ライフサイエンスコーパス: double-strand DNA break

1 AN deletion reduced recruitment of Tel1 to a double-strand DNA break.

2 ctively cope with severe DNA lesions such as double strand DNA breaks.

3 f neuroblastoma cell lines, directly causing double strand DNA breaks.

4 promoting homology-directed repair (HDR) of double strand DNA breaks.

5 sensitivity and decreased ability to repair double strand DNA breaks.

6 nes, whereas ATM is activated in response to double strand DNA breaks.

7 revealing the initial step in the repair of double-strand DNA breaks.

8 not required for NHEJ repair of chromosomal double-strand DNA breaks.

9 es that mediate DNA cross-linking and induce double-strand DNA breaks.

10 ase involved in the ATM-mediated response to double-strand DNA breaks.

11 articipates in non-homologous end joining of double-strand DNA breaks.

12 enhances Rad51 accumulation during repair of double-strand DNA breaks.

13 orylation of histone H2AX, a known marker of double-strand DNA breaks.

14 d51) is central to recombinational repair of double-strand DNA breaks.

15 ts in recombinogenic DNA lesions, presumably double-strand DNA breaks.

16 omic deletions and rearrangements as well as double-strand DNA breaks.

17 NHEJ is the major pathway for the repair of double-strand DNA breaks.

18 le-strand DNA nicks, whereas Mn(2+) promotes double-strand DNA breaks.

19 fragmentation in dut rec mutants, indicating double-strand DNA breaks.

20 BC recombinational repair pathway that mends double-strand DNA breaks.

21 binational repair after being converted into double-strand DNA breaks.

22 f neuroblastoma cell lines, directly causing double-strand DNA breaks.

23 epair gene XPB, is involved in the repair of double-strand DNA breaks.

24 pathway that in normal cells acts to repair double-strand DNA breaks.

25 regulate DNA topology by creating transient double-strand DNA breaks.

26 leading to further processing of the initial double-stranded DNA break.

27 , suggests sequence capture during repair of double-stranded DNA breaks.

28 ed in homologous recombination and repair of double-stranded DNA breaks.

29 forms distinct foci, and can associate with double-stranded DNA breaks.

30 defective lentiviruses into nuclease-induced double-stranded DNA breaks.

31 ved in the early recognition and response to double-stranded DNA breaks.

32 with other telomeric loci, or non-telomeric double-stranded DNA breaks.

33 ase/nuclease that initiates recombination at double-stranded DNA breaks.

34 ferred DNA and protecting the genome against double-stranded DNA breaks.

35 maximal activity and induced a high ratio of double-stranded DNA breaks.

36 us for homology-directed DNA repair (HDR) of double-stranded DNA breaks.

37 identify SMARCAL1 as a protein recruited to double-stranded DNA breaks.

38 cells through an accumulation of persistent double-stranded DNA breaks.

39 es responsible for homology-driven repair of double-stranded DNA breaks.

40 phosphorylated histone H2AX, an indicator of double-stranded DNA breaks.

41 ad3-related (ATR) kinase to induce transient double-stranded DNA breaks.

42 tivity and might prevent DME from generating double-stranded DNA breaks.

43 nation, which is essential for the repair of double-stranded DNA breaks.

44 e that initiates homologous recombination at double-stranded DNA breaks.

45 nonhomologous end-joining pathways to repair double-stranded DNA breaks.

46 rays and ultraviolet light that can lead to double-stranded DNA breaks.

47 nation, an important mechanism for repair of double-stranded DNA breaks.

48 l DNA replication in egg extracts containing double-stranded DNA breaks.

49 maternally or paternally derived and display double-stranded DNA breaks.

50 Mre11 and Rad50 to coordinate the repair of double-stranded DNA breaks.

51 converting single-stranded DNA lesions into double-stranded DNA breaks.

52 ls by inhibiting topoisomerases and inducing double-stranded DNA breaks.

53 gether with experimentally induced telomeric double-stranded DNA breaks.

54 on, and is a major pathway for the repair of double-stranded DNA breaks.

55 sions, small duplications, and generation of double-stranded DNA breaks.

56 Cas9 as an RNA-guided nuclease that creates double-stranded DNA breaks.

57 striction sites as non-self and introduces a double-stranded DNA break [3].

58 colibactin, a genotoxic molecule(s) causing double-stranded DNA breaks(4) and enhanced colorectal ca

59 on (HR) is a major pathway for the repair of double-strand DNA breaks, a highly deleterious form of D

60 mit capture of the second processed end of a double-stranded DNA break, a step which is required for

61 und that the frequency and position of local double-strand DNA breaks affect the ratio of mismatch re

62 ned phosphorylated only during the repair of double strand DNA breaks, after which Chk1 was inactivat

63 Myc or GpIb alpha overexpression and include double-stranded DNA breaks, altered nuclear size and mor

64 mediated knockdown of ODC1, UC cells undergo double-strand DNA breaks and apoptosis.

65 is central to Red-mediated recombination at double-strand DNA breaks and chromosomal ends.

66 ylation, induction of LINE-1 transcripts and double-strand DNA breaks and decreases viability in prim

67 HCV causes double-strand DNA breaks and enhances the mutation frequ

68 small interfering RNA blocked the E2-induced double-strand DNA breaks and hypermutation of the V(H) g

69 ponse where it participates in the repair of double-strand DNA breaks and in base excision repair of

70 stasising OMMs may indicate APOBEC3A-induced double-strand DNA breaks and pro-metastatic hypermutatio

71 esulted from nuclear entry by Dox, promoting double-stranded DNA breaks and apoptosis.

72 s, probably due to the dramatic induction of double-stranded DNA breaks and chromosomal fragmentation

73 urthermore, these tumors were aneuploid with double-stranded DNA breaks and end-to-end telomere fusio

74 usly we have shown that HCV infection causes double-stranded DNA breaks and enhances the mutation fre

75 sophila, a meiotic checkpoint which monitors double-stranded DNA breaks and involves Drosophila ATR a

76 Depletion of WRN induced double-stranded DNA breaks and promoted apoptosis and ce

77 various stressors, such as for the repair of double-stranded DNA breaks and protein quality control,

78 that has primarily evolved for the repair of double-stranded DNA breaks and stalled replication forks

79 CD complex, which acts in both the repair of double-stranded DNA breaks and the degradation of bacter

80 t during homologous recombination, repair of double stranded DNA breaks, and integron recombination.

81 ation, leading to replication fork collapse, double-strand DNA breaks, and cell death.

82 and DNA ligases in the repair of single- and double-strand DNA breaks, and discusses the notion that

83 osphorylated H2AX (gammaH2AX) in response to double-strand DNA breaks, and impaired growth after DNA

84 vate the aryl hydrocarbon receptor, increase double-strand DNA breaks, and increase the expression of

85 ed replication forks, insufficient repair of double-stranded DNA breaks, and improper segregation of

86 Finally, GpIbalpha also promotes double-stranded DNA breaks, and induces profound nuclear

87 etabolism, archazolid caused S-phase arrest, double-stranded DNA breaks, and p53 stabilization, leadi

88 Double-strand DNA breaks are common events in eukaryotic

89 Double-strand DNA breaks are the most cytotoxic form of

90 and to map the frequency of meiosis-specific double-strand DNA breaks (as an estimate of the recombin

91 NN, like NRG, attenuated the double-stranded DNA breaks associated with DOXO exposure

92 Double strand DNA breaks at distant, random sites were o

93 stic of a bias in the frequencies of meiotic double-strand DNA breaks at the hotspot near the His4 lo

94 pyogenes (SpCas9) is more active in creating double-stranded DNA breaks at 37 degrees C than at 22 de

95 diation-induced foci (IRIF) that result from double-strand DNA breaks because they correlate with 53B

96 et (UV)-C radiation and reagents that induce double-stranded DNA breaks, but exhibit normal responses

97 The role of BRCA1 in the repair of double-strand DNA breaks by homologous recombination (HR

98 Tumors with compromised ability to repair double-strand DNA breaks by homologous recombination, in

99 oteins have been implicated in the repair of double-strand DNA breaks by homologous recombination.

100 ATM) protein kinase is recruited to sites of double-strand DNA breaks by the Mre11/Rad50/Nbs1 (MRN) c

101 plex that is essential for the repair of all double-strand DNA breaks by the nonhomologous DNA end jo

102 genome, it is not required for the repair of double-strand DNA-breaks by homologous recombination.

103 ATM is recruited to double-stranded DNA breaks by a complex of sensor protei

104 In diploid eukaryotes, repair of double-stranded DNA breaks by homologous recombination o

105 The error-free repair of double-stranded DNA breaks by homologous recombination r

106 tumours are often deficient in the repair of double-stranded DNA breaks by homologous recombination(8

107 o prevent telomeres from being recognized as double-stranded DNA breaks by sequestering the 3' single

108 Double-strand DNA breaks can be repaired by any of sever

109 quinolones predominantly results from lethal double-strand DNA breaks caused by incomplete repair of

110 l cells and bone marrow cells in response to double-strand DNA breaks caused by ionizing radiation an

111 found that some cells within biofilms incur double-stranded DNA breaks caused by endogenous oxidativ

112 In response to even a single chromosomal double-strand DNA break, cells enact the DNA damage chec

113 of linked loci is limited as multiple nearby double-stranded DNA breaks created by Cas9 routinely res

114 g cellular metabolism; these lesions include double-stranded DNA breaks, daughter-strand gaps, and DN

115 3'ss control and ATM-dependent responses to double-strand DNA breaks, demonstrate functional plastic

116 Cell-cycle arrest induced by double-stranded DNA breaks depends on activation of the

117 ding its role in homology-directed repair of double-strand DNA breaks, do not depend on the E3 ligase

118 DK4 activity, transcriptional regulation and double strand DNA break (DSB) induction.

119 ature B cells displayed significantly higher double-strand DNA break (DSB) accumulation and p53 activ

120 limit checkpoint signalling at a persistent double-strand DNA break (DSB) and at uncapped telomeres.

121 most central questions about the repair of a double-strand DNA break (DSB) concerns how the two free

122 ssovers at the expense of noncrossovers when double-strand DNA break (DSB) frequency is reduced.

123 y the host during infection, but the role of double-strand DNA break (DSB) repair systems is unclear.

124 We focus on regulation of double-strand DNA break (DSB) repair via the non-homolog

125 Consistent with the role of DBHS proteins in double-strand DNA break (DSB) repair, elevated DSBs were

126 A1, a cancer susceptibility gene involved in double-strand DNA break (DSB) repair, lead to breast can

127 ia nonhomologous end-joining (NHEJ)-mediated double-strand DNA break (DSB) repair.

128 In Drosophila, the persistent presence of double-strand DNA breaks (DSB) activates the ATR/Mei-41

129 s associated with single-strand DNA (ssDNA), double-strand DNA breaks (DSB), and genomic rearrangemen

130 ted T helper 17 cell differentiation through double-stranded DNA break (DSB) and ASC-mediated inflamm

131 ern expected as a consequence of repair of a double-stranded DNA break (DSB) of an unreplicated chrom

132 Impairment of double-stranded DNA break (DSB) repair is essential to m

133 recombination (HR) is a crucial pathway for double-stranded DNA break (DSB) repair.

134 ressing cells during the early stages of the double-stranded DNA break (DSB) response, accelerating a

135 al chromatin organization before and after a double-stranded DNA break (DSB), to estimate the level o

136 ) are ancient selfish elements that catalyze double-stranded DNA breaks (DSB) in a highly specific ma

137 Recognition and repair of double-stranded DNA breaks (DSB) involves the targeted r

138 oci over large chromatin domains surrounding double-stranded DNA breaks (DSB).

139 Repair of double strand DNA breaks (DSBs) can result in gene disru

140 (NHEJ) is an important process that repairs double strand DNA breaks (DSBs) in eukaryotic cells.

141 bivalent is also prone to exhibit persistent double strand DNA breaks (DSBs).

142 ubiquitin ligase is activated in response to double stranded DNA breaks (DSBs) where it mono-ubiquiti

143 an upstream activator of ATM in response to double-strand DNA breaks (DSBs) and as a downstream effe

144 or suppressor that is critical for resolving double-strand DNA breaks (DSBs) and interstrand crosslin

145 and ATR kinases, which respond primarily to double-strand DNA breaks (DSBs) and replication stress,

146 Double-strand DNA breaks (DSBs) are continuously induced

147 human cells and can induce the formation of double-strand DNA breaks (DSBs) at a site complementary

148 acilitates homology-directed repair (HDR) of double-strand DNA breaks (DSBs) by initiating DNA resect

149 Repair of double-strand DNA breaks (DSBs) by the homologous recomb

150 Furthermore, we demonstrate that double-strand DNA breaks (DSBs) cause inhibition of Cdc4

151 he cell cycle to progress in the presence of double-strand DNA breaks (DSBs) caused by ionizing radia

152 Double-strand DNA breaks (DSBs) continuously arise and c

153 g V regions (somatic hypermutation, SHM) and double-strand DNA breaks (DSBs) into switch (S) regions,

154 Here we demonstrate that double-strand DNA breaks (DSBs) introduced a large dista

155 lay of cell cycle progression in response to double-strand DNA breaks (DSBs) is critical to allow tim

156 easure the frequency of the meiosis-specific double-strand DNA breaks (DSBs) of all 6,000 yeast genes

157 l translocation requires formation of paired double-strand DNA breaks (DSBs) on heterologous chromoso

158 atocytes exhibit up to a 25-fold increase in double-strand DNA breaks (DSBs) throughout meiotic proph

159 is responsible for recognizing and repairing double-strand DNA breaks (DSBs) via non-homologous end j

160 2A.X foci, indicative of an accumulation of double-strand DNA breaks (DSBs), and increased sensitivi

161 ons that mistake natural chromosome ends for double-strand DNA breaks (DSBs), and the progressive los

162 ntioxidants was shown to reduce formation of double-strand DNA breaks (DSBs), as indicated by phospho

163 is initiated by the programmed induction of double-strand DNA breaks (DSBs), lesions that pose a pot

164 se excision repair (BER) enzymes can produce double-strand DNA breaks (DSBs).

165 NA damage, where BRCA1 facilitates repair of double-strand DNA breaks (DSBs).

166 into not identifying them as damage-induced double-strand DNA breaks (DSBs).

167 ay in multicellular eukaryotes for repairing double-strand DNA breaks (DSBs).

168 amages mitochondria, leading to induction of double-stranded DNA breaks (DSBs) and accumulation of ox

169 In mammalian cells, double-stranded DNA breaks (DSBs) are preferentially rep

170 are particularly susceptible to formation of double-stranded DNA breaks (DSBs) arising from physiolog

171 by ATR (ATM and Rad3-related) in response to double-stranded DNA breaks (DSBs) but not to DNA replica

172 Double-stranded DNA breaks (DSBs) can result in chromoso

173 The activation of ATR-ATRIP in response to double-stranded DNA breaks (DSBs) depends upon ATM in hu

174 J) and homologous recombination (HR), repair double-stranded DNA breaks (DSBs) in all eukaryotes.

175 cent reports show it is enriched at sites of double-stranded DNA breaks (DSBs) in mammalian cells.

176 participates in the detection of chromosomal double-stranded DNA breaks (DSBs) in this system.

177 and acceptor genomic sequences subjected to double-stranded DNA breaks (DSBs) made by programmable n

178 functionally dicentric chromosome undergoes double-stranded DNA breaks (DSBs) that can be repaired b

179 regions and by the subsequent generation of double-stranded DNA breaks (DSBs).

180 Rad52 and RPA participate in the repair of double-stranded DNA breaks (DSBs).

181 e two master checkpoint kinases activated by double-stranded DNA breaks (DSBs).

182 ions have been implicated in the response to double-stranded DNA breaks (DSBs).

183 topoisomerase II generates a protein-linked double-stranded DNA break during its catalytic cycle, it

184 important for the recombinational repair of double-stranded DNA breaks during meiosis.

185 gous recombination compete for the repair of double-stranded DNA breaks during the cell cycle.

186 In Escherichia coli, RecBCD processes double-stranded DNA breaks during the initial stages of

187 ous recombination and avoids the creation of double-strand DNA breaks, enabling precise chromosome mo

188 utant was shown to have a capacity to repair double-stranded DNA breaks equivalent to wild-type.

189 ypermutation on both DNA strands to generate double-strand DNA breaks for efficient class switch reco

190 In bacterial cells, processing of double-stranded DNA breaks for repair by homologous reco

191 In bacterial cells, processing of double-stranded DNA breaks for repair by homologous reco

192 AddAB is a helicase-nuclease that processes double-stranded DNA breaks for repair by homologous reco

193 In bacterial cells, processing of double-stranded DNA breaks for repair by homologous reco

194 onents, in meiotic recombination by enabling double-strand DNA break formation by Rec12.

195 and replication fork restart, prevention of double-stranded DNA break formation, and avoidance of re

196 s recombination events that are initiated by double-stranded DNA breaks formed prior to replication.

197 non-homologous end-joining (NHEJ) repair of double-stranded DNA breaks generated by Cas9 are much le

198 ignificant improvement in tumor cell damage (double strand DNA breaks), growth suppression, and overa

199 F, XPC and AP-endonuclease-1), and repair of double-stranded DNA breaks (homologs of BRCA2, XRCC3, KU

200 because AID(+) dividing cells exhibited more double-stranded DNA breaks, IGH class switching, and new

201 g intermediates that are converted to lethal double strand DNA breaks in DNA replication fork collisi

202 ce homologous recombination (HR) at a unique double-strand DNA break in a GFP reporter in mammalian c

203 ced cytidine deaminase (AID), which produces double-strand DNA breaks in both genes.

204 bineering accompanied by the introduction of double-strand DNA breaks in the chromosome and a donor p

205 Cas9 can be reprogrammed to create double-strand DNA breaks in the genomes of a variety of

206 e and nuclease complex is used for repairing double-strand DNA breaks in the many bacteria that do no

207 nd the Mre11-Rad50 complex for the repair of double-strand DNA breaks in thermophilic archaea.

208 nuclease, which is involved in the repair of double-stranded DNA breaks in Bacillus subtilis.

209 Repair of double-stranded DNA breaks in Escherichia coli is initia

210 Although Cas9 efficiently induces double-stranded DNA breaks in the early embryo and male

211 Cas9 can be reprogrammed to create specific double-stranded DNA breaks in the genomes of a variety o

212 20 are colocalized at the gamma-H2AX foci of double-stranded DNA breaks in the nucleus.

213 point mutations in the Ig variable region or double-stranded DNA breaks in the switch region DNA.

214 ions, and H2AX phosphorylation, a marker for double-stranded DNA breaks, in Hus1(neo/neo) and Hus1(ne

215 Rad51 localization, but only in presence of double strand DNA breaks, indicating that each of these

216 frequency of sister chromatid exchanges and double strand DNA breaks, indicating the formation of mi

217 BRCA1 has no equivalent role at chromosomal double-stranded DNA breaks, indicating that tandem dupli

218 initiate recombination between homologs are double-stranded DNA breaks induced during S or G2 of the

219 Here we introduced double-stranded DNA breaks into the nuclear genome of to

220 The cellular response to the introduction of double strand DNA breaks involves complexes of protein i

221 The postulated mechanism for the double-strand DNA breaks is clustered uracil excision, w

222 eptor (GR)/BRG1-dependent, TOP2beta-mediated double-strand DNA breaks is required for efficient GR-st

223 The mechanism by which a double-stranded DNA break is produced following collisio

224 In bacteria, the repair of double-stranded DNA breaks is modulated by Chi sequences

225 es depending on the stimulus; in response to double-strand DNA breaks, it shows a series of repeated

226 dk5 induces aberrant cell-cycle activity and double-strand DNA breaks leading to neurotoxicity.

227 cycle progression through mitosis following double-stranded DNA breaks leads to the formation of mic

228 ton beam irradiation induces more single and double strand DNA breaks, less H2AX phosphorylation, inc

229 e mtDNA deletions in muscle, suggesting that double-strand DNA breaks mediate the formation of large

230 r CRISPR-Cas9 system couples a site-specific double-strand DNA break mediated by two Cas9 ribonucleop

231 f homologous sites can explain how repair of double strand DNA breaks might occur in a mechanism that

232 The TALEN pairs were designed to induce double-strand DNA break near the starting codon of each

233 al decline in viability following an induced double-strand DNA break, of a magnitude comparable with

234 oksani et al. examine the impact of a single double-stranded DNA break on replication in the budding

235 inase to specific loci and (2) generation of double-strand DNA breaks only after recognition of a pai

236 The complexes failed to induce double-strand DNA breaks or DNA cross-linking but induce

237 antage that it does not require formation of double-stranded DNA breaks or provision of a donor DNA t

238 reaction of topoisomerase II, which creates double-stranded DNA breaks, plays a central role in both

239 Correction of double strand DNA breaks proceeds in an error-free pathw

240 During recombinational repair of double-stranded DNA breaks, RAD51 recombinase assembles

241 We propose that DNA damage-elicited double-strand DNA breaks releases DNA fragments, which m

242 Our results suggest that FANCD2 mediates double strand DNA break repair independently of Rad51-as

243 cesses including transcriptional activation, double strand DNA break repair, and apoptosis.

244 dual roles for DNMT1 in DNA methylation and double strand DNA break repair.

245 cil-DNA excision (ung, polA, and xthA); (ii) double-strand DNA break repair (recA, recBC, and ruvABC)

246 We show elevated levels of Mdmx-inhibited double-strand DNA break repair and induced chromosome an

247 pon radiation exposure such as regulation of double-strand DNA break repair and tumor cell metabolism

248 nal signature was associated with failure of double-strand DNA break repair by homologous recombinati

249 that 7-12% of gastric cancers have defective double-strand DNA break repair by homologous recombinati

250 of the RecBCD enzyme, which is essential for double-strand DNA break repair in Escherichia coli and m

251 The double-strand DNA break repair pathway, non-homologous D

252 nonhomologous end-joining (NHEJ) pathway of double-strand DNA break repair.

253 vates DNA-PKcs, a protein kinase critical in double-strand DNA break repair.

254 critical role in sister chromatid cohesion, double-stranded DNA break repair and regulation of gene

255 Double-stranded DNA break repair by homologous recombina

256 5%) breakpoint junctions are consistent with double-stranded DNA break repair by nonhomologous end-jo

257 s a key regulator of DNA replication timing, double-stranded DNA break repair, and replication fork r

258 n to their implications for the mechanism of double-stranded DNA break repair, these observations may

259 A-dependent protein kinase (DNA-PK) mediates double-stranded DNA break repair, V(D)J recombination an

260 ast DNAs insert into nuclear genomes through double-stranded DNA break repair.

261 is a DNA helicase/nuclease that functions in double-stranded DNA break repair.

262 kinase family, is a master regulator of the double strand DNA break-repair pathway after genotoxic s

263 coli, homologous recombination initiated at double-stranded DNA breaks requires the RecBCD enzyme, a

264 AB translocation and hotspot scanning during double-stranded DNA break resection.

265 merase I and II create transient single- and double-stranded DNA breaks, respectively, it has been as

266 Remarkably, TALENs or CRISPR-Cas9-mediated double-strand DNA breaks resulted in up to 100% targetin

267 The double-strand DNA breaks resulting from replication fork

268 parallel with CRISPRi/a, which do not induce double-stranded DNA breaks, revealed that a distinct set

269 method, which predicts the extent to which a double-stranded DNA break site will utilize the microhom

270 engagement of B cells by purified E2 induced double-strand DNA breaks specifically in the variable re

271 Both ROS-induced single- and double-strand DNA breaks (SSBs and DSBs) contribute to R

272 Unrepaired DNA lesions, such as single- and double-stranded DNA breaks (SSBs and DSBs), and single-s

273 ific, direct in situ detection of single- or double-strand DNA breaks (sSTRIDE or dSTRIDE), in nuclei

274 Gmnn(-/-) spermatogonia exhibit more double-stranded DNA breaks than control cells, consisten

275 fusion of sister chromatids bearing targeted double strand DNA breaks that is entirely uncoupled from

276 uirement for crossovers and an excess of the double-strand DNA breaks that are the initiating events

277 It is suggested that for double-strand DNA breaks that have initially formed a co

278 VI topoisomerases and is thought to catalyze double-strand DNA breaks that initiate recombination.

279 k5 activity elicited cell-cycle activity and double-strand DNA breaks that preceded neuronal death.

280 hat the two regions differ in the density of double-stranded DNA breaks that are generated.

281 CRISPR/Cas9 causes double-stranded DNA breaks that can undergo DNA repair e

282 omosome throughout the genome and can induce double-stranded DNA breaks that lead to chromosome trans

283 midinic endonucleases, eventually generating double strand DNA breaks, the obligatory intermediates o

284 Although fluoroquinolones stabilize double-stranded DNA breaks, the antibacterial thiophenes

285 horylated H2AX is a characteristic marker of double-stranded DNA breaks, this modification was widely

286 II topoisomerases (TOP2) introduce transient double-stranded DNA breaks through a covalent TOP2-DNA i

287 In all domains of life, the resection of double-stranded DNA breaks to form long 3'-ssDNA overhan

288 far apart (>30 bp) to dimerise and produce a double-strand DNA break using just two strand-cleavage e

289 d repair (HDR) of Cas9-induced site-specific double-strand DNA breaks using timed delivery of Cas9-gu

290 aks resulted in the generation of persistent double-stranded DNA breaks was found to be a primary cau

291 gly, CSR induced by staggered but not blunt, double-stranded DNA breaks was impaired by SAMHD1 deplet

292 by the presence of pyknotic cells containing double-strand DNA breaks, was apparent throughout these

293 Because T-DNA preferentially integrates into double-strand DNA breaks, we adapted a CRISPR/Cas9 syste

294 Ty elements constitutes a preferred site for double-strand DNA breaks when DNA replication is comprom

295 the BNP-based sunblock significantly reduced double-stranded DNA breaks when compared with a commerci

296 ATM is central to a pathway that responds to double-strand DNA breaks, whereas the related kinase ATR

297 predictably and independent of Cas9-induced double-stranded DNA breaks (which causes substantial ind

298 r growth by causing apoptotic cell death via double-stranded DNA breaks while causing a remodeling of

299 for genome editing through the catalysis of double-strand DNA breaks within target loci and subseque

300 fork stalling, we suggest that formation of double-stranded DNA breaks within the Ytel sequences mig