) from compromised replication fork repair(6).

229 created by Scc2-dependent de novo loading at replication forks requires the Ctf18-RFC complex.

230 In bacteria, the restart of stalled DNA replication forks requires the DNA helicase PriA.

231 ent to DNA repair foci and, secondly, during replication fork restart following replication fork stal

232 s CtBP interacting protein (CtIP) to promote replication fork restart while suppressing new origin fi

233 h TopBP1 and PHF8 are required for efficient replication fork restart.

234 r pathways, replication-stress signaling and replication-fork restart factors.

235 pathways assist fork progression, promoting replication fork reversal, translesion DNA synthesis (TL

236 DNA topological stress inhibits DNA replication fork (RF) progression and contributes to DNA

237 A synthesis, and the recovery of stalled DNA replication forks (RFs).

238 n in BRCA2-deficient cells protected stalled replication forks (RFs).

239 f FAM111A in overcoming protein obstacles to replication forks, shedding light on cellular responses

240 eading of gamma-H2AX on chromatin and global replication fork slowdown.

241 K expression initially enhances cellular DNA replication fork speed but ultimately leads to increased

242 ve sister chromatid cohesion and reduced DNA replication fork speed.

243 Epigenetic mechanisms of replication fork stability are emerging but remain poorl

244 y unrecognized role in DNA damage repair and replication fork stability by counteracting 53BP1 functi

245 Replication fork stability during DNA replication is vit

246 tensive transcriptional activity compromises replication fork stability, potentially leading to gene

247 2 monoubiquitination is a critical event for replication fork stabilization by the Fanconi anemia (FA

248 lar events in recombinational DNA repair and replication fork stabilization.

249 icity island of H. pylori, is accompanied by replication fork stalling and can be observed also in pr

250 es revealed increased amounts of spontaneous replication fork stalling and chromosomal aberrations, a

251 renders cells specifically sensitive to the replication fork stalling and collapse caused by methyl

252 fork speed but ultimately leads to increased replication fork stalling and the attenuation of cellula

253 best modeled as mtDNA deletions initiated by replication fork stalling during strand displacement mtD

254 One way to prevent replication fork stalling is through the recruitment of

255 eplication blocks, most genome-destabilizing replication fork stalling likely occurs because of prote

256 ng primary cells, significant differences in replication fork stalling, collapse, and DNA damage were

257 In BLBC cells, POLE suppression leads to replication fork stalling, DNA damage, and a senescence-

258 els, correlate with synergistic increases in replication fork stalling, double-strand breaks, and apo

259 s replication stress, possibly by increasing replication fork stalling, providing a molecular mechani

260 ce inhibition of DNA replication can lead to replication fork stalling, resulting in DNA damage and a

261 In response to DNA damage or replication fork stalling, the basal activity of Mec1(AT

262 d DNA is transient, but can be stabilized by replication fork stalling.

263 ion, R-loop-mediated genome instability, and replication fork stalling.

264 y, during replication fork restart following replication fork stalling.

265 d replication fork progression and increased replication fork stalling.

266 ia pathway of ICL repair is activated when a replication fork stalls at an ICL(2); this triggers mono

267 passively replicated from distal-originating replication forks, suggesting distinct chromatin assembl

268 tly at single-ended DSBs formed at collapsed replication forks than at double-ended DSBs.

269 structures appear to arise from arrested DNA replication forks that accumulate in the absence of CtIP

270 DNA replication forks that are stalled by DNA damage activat

271 udied the convergence of reconstituted yeast replication forks that include all core replisome compon

272 ing and inhibit Exo1 recruitment to stressed replication forks, thereby avoiding unscheduled fork res

273 ewly synthesized histones in the wake of the replication fork through the activity of the replication

274 DNA replication requires the progression of replication forks through DNA damage, actively transcrib

275 Factor 1 (CAF-1), which is recruited to DNA replication forks through its interaction with prolifera

276 G helicase, which stably associates with DNA replication forks throughout elongation.

277 cherichia coli by monitoring the location of replication forks throughout on average >500 cell cycles

278 AD52 limits excessive remodelling of stalled replication forks, thus indirectly assisting RAD51 and B

279 repair DNA double-strand breaks and stalled replication forks to maintain genome stability.

280 asic sites in single-stranded DNA at stalled replication forks to prevent genome instability.

281 In vitro, purified replisomes drive model replication forks to synthesize continuous leading stran

282 d homologous recombination (HR), accelerated replication forks under stress, and increased resistance

283 visualize chromatin components at individual replication forks undergoing DNA replication.

284 PriA can recognize and remodel abandoned DNA replication forks, unwind DNA in the 3'-to-5' direction,

285 he requirement of both proteins to stabilize replication forks upon Myc dysregulation in a nonredunda

286 2 or Aurora A causes deprotection of stalled replication forks upon replication stress induction.

287 We also detected LANA along with MCMs at the replication forks using a novel approach, isolation of p

288 ably, we also showed that the progression of replication forks was altered in ORSCs from hair follicl

289 mics of chromatin restoration behind the DNA replication fork, we developed nascent chromatin occupan

290 complexes co-directionally oriented with the replication fork were transient blockages, whereas those

291 Moreover, in the absence of HAT1, stalled replication forks were unstable, and newly synthesized D

292 ATRX and FANCD2 localize to stalled replication forks where they cooperate to recruit CtIP a

293 essivity of unwinding in the presence of the replication fork, which acts as a barrier to progress.

294 DNA-binding factors following passage of the replication fork, which may provide a mechanism for pert

295 ficient cells by acetylating H4K8 at stalled replication forks, which recruits MRE11 and EXO1.

296 Cdc45 also recruits Rad53 to stalled replication forks, which we demonstrate is important for

297 dentify the location, direction and speed of replication forks with high resolution.

298 In Xenopus egg extracts, the collision of replication forks with interstrand crosslinks initiates

299 he interactions between PriA and stalled DNA replication forks with or without SSB.

300 demonstrate that Rep colocalizes with 70% of replication forks, with a hexameric stoichiometry, indic