ライフサイエンスコーパス: fork

1 single strand gap at the stalled replication fork.

2 or the formation of a functional replication fork.

3 by an active fork converging on a collapsed fork.

4 0 or more protein factors into a replication fork.

5 could impede progression of the replication fork.

6 ies on the lagging strand of the replication fork.

7 separately and as an integrated replication fork.

8 T7 assembled on DNA resembling a replication fork.

9 DNA synthesis at an undisturbed replication fork.

10 o ssDNA sequences located at the replication fork.

11 to follow the advancement of the replication fork.

12 e the structure of CMG in complex with a DNA fork.

13 within the host specific niche, from farm to fork.

14 primase at the top of CMG at the replication fork.

15 ding the trimeric complex onto a replication fork.

16 WRN helicase-mediated degradation of stalled forks.

17 nucleolytic cleavage of stalled replication forks.

18 ase Chk1 by Rad3 (ATR) at broken replication forks.

19 driven by the progression of the replication forks.

20 ent upon HR-mediated resolution of collapsed forks.

21 2 are required for RTF2 removal from stalled forks.

22 pha and delta binding to stalled replication forks.

23 section to mediate DNA processing at stalled forks.

24 8, and Smc5/6 complex at damaged replication forks.

25 ercoils that accumulate ahead of replication forks.

26 h significantly restored PCNA at replication forks.

27 to ubiquitylated PCNA accumulated at stalled forks.

28 ading strand on active forks than on stalled forks.

29 h DNA damage frequently stalling replication forks.

30 not elongating) Okazaki fragments of stalled forks.

31 ding Okazaki fragments of active and stalled forks.

32 double-strand breaks and stalled replication forks.

33 lie in the processing of halted replication forks.

34 evolved to support multiple DNA replication forks.

35 lymerase with active and stalled replication forks.

36 ssing and protection of stressed replication forks.

37 ociation with active and stalled replication forks.

38 signaling and restart of stalled replication forks.

39 em duplications form specifically at stalled forks.

40 ntegrity and repair of collapsed replication forks.

41 elongation to dissipate torsion ahead of the forks.

42 nks and stabilization of stalled replication forks.

43 tion and protect, repair and restart damaged forks.

44 f HR-mediated repair and restart of stressed forks.

45 present in non-reversed stalled replication forks.

46 DNA polymerase alpha function at replication forks.

47 tion of the newly synthesized DNA at stalled forks.

48 ress by inducing abasic sites at replication forks.

49 hat modulates ZRANB3 activity at replication forks.

50 responses during conflicts with replication forks.

51 Mre11 inhibition instead promotes reversed fork accumulation in the absence of Brca2.

52 Replication forks also appear to stall at an unusually high rate thr

53 rmation activates MUS81-EME1 for replication fork and flap structure cleavage by relaxing substrate s

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

55 is a key component of eukaryotic replicative forks and is composed of four subunits (Sld5, Psf1, Psf2

56 r, rescue, and repair of stalled replication forks and meiosis.

57 sms of ssDNA binding proteins at replication forks and other ss duplex junctions.

58 ATR kinase activity slows replication forks and prevents origin firing in damaged cells.

59 protein SMARCAL1 stabilizes DNA replication forks and prevents replication fork collapse, a cause of

60 nucleases, efficiently cleaving replication forks and recombination intermediates.

61 which recruits ZRANB3 to stalled replication forks and stimulates its endonuclease activity.

62 ld to tether PCNA and RPA at the replication fork, and that post-translational modifications on the U

63 oteins are chaperoned around the replication fork, and the strategies that ensure that this process i

64 n of RNA-DNA hybrids, slowing of replication forks, and increased DNA damage.

65 cation origin firing, stabilizes replication forks, and promotes micronuclei formation, thus facilita

66 oops are known to interfere with replication forks, and sensitivity of the double rnhAB mutants to tr

67 Here, we establish that reversed replication forks are a pathological substrate for telomerase and th

68 he authors describe how reversed replication forks are degraded in the absence of BRCA2, and a MUS81

69 ediates, we report that reversed replication forks are entry points for fork degradation in BRCA2-def

70 In their absence, stalled replication forks are extensively degraded by the MRE11 nuclease, le

71 Stressed replication forks are most commonly repaired via homologous recombin

72 The unprotected regressed arms of reversed forks are the entry point for MRE11 in BRCA-deficient ce

73 ircumvent the process leading to replication fork arrest and minimize replicative stress.

74 n aberrant processing of stalled replication forks as the cause of increased mutagenesis.

75 form the core of the eukaryotic replication fork, as this complex undergoes major structural rearran

76 belling and combing to visualise replication forks at a single-molecule level.

77 51 filaments stabilizing stalled replication forks at CFSs and hence facilitates CFS cleavage by MUS8

78 he 5'-endonuclease EEPD1 cleaves replication forks at the junction between the lagging parental stran

79 s at a site-specific chromosomal replication fork barrier imposed by the binding of Tus proteins to a

80 Replication fork barriers are a commonly encountered problem, which

81 Consequently, the damaged forks become unstable and resistant to repair.

82 cued by XPA, suggesting that XPA-replication fork binding may prevent apoptosis in HGPS cells.

83 PCNA allows the helicase activity to unwind fork-blocking CAG/CTG hairpin structures to prevent brea

84 of Srs2 in facilitating replication through fork-blocking hairpin lesions.

85 t may originate in vivo from DNA replication fork bypass of an ICL.

86 s suggest that DNA damage at the replication fork can be replicated directly by the replisome without

87 ch cellular responses to stalled replication forks can actively generate genomic alterations and gene

88 Collapsed forks can be rescued by homologous recombination, which

89 Aberrant repair of stressed replication forks can result in cell death or genome instability and

90 can block progression of the DNA replication fork, causing replicative stress and/or cell cycle arres

91 ously showed that Metnase possesses a unique fork cleavage activity necessary for its function in rep

92 for replication fork repair by mediating the fork cleavage that permits initiation of HR-mediated rep

93 ommonly encountered problem, which can cause fork collapse and act as hotspots for replication termin

94 This prevents replication fork collapse and controls their progression.

95 n sequestration of PCNA promotes replication fork collapse and mislocalization of XPA in laminopathy-

96 ited to replication forks, where it prevents fork collapse by regulating RAD51.

97 ased origin firing and a higher frequency of fork collapse in isogenic cells, explaining their poorer

98 A replication forks and prevents replication fork collapse, a cause of DNA breaks and apoptosis.

99 tivated during replication stress to prevent fork collapse, an essential but poorly understood proces

100 block to replication, leading to replication fork collapse, double-strand DNA breaks, and cell death.

101 occurred at stalled or collapsed replication forks, concurrent with a significant loss of PCNA at the

102 We find that this type of non-canonical fork convergence in fission yeast is prone to trigger de

103 ermination may frequently occur by an active fork converging on a collapsed fork.

104 Replication forks could thus be rescued in a manner that does not in

105 g the Chk1-dependent response to replication fork damage.

106 nd PTIP, we show that RAD52 promotes stalled fork degradation and chromosomal breakage in BRCA2-defec

107 ersed replication forks are entry points for fork degradation in BRCA2-defective cells.

108 Conversely, impairing fork reversal prevents fork degradation, but increases chromosomal breakage, un

109 ell response to chemotherapeutics that cause fork degradation.BRCA proteins have emerged as key stabi

110 he prespacer is bound by Cas1-Cas2 as a dual-forked DNA, and the terminal 3'-OH of each 3' overhang s

111 and stimulates its helicase activity on DNA fork duplexes.

112 x is critical to restart stalled replication forks during checkpoint recovery.

113 SON is a replisome component that stabilizes forks during genome replication.

114 tructures that stall or collapse replication forks during the S phase.

115 cally, cDKO HSPCs showed altered replication fork dynamics, massive accumulation of DNA damage, genom

116 phosphorylation also facilitates replication fork elongation.

117 randed breaks (DSBs) and stalled replication forks, enabling two distinct mechanisms of PARPi resista

118 yde, stalls and destabilizes DNA replication forks, engendering structural chromosomal aberrations.

119 configuration of DNA polymerases at stalled forks facilitates the resumption of DNA synthesis after

120 g factors for the maintenance of replication forks following replication stress.

121 ly exposed ds-ssDNA junctions at replication forks for XPA binding.

122 n of DNA replication, convergent replication forks form a palindrome-like structural intermediate tha

123 over key molecular determinants for reversed fork formation and describe how the homologous recombina

124 ctivation of these factors restores reversed fork frequency and chromosome integrity in BRCA2-defecti

125 R) and the protection of stalled replication forks from degradation.

126 uppressor BRCA2 protects stalled replication forks from nucleolytic degradation.

127 dependent nucleolytic processing of reversed forks generated by fork remodelers.

128 Stalling at DNA replication forks generates stretches of single-stranded (ss) DNA on

129 ion of folded gastrulation expression by the Fork head transcription factor is required for apicomedi

130 The assembly of the replication fork helicase during S phase is key to the initiation of

131 The replication fork helicase is composed of Cdc45, Mcm2-7 and GINS (CMG

132 ation factors in assembly of the replication fork helicase remain unclear.

133 m to trigger the assembly of the replication fork helicase.

134 on of genes co-oriented with the replication fork in Ehmt1(-/-) and Ehmt2(-/-) ESCs, indicating that

135 he DNA2/WRN-dependent degradation of stalled forks in Abro1-deficient cells.

136 plication fork repair and restart of stalled forks in human is Metnase (also known as SETMAR), a chim

137 y, after HU induction of stalled replication forks in MCL-1-depleted cells, there was a decreased abi

138 ndependent RAD51 loading to DSBs and stalled forks in PARPi-resistant BRCA1-deficient cells, overcomi

139 equired for repriming of stalled replication forks in the nucleus, its role in mitochondria has remai

140 fficulties in analyzing specific replication forks in vivo.

141 PrimPol's recruitment to stalled replication forks in vivo.

142 dependent and exhibit properties of reversed forks, including being processed by the Exo1 nuclease.

143 t telomerase binding to reversed replication forks inhibits telomere replication, which can be mimick

144 Ribonuclease H1 ameliorates replication fork instability and chromosomal aberrations provoked by

145 ore, we show that FAN1 preserves replication fork integrity by a mechanism that is distinct from BRCA

146 g factors for the maintenance of replication fork integrity following replication stress.

147 o1, in the protection of stalled replication fork integrity.

148 Protection of the stalled replication fork is crucial for responding to replication stress and

149 DNA damage when progression of a replication fork is hampered causing replicative stress.

150 and efficient restart of stalled replication forks is critical for the maintenance of genome integrit

151 ted RFWD3 recruitment to stalled replication forks is important for ICL repair.

152 ascent lagging strands of active and stalled forks, it binds to only the matured (and not elongating)

153 ng that the NGN domain binds at the upstream fork junction of the transcription elongation complex, s

154 helicase partially encircles duplex DNA at a forked junction and is stopped by a block on the non-tra

155 stranded DNA gap accumulation at replication fork junctions and behind them by promoting Rad51 bindin

156 endent degradation of nascent DNA at stalled forks, leading to cell lethality.

157 es with WRN on synthetic stalled replication fork-like structures and stimulates its helicase activit

158 NA is a pivotal component of the replication fork machinery and a main regulator of the DNA damage to

159 cellular processes during which alternative forks may be utilized, and new biochemical studies with

160 This study introduces a simple cylinder fork model (CFM) and investigates the effects of vessel

161 RNH1) plays an important role in replication fork movement in the mammalian nucleus by resolving R-lo

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

163 otein cross-links, if present at replication forks or actively transcribed regions, may interfere wit

164 r predicament lies ahead for the replication fork, PCNA is there to orchestrate the events necessary

165 competitive than XPA in binding replication forks, PCNA sequestration by progerin may shift the equi

166 tively, and Exo1 repairs stalled replication forks poorly without EEPD1.

167 A double-strand break repair and replication fork processing, RAD51 is also implicated in the suppres

168 ting fork reversal also induced unrestrained fork progression and chromosomal breakage, suggesting fo

169 Reduced rate of DNA replication fork progression and chromosomal shattering were also ob

170 transcription can interfere with replication fork progression and stability, leading to increased mut

171 function to genome integrity and replication fork progression at particular G-rich motifs.

172 Our results demonstrate that replication fork progression in BRCA2-deficient cells requires MUS81

173 on track analyses showed reduced replication fork progression in some homozygous cells following DNA

174 tudy raises the possibility that replication fork progression might be impeded, adding to increased g

175 plication by slowing or impeding replication fork progression.

176 n origin firing that compensated for reduced fork progression.

177 uctures that are known to impede replication fork progression.

178 ligase complex that is linked to replication fork progression.

179 reating an additional barrier to replication fork progression.

180 omologous recombination (HR) and replication fork protection are sequentially bypassed during the acq

181 The replication fork protection complex (FPC) coordinates multiple proce

182 Furthermore, we show that the fork protection complex Mrc1-Tof1-Csm3 (MTC) enhances th

183 wnstream neighbor of SON (DONSON) as a novel fork protection factor and report biallelic DONSON mutat

184 chanism is distinct from the BRCA2-dependent fork protection pathway, in which stable RAD51 filament

185 Targeting these fork protection systems represents a promising strategy

186 ed origin firing, micronuclei formation, and fork protection were traced to the ability of GOF p53 to

187 cells lacking BRCA2, RADX deletion restores fork protection without restoring HDR.

188 t increases chromosomal breakage, uncoupling fork protection, and chromosome stability.

189 ecombination, but not in stalled replication fork protection, is primarily associated with supporting

190 ATRis also overcome the bypass of BRCA1/2 in fork protection.

191 HDR), replication fork reversal, and stalled fork protection.

192 established DONSON as a critical replication fork protein required for mammalian DNA replication and

193 icase associates stably with the replication fork, providing the molecular basis for how the E. coli

194 frequency and Q-factor of the quartz tuning fork (QTF) as well as the trace-gas concentration can be

195 ntegrating nanoelectrodes with quartz tuning forks (QTFs).

196 By antagonizing RAD51 at forks, RADX allows cells to maintain a high capacity for

197 chromatin factors might modulate replication fork rates in vivo.

198 We propose that Bre1-H2Bub facilitates fork recovery and gap-filling repair by controlling chro

199 y a regulatory pathway that promotes stalled forks recovery from replication stress.

200 erent spatial arrangement at the replication fork, reflecting their roles in leading- and lagging-str

201 While the fork regression/remodeling functions of SMARCAL1 have be

202 architecture and dynamics of the replication fork remain only partially understood, preventing a mole

203 In addition to SMARCAL1, other SNF2-family fork remodelers, including ZRANB3 and HLTF, cause nascen

204 ic processing of reversed forks generated by fork remodelers.

205 rplay of homologous recombination factors in fork remodeling and stability.BRCA2 is involved in both

206 However, whether this interaction promotes fork remodeling and template switching in vivo was unkno

207 ression and chromosomal breakage, suggesting fork remodeling as a global fork slowing and protection

208 e authors reveal how HR factors cooperate in fork remodeling, showing that BRCA2 supports RAD51 loadi

209 One enzyme crucial for DNA replication fork repair and restart of stalled forks in human is Met

210 ward both Rad18-dependent TS and replication fork repair by HR.

211 rforms a gatekeeper function for replication fork repair by mediating the fork cleavage that permits

212 s with a ssDNA tail promotes POLD3-dependent fork rescue.

213 We also discuss the effects of deregulated fork resection on genomic instability and on the unsched

214 scent DNA, a process commonly referred to as fork resection.

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

216 sistence of RTF2 at stalled forks results in fork restart defects, hyperactivation of the DNA damage

217 respectively) in the recombination-mediated fork restart pathway.

218 ch can be mimicked by preventing replication fork restart through depletion of RECQ1 or PARG.

219 logous to S. pombe Rtf2) must be removed for fork restart to be optimal.

220 S81 endonuclease is required for replication fork restart under replication stress elicited by exogen

221 ication stress, including slowed replication fork restart, although DNA replication checkpoints are f

222 family DNA translocase that remodels stalled forks, restores replication fork stability and reduces t

223 Persistence of RTF2 at stalled forks results in fork restart defects, hyperactivation o

224 ed in a surge of abasic sites at replication forks, revealing an ATR-mediated negative feedback loop

225 Mutations affecting fork reversal also induced unrestrained fork progression

226 uncover the physiopathological relevance of fork reversal and illuminate a complex interplay of homo

227 Here we show that damage-induced fork reversal in mammalian cells requires PCNA ubiquitin

228 Fork reversal in vivo also requires ZRANB3 translocase a

229 Replication fork reversal is a rapidly emerging and remarkably frequ

230 Fork reversal is driven in vitro by multiple enzymes, in

231 Conversely, impairing fork reversal prevents fork degradation, but increases c

232 ut not its activity, or blocking replication fork reversal through PARP1 inhibition or depleting UBC1

233 ecting replication forks that have undergone fork reversal upon drug treatment.

234 homology-directed repair (HDR), replication fork reversal, and stalled fork protection.

235 that BRCA2 is dispensable for RAD51-mediated fork reversal, but assembles stable RAD51 nucleofilament

236 it interacts with and stabilizes replication forks (RFs), resulting in elevated cell proliferation ra

237 ion termination, suggesting that replication forks rotate during replication elongation to dissipate

238 downstream to the confluence with the South Fork Shenandoah River.

239 y unwound single-stranded DNA at replication fork showed that RPA promotes DNA-(H3-H4) complex format

240 kage, suggesting fork remodeling as a global fork slowing and protection mechanism.

241 ibutable to a combination of DNA replication fork slowing and reduced replication origin firing.

242 (increased gammaH2AX, decreased replication fork speed, and increased R-loops), an apoptotic respons

243 rtant connection between meiotic replication fork stability and chromosome segregation, two processes

244 remodels stalled forks, restores replication fork stability and reduces the formation of replication

245 show that Abro1 protects stalled replication fork stability by inhibiting DNA2 nuclease/WRN helicase-

246 Defective fork stability contributes to chemotherapeutic sensitivi

247 FPC components, to elucidate how replication fork stability contributes to DNA integrity in meiosis.

248 ally reduce DONSON protein levels and impair fork stability in cells from patients, consistent with d

249 nd PARP inhibition to compromise replication fork stability in HR-deficient cancer cells, leading to

250 merging and remarkably frequent mechanism of fork stabilization in response to genotoxic insults.

251 Human Timeless is involved in replication fork stabilization, S-phase checkpoint activation and es

252 gly broad view of DNA repair and replication fork stabilizing proteins as modulators of R-loop-mediat

253 Failure to restart replication forks stalled at genomic regions that are difficult to r

254 process that helps resume DNA replication at forks stalled near bulky adducts on the DNA.

255 Replication stress or DNA damage triggers fork stalling and checkpoint signaling to activate repai

256 ed the mutagenic consequences of replication fork stalling at a single, site-specific replication bar

257 Furthermore, we observed frequent fork stalling at the junction of the common deletion, su

258 Because fork stalling in FAN1-deficient cells causes chromosomal

259 for overcoming cisplatin-induced replication fork stalling, as replication-restart was impaired in bo

260 e of genome instability, causing replication fork stalling, chromosome fragility, and impaired repair

261 Upon aberrant fork stalling, DNA damage signaling and concomitant H2AX

262 sions during replication, thereby preventing fork stalling, replication stress, and secondary DNA dam

263 stress, and secondary DNA damage related to fork stalling.

264 ruitment to sites of ICL-induced replication fork stalling.

265 ells caused G1 cell cycle arrest and S phase fork stalling.

266 DNA sequences via a mechanism we call Inter-Fork Strand Annealing (IFSA) that depends on the recombi

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

268 the nascent leading strand of a replication fork strikes the ICL Here, we report that while purified

269 UL8 has a very high affinity for replication fork structures containing a gap in the lagging strand a

270 ises simple ICL-containing model replication fork structures, the presence of a nascent leading stran

271 HJs, 5 flaps, splayed arms, and replication fork structures.

272 transfer donor-bridge-acceptor-bridge-donor 'fork' system: asymmetric (13)C isotopic labelling of one

273 DNA (ssDNA) of the leading strand on active forks than on stalled forks.

274 uced origins generate additional replication forks that are targeted by subsequent exposure to DNA da

275 olytic degradation by protecting replication forks that have undergone fork reversal upon drug treatm

276 regulated protection of stalled replication forks that involves Abro1.

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

278 by eviction of incorrect polymerases at the fork, the clamp machinery directs quality control on the

279 e restart of temporarily stalled replication forks thereby suppressing the firing of new replication

280 mosome breaks and restore broken replication forks, thereby ensuring genome stability and cell surviv

281 UNG2 remains associated with the replication fork through its interactions with two proteins, Prolife

282 x mechanisms to process and restart arrested forks through the coordinated action of multiple nucleas

283 targeting histone deposition to replication fork, through which RPA couples nucleosome assembly with

284 nto PrimPol's mode of recruitment to stalled forks to facilitate repriming and restart.

285 mplicated in cleavage of stalled replication forks to permit end resection, the identity of such an e

286 pressor and HR effector BRCA1 at replication forks to protect from RS-induced DNA damage.

287 n the regressed arms of reversed replication forks to protect them from degradation.

288 gaps are converted by Smarcal1 into reversed forks, triggering extensive Mre11-dependent nascent DNA

289 A repair factors protect stalled replication forks upon replication stress.

290 d 'mismatches' directly into the replication fork via oligonucleotide recombination, examine the dire

291 RADX is recruited to replication forks, where it prevents fork collapse by regulating RAD

292 rrent with a significant loss of PCNA at the forks, whereas PCNA efficiently bound to progerin.

293 e newly replicated region behind the stalled fork, which primarily consist of localized losses and du

294 task is executed by thousands of replication forks, which progress along the chromosomes and frequent

295 ein reduces the number of active replication forks, which reduces the consumption of thymidine and in

296 nd regulation of nucleases acting at stalled forks with a focus on the nucleolytic degradation of nas

297 In turn, MUS81 cleavage of regressed forks with a ssDNA tail promotes POLD3-dependent fork re

298 Without Brca2, forks with persistent gaps are converted by Smarcal1 int

299 omposition of the eukaryotic DNA replication fork, with an emphasis on the enzymes that synthesize DN

300 and inhibits restart of reversed replication forks within telomeres, which compromises replication an