ライフサイエンスコーパス: replication fork

1 present that could impede progression of the replication fork.

2 essential for the formation of a functional replication fork.

3 NA synthesis separately and as an integrated replication fork.

4 cteriophage T7 assembled on DNA resembling a replication fork.

5 ading strand DNA synthesis at an undisturbed replication fork.

6 protein onto ssDNA sequences located at the replication fork.

7 along ssDNA to follow the advancement of the replication fork.

8 discontinuities on the lagging strand of the replication fork.

9 H's functions in protecting the integrity of replication fork.

10 azaki fragments on the lagging strand of the replication fork.

11 eading and lagging strand polymerases at the replication fork.

12 -link from chromatin and resolve the stalled replication fork.

13 cting or loading the trimeric complex onto a replication fork.

14 d Pol alpha-primase at the top of CMG at the replication fork.

15 ding onto a single strand gap at the stalled replication fork.

16 ssembly of 50 or more protein factors into a replication fork.

17 mmaH2A, Rhp18, and Smc5/6 complex at damaged replication forks.

18 positive supercoils that accumulate ahead of replication forks.

19 thought, with DNA damage frequently stalling replication forks.

20 pair of DNA double-strand breaks and stalled replication forks.

21 progerin each significantly restored PCNA at replication forks.

22 f FAN1 might lie in the processing of halted replication forks.

23 n of each polymerase with active and stalled replication forks.

24 or the processing and protection of stressed replication forks.

25 ttern of association with active and stalled replication forks.

26 checkpoint signaling and restart of stalled replication forks.

27 chromosome integrity and repair of collapsed replication forks.

28 DNA cross-links and stabilization of stalled replication forks.

29 hanism which evolved to support multiple DNA replication forks.

30 ociated DNA damage and protection of stalled replication forks.

31 n origins activate to initiate bidirectional replication forks.

32 cleosome assembly onto nascent DNA at active replication forks.

33 itylation and Pol eta recruitment to stalled replication forks.

34 with changes in histone H4 deacetylation at replication forks.

35 not commonly present in non-reversed stalled replication forks.

36 acilitating DNA polymerase alpha function at replication forks.

37 participates in the recovery of the stalled replication forks.

38 omains and is therefore recruited to stalled replication forks.

39 a new member in guarding genome stability at replication forks.

40 ak-induced replication (BIR) for damaged DNA replication forks.

41 plication stress by inducing abasic sites at replication forks.

42 mechanism that modulates ZRANB3 activity at replication forks.

43 c DNA damage responses during conflicts with replication forks.

44 eckpoint kinase Chk1 by Rad3 (ATR) at broken replication forks.

45 e primarily driven by the progression of the replication forks.

46 arising from nucleolytic cleavage of stalled replication forks.

47 oting Pol alpha and delta binding to stalled replication forks.

48 viable, have a reduced capacity to maintain replication forks active during a transient hydroxyurea-

49 enome surveillance and DNA repair factors to replication forks, allowing cells to mitigate the threat

50 Replication forks also appear to stall at an unusually h

51 alytic activity of Twinkle helicase on model replication fork and DNA repair structures.

52 SMX formation activates MUS81-EME1 for replication fork and flap structure cleavage by relaxing

53 fork model that can explain how passage of a replication fork and regulation of origin firing affect

54 ith Mph1 and DNA species that resemble a DNA replication fork and the D loop formed during recombinat

55 erstrand crosslink repair, repair of stalled replication forks and DNA end joining-it fills a unique

56 to chromatin and accumulation at challenged replication forks and DNA lesions.

57 X-5461, and its related drug CX-3543, blocks replication forks and induces ssDNA gaps or breaks.

58 break repair, rescue, and repair of stalled replication forks and meiosis.

59 mbly mechanisms of ssDNA binding proteins at replication forks and other ss duplex junctions.

60 ATR kinase activity slows replication forks and prevents origin firing in damaged

61 ess response protein SMARCAL1 stabilizes DNA replication forks and prevents replication fork collapse

62 e individual nucleases, efficiently cleaving replication forks and recombination intermediates.

63 treatment increased the frequency of stalled replication forks and reduced fork speed.

64 3 function, which recruits ZRANB3 to stalled replication forks and stimulates its endonuclease activi

65 xible scaffold to tether PCNA and RPA at the replication fork, and that post-translational modificati

66 l histone proteins are chaperoned around the replication fork, and the strategies that ensure that th

67 sed the ability to challenge pre-established replication forks, and displayed equivalent susceptibili

68 accumulation of RNA-DNA hybrids, slowing of replication forks, and increased DNA damage.

69 es DNA replication origin firing, stabilizes replication forks, and promotes micronuclei formation, t

70 R-loops are known to interfere with replication forks, and sensitivity of the double rnhAB m

71 interaction enables its function at stalled replication forks, and that the inhibition of RAD52-ssDN

72 gression by affecting the chromatin state at replication forks, and we propose histone H2B ubiquitina

73 ed by RNA polymerase I (pol I) and arrest of replication forks approaching the Ter sites from the opp

74 Here, we establish that reversed replication forks are a pathological substrate for telom

75 Here the authors describe how reversed replication forks are degraded in the absence of BRCA2,

76 ation intermediates, we report that reversed replication forks are entry points for fork degradation

77 In their absence, stalled replication forks are extensively degraded by the MRE11

78 Stressed replication forks are most commonly repaired via homolog

79 Replication forks are vulnerable to wayward nuclease act

80 cellular differentiation, require programmed replication fork arrest (PFA).

81 which can circumvent the process leading to replication fork arrest and minimize replicative stress.

82 suggested an aberrant processing of stalled replication forks as the cause of increased mutagenesis.

83 teins, which form the core of the eukaryotic replication fork, as this complex undergoes major struct

84 DNA fibre labelling and combing to visualise replication forks at a single-molecule level.

85 removes RAD51 filaments stabilizing stalled replication forks at CFSs and hence facilitates CFS clea

86 leosomes and other chromatin proteins behind replication forks at high temporal and spatial resolutio

87 show that the 5'-endonuclease EEPD1 cleaves replication forks at the junction between the lagging pa

88 duplications at a site-specific chromosomal replication fork barrier imposed by the binding of Tus p

89 To avoid this problem, a replication fork barrier protein is situated downstream

90 Exo1 promotes replication fork barrier-induced direct repeat recombina

91 e sites, called replication termini (Ter) or replication fork barriers (RFB), that are located in eac

92 Replication fork barriers are a commonly encountered pro

93 nces, including telomeres, represent natural replication fork barriers.

94 could be rescued by XPA, suggesting that XPA-replication fork binding may prevent apoptosis in HGPS c

95 A polymerase I (Pol I), and to a pair of DNA replication fork block sites (Ter1 and Ter2) through int

96 ty that DSBs might be arising as a result of replication fork breakdown.

97 ly refines the current model of the poxvirus replication fork but also will lead in the long run to a

98 ructures that may originate in vivo from DNA replication fork bypass of an ICL.

99 ammalian mitochondria, did not promote mtDNA replication fork bypass of the damage.

100 hese findings suggest that DNA damage at the replication fork can be replicated directly by the repli

101 anism by which cellular responses to stalled replication forks can actively generate genomic alterati

102 Stalled replication forks can be stabilized and restarted by hom

103 Aberrant repair of stressed replication forks can result in cell death or genome ins

104 randed gaps can block progression of the DNA replication fork, causing replicative stress and/or cell

105 on profoundly impairs the progression of DNA replication forks, causing unscheduled termination event

106 This prevents replication fork collapse and controls their progression

107 s with the transcription apparatus can cause replication fork collapse and genomic instability.

108 Progerin sequestration of PCNA promotes replication fork collapse and mislocalization of XPA in

109 ng replication fork integrity and preventing replication fork collapse in the presence of triplex str

110 tabilizes DNA replication forks and prevents replication fork collapse, a cause of DNA breaks and apo

111 DNA synthesis or reprime DNA synthesis after replication fork collapse, but the origin of this activi

112 re a potent block to replication, leading to replication fork collapse, double-strand DNA breaks, and

113 the intra-S-phase checkpoint, which prevents replication fork collapse, late origin firing and stabil

114 In vertebrates, ICL repair is triggered when replication forks collide with the lesion, leading to FA

115 When a replication fork collides with an ICL, it triggers a dam

116 ion to DSBs occurred at stalled or collapsed replication forks, concurrent with a significant loss of

117 Replisome assembly at eukaryotic replication forks connects the DNA helicase to DNA polym

118 Replication forks could thus be rescued in a manner that

119 promoting homologous recombination (HR) upon replication fork damage.

120 d by blocking the Chk1-dependent response to replication fork damage.

121 er the temporal profiles of initiation rate, replication fork density and fraction of replicated DNA,

122 FDia2 complex is critical to restart stalled replication forks during checkpoint recovery.

123 s or other structures that stall or collapse replication forks during the S phase.

124 GINS on chromatin, causing severe defects in replication fork dynamics accompanied by pronounced repl

125 2 Mechanistically, cDKO HSPCs showed altered replication fork dynamics, massive accumulation of DNA d

126 gently regulated and intrinsically linked to replication fork dynamics.

127 SIRT1 phosphorylation also facilitates replication fork elongation.

128 NA double-stranded breaks (DSBs) and stalled replication forks, enabling two distinct mechanisms of P

129 Replication forks encounter obstacles that must be repai

130 te a direct role of p53 in the processing of replication forks encountering obstacles on the template

131 n, formaldehyde, stalls and destabilizes DNA replication forks, engendering structural chromosomal ab

132 y stabilizing factors for the maintenance of replication forks following replication stress.

133 tration likely exposed ds-ssDNA junctions at replication forks for XPA binding.

134 he completion of DNA replication, convergent replication forks form a palindrome-like structural inte

135 mbination (HR) and the protection of stalled replication forks from degradation.

136 in Brca2(ko/ko) cells, but protects stalled replication forks from MRE11-mediated degradation throug

137 the tumor suppressor BRCA2 protects stalled replication forks from nucleolytic degradation.

138 Stalling at DNA replication forks generates stretches of single-stranded

139 The machinery at the eukaryotic replication fork has seen many new structural advances u

140 The assembly of the replication fork helicase during S phase is key to the i

141 The replication fork helicase is composed of Cdc45, Mcm2-7 a

142 these initiation factors in assembly of the replication fork helicase remain unclear.

143 e DNA replication after the formation of the replication fork helicase.

144 ion mechanism to trigger the assembly of the replication fork helicase.

145 DR) pathways involved in protecting stressed replication forks: homologous recombination repair, DNA

146 ion initiation of genes co-oriented with the replication fork in Ehmt1(-/-) and Ehmt2(-/-) ESCs, indi

147 an RAD52 facilitates repair of collapsed DNA replication forks in cancer cells.

148 that RNA polymerase complexes also encounter replication forks in higher eukaryotes.

149 Similarly, after HU induction of stalled replication forks in MCL-1-depleted cells, there was a d

150 al from chromatin and degradation of stalled replication forks in S phase.

151 romotes intramolecular resolution of stalled replication forks in telomeric DNA while BLM facilitates

152 hown to be required for repriming of stalled replication forks in the nucleus, its role in mitochondr

153 dological difficulties in analyzing specific replication forks in vivo.

154 ritical for PrimPol's recruitment to stalled replication forks in vivo.

155 stablish that telomerase binding to reversed replication forks inhibits telomere replication, which c

156 Ribonuclease H1 ameliorates replication fork instability and chromosomal aberrations

157 hich leads to impaired resolution of stalled replication forks, insufficient repair of double-strande

158 on by XPC and XPA is critical to maintaining replication fork integrity and preventing replication fo

159 Furthermore, we show that FAN1 preserves replication fork integrity by a mechanism that is distin

160 y stabilizing factors for the maintenance of replication fork integrity following replication stress.

161 mponent, Abro1, in the protection of stalled replication fork integrity.

162 Here, we report that progression of the DNA replication fork is coordinated by UBXN-3/FAF1.

163 Protection of the stalled replication fork is crucial for responding to replicatio

164 n errors or DNA damage when progression of a replication fork is hampered causing replicative stress.

165 protection and efficient restart of stalled replication forks is critical for the maintenance of gen

166 at RPA-mediated RFWD3 recruitment to stalled replication forks is important for ICL repair.

167 of TopBP1 to sites of DNA damage and stalled replication forks is necessary for downstream events in

168 ents single-stranded DNA gap accumulation at replication fork junctions and behind them by promoting

169 mulate in early S-phase, exhibiting retarded replication fork kinetics and reduced ATR kinase signali

170 bilizing compounds retard the progression of replication forks leading to a reduction in DNA replicat

171 es resection and lastly, it resolves stalled replication forks, leading to initiation of DNA replicat

172 L5 co-operates with WRN on synthetic stalled replication fork-like structures and stimulates its heli

173 PCNA is a pivotal component of the replication fork machinery and a main regulator of the D

174 xchange protein, RAD51, is also required for replication fork maintenance, and here we show that recr

175 Here I present an alternative model: the replication fork model that can explain how passage of a

176 uclease H1 (RNH1) plays an important role in replication fork movement in the mammalian nucleus by re

177 gs reveal that redundant interactions at the replication fork must stabilize complexes containing onl

178 Importantly, the number of replication forks must be quickly adjusted in response t

179 To generate a free 5' end, stalled replication forks must therefore be cleaved.

180 sibility of exchange at the Escherichia coli replication fork on a rolling circle template.

181 iated DNA-protein cross-links, if present at replication forks or actively transcribed regions, may i

182 lexes, which in turn interact with advancing replication forks or transcription complexes to generate

183 an cause mutations in the cellular genome at replication forks or within transcription bubbles depend

184 of TFs, RNAPII, and remodelers minutes after replication fork passage.

185 nome must be disrupted and reformed when the replication fork passes, but how chromatin organization

186 Whatever predicament lies ahead for the replication fork, PCNA is there to orchestrate the event

187 is much more competitive than XPA in binding replication forks, PCNA sequestration by progerin may sh

188 act constitutively, and Exo1 repairs stalled replication forks poorly without EEPD1.

189 -mediated DNA double-strand break repair and replication fork processing, RAD51 is also implicated in

190 Reduced rate of DNA replication fork progression and chromosomal shattering

191 cate ruthenium-based intercalation can block replication fork progression and demonstrate how these D

192 an1 recruitment--and activity--restrains DNA replication fork progression and prevents chromosome abn

193 replisomal interaction hub that coordinates replication fork progression and sister chromatid cohesi

194 on defects; transcription can interfere with replication fork progression and stability, leading to i

195 nected Mms1 function to genome integrity and replication fork progression at particular G-rich motifs

196 Our results demonstrate that replication fork progression in BRCA2-deficient cells re

197 5-f][1,10]phenanthroline) immediately stalls replication fork progression in HeLa human cervical canc

198 ally interact and act in concert to preserve replication fork progression in perturbed conditions.

199 Replication track analyses showed reduced replication fork progression in some homozygous cells fo

200 rders, our study raises the possibility that replication fork progression might be impeded, adding to

201 The Chl1 helicase facilitates replication fork progression under conditions of nucleot

202 tides that chromosomal triplexes perturb DNA replication fork progression, eventually resulting in fo

203 Mcm4 intersect to control origin firing and replication fork progression, thereby ensuring genome st

204 her initiation rate is accompanied by slower replication fork progression, thereby maintaining a norm

205 able DNA structures that are known to impede replication fork progression.

206 , which is a direction dependent barrier for replication fork progression.

207 lation of both replication origin firing and replication fork progression.

208 3 ubiquitin ligase complex that is linked to replication fork progression.

209 nflicts by creating an additional barrier to replication fork progression.

210 with DNA replication by slowing or impeding replication fork progression.

211 f BRCA1 in homologous recombination (HR) and replication fork protection are sequentially bypassed du

212 The replication fork protection complex (FPC) coordinates mu

213 and cisplatin resistance is associated with replication fork protection in Brca2-deficient tumour ce

214 RP1 and CHD4, leads to the same end point of replication fork protection, highlighting the complexiti

215 homologous recombination, but not in stalled replication fork protection, is primarily associated wit

216 warfism and established DONSON as a critical replication fork protein required for mammalian DNA repl

217 the DnaB helicase associates stably with the replication fork, providing the molecular basis for how

218 ow multiple chromatin factors might modulate replication fork rates in vivo.

219 PolDIP2 in human cells causes a decrease in replication fork rates, similar to that observed in Prim

220 cells does not produce a further decrease in replication fork rates.

221 adopt a different spatial arrangement at the replication fork, reflecting their roles in leading- and

222 however the architecture and dynamics of the replication fork remain only partially understood, preve

223 One enzyme crucial for DNA replication fork repair and restart of stalled forks in

224 ntributes toward both Rad18-dependent TS and replication fork repair by HR.

225 us, EEPD1 performs a gatekeeper function for replication fork repair by mediating the fork cleavage t

226 hieve distinct outcomes in recombination and replication fork repair.

227 with Mph1 and the associated MHF complex in replication fork repair.

228 ordinate sequestration of RPA at stalled DNA replication forks, represents a conserved feature of the

229 This interaction likely promotes replication fork restart and gap avoidance.

230 ication, which can be mimicked by preventing replication fork restart through depletion of RECQ1 or P

231 tivity of MUS81 endonuclease is required for replication fork restart under replication stress elicit

232 creased replication stress, including slowed replication fork restart, although DNA replication check

233 , promotion of deoxynucleotide synthesis and replication fork restart, prevention of double-stranded

234 cells resulted in a surge of abasic sites at replication forks, revealing an ATR-mediated negative fe

235 Replication fork reversal is a rapidly emerging and rema

236 telomeres, but not its activity, or blocking replication fork reversal through PARP1 inhibition or de

237 D51 promotes homology-directed repair (HDR), replication fork reversal, and stalled fork protection.

238 ells, where it interacts with and stabilizes replication forks (RFs), resulting in elevated cell prol

239 ore replication termination, suggesting that replication forks rotate during replication elongation t

240 imics freshly unwound single-stranded DNA at replication fork showed that RPA promotes DNA-(H3-H4) co

241 together with R-loop accumulation results in replication fork slowing and DNA damage.

242 hat was attributable to a combination of DNA replication fork slowing and reduced replication origin

243 cogene-induced replication stress, including replication fork slowing, DNA damage and senescence.

244 y reducing DNA repair but also by preventing replication fork slowing.

245 fork stress (increased gammaH2AX, decreased replication fork speed, and increased R-loops), an apopt

246 veal an important connection between meiotic replication fork stability and chromosome segregation, t

247 s in DNA can serve as natural impediments to replication fork stability and progression, resulting in

248 locase that remodels stalled forks, restores replication fork stability and reduces the formation of

249 We show that Abro1 protects stalled replication fork stability by inhibiting DNA2 nuclease/W

250 t's primary FPC components, to elucidate how replication fork stability contributes to DNA integrity

251 Here we find PARP inhibition to compromise replication fork stability in HR-deficient cancer cells,

252 , and its absence in S phase is required for replication fork stability.

253 Human Timeless is involved in replication fork stabilization, S-phase checkpoint activ

254 an increasingly broad view of DNA repair and replication fork stabilizing proteins as modulators of R

255 In the absence of FANCD2, replication forks stall within the AT-rich fragility cor

256 mosome abnormalities from occurring when DNA replication forks stall, even in the absence of ICLs.

257 Failure to restart replication forks stalled at genomic regions that are di

258 s, we analyzed the mutagenic consequences of replication fork stalling at a single, site-specific rep

259 ndent direct repeat recombination induced by replication fork stalling but only a minor role in const

260 exes in DNA replication foci and counteracts replication fork stalling in RNAPI- and RNAPII-transcrib

261 mploys specialized DNA polymerases to bypass replication fork stalling lesions.

262 delays, defective HRR, inability to overcome replication fork stalling, and replication stress.

263 s necessary for overcoming cisplatin-induced replication fork stalling, as replication-restart was im

264 are a source of genome instability, causing replication fork stalling, chromosome fragility, and imp

265 that form non-B structures are implicated in replication fork stalling, DNA double strand breaks (DSB

266 ng RFWD3 recruitment to sites of ICL-induced replication fork stalling.

267 A polymerases to sites of DNA-damage-induced replication fork stalling.

268 in DNA damage response signalling following replication fork stalling/collapse.

269 haracterized by an increase in biomarkers of replication fork stress (increased gammaH2AX, decreased

270 iggered when the nascent leading strand of a replication fork strikes the ICL Here, we report that wh

271 Finally, UL8 has a very high affinity for replication fork structures containing a gap in the lagg

272 PF-ERCC1 incises simple ICL-containing model replication fork structures, the presence of a nascent l

273 ntly cleaves HJs, 5 flaps, splayed arms, and replication fork structures.

274 nhibitor-induced origins generate additional replication forks that are targeted by subsequent exposu

275 TRAIP as a new factor at active and stressed replication forks that directly interacts with PCNA via

276 age tolerance facilitates the progression of replication forks that have encountered obstacles on the

277 revent nucleolytic degradation by protecting replication forks that have undergone fork reversal upon

278 ew aspect of regulated protection of stalled replication forks that involves Abro1.

279 sensitizes cells to DSBs from IR or stalled replication forks that require HR for repair.

280 mediating the restart of temporarily stalled replication forks thereby suppressing the firing of new

281 to mend chromosome breaks and restore broken replication forks, thereby ensuring genome stability and

282 ng S-phase, UNG2 remains associated with the replication fork through its interactions with two prote

283 platform for targeting histone deposition to replication fork, through which RPA couples nucleosome a

284 del where Pol iota occasionally accesses the replication fork to generate a first mutation, and Pol z

285 servations demonstrate the resilience of the replication fork to natural barriers and the sensitivity

286 i indicating increased conversion of stalled replication forks to double-strand breaks (DSBs).

287 n are required for ETAA1 function at stalled replication forks to maintain genome stability.

288 have been implicated in cleavage of stalled replication forks to permit end resection, the identity

289 he tumor suppressor and HR effector BRCA1 at replication forks to protect from RS-induced DNA damage.

290 51 loading on the regressed arms of reversed replication forks to protect them from degradation.

291 Cs 1 and 2 to facilitate activity of stalled replication forks under conditions of replication stress

292 cule FRET measurements, lead us to suggest a replication fork unwinding mechanism whereby the N-termi

293 ntegrity, DNA repair factors protect stalled replication forks upon replication stress.

294 duce targeted 'mismatches' directly into the replication fork via oligonucleotide recombination, exam

295 RADX is recruited to replication forks, where it prevents fork collapse by re

296 activity such as removal of proteins at the replication fork, whereas the association of ssDNA reeli

297 is daunting task is executed by thousands of replication forks, which progress along the chromosomes

298 ing Hda protein reduces the number of active replication forks, which reduces the consumption of thym

299 enesis and composition of the eukaryotic DNA replication fork, with an emphasis on the enzymes that s

300 ly binds to and inhibits restart of reversed replication forks within telomeres, which compromises re