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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

19 pendent and coincident with the formation of double-strand DNA breaks.

20 fore mismatches are converted to single- and double-strand DNA breaks.

21 the genetic material by generating transient double-strand DNA breaks.

22 romatids together during mitosis and repairs 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 double helix and generate an enzyme-mediated double-stranded DNA break.

28 resent at both scissile bonds to stabilize a double-stranded DNA break.

29 Mre11 and Rad50 to coordinate the repair of 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 identify SMARCAL1 as a protein recruited to double-stranded DNA breaks.

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

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

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

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

41 ls by inhibiting topoisomerases and inducing 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 is, which leads to excessive accumulation of double-stranded DNA breaks.

50 with, 53BP1 after exposure to agents causing double-stranded DNA breaks.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

84 Double-strand DNA breaks are also generated by cleavage

85 Double-strand DNA breaks are common events in eukaryotic

86 is an integral part of the process by which double-strand DNA breaks are repaired to maintain genome

87 ical organisms are largely unknown, although double-strand DNA breaks are required in all proposed me

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

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

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

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

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

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

94 eplacement "footprints" in IgH sequences and double-stranded DNA breaks at V(H) cRSS sites in immatur

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

96 NA damage, rather than the failure to repair double-strand DNA breaks, because asf1 mutants are fully

97 ells rely heavily on recombination to repair double-strand DNA breaks, but the specific pathways used

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

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

100 The repair of double-strand DNA breaks by homologous recombination is

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

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

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

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

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

106 s sufficient to stimulate the formation of a double-stranded DNA break by human topoisomerase IIalpha

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

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

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

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

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

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

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

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

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

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

117 3'ss control and ATM-dependent responses to double-strand DNA breaks, demonstrate functional plastic

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

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

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

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

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

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

124 In Drosophila, mutations in double-strand DNA break (DSB) repair enzymes, such as sp

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 ) genes appears to involve the generation of double-strand DNA breaks (DSBs) and their error-prone re

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

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

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

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

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

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

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

154 leading contenders, but in the last decade, double-strand DNA breaks (DSBs) have reigned.

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

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

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

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

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

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 Ionizing radiation (IR) primarily leads to double-strand DNA breaks (DSBs), which activate DNA dama

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

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

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

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

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

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

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

175 tein essential for recombinational repair of double-stranded DNA breaks (DSBs) in somatic cells and d

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

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

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

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

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

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

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

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

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

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

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

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

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

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

190 AddAB is a helicase-nuclease that processes 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 In bacterial cells, processing of double-stranded DNA breaks for repair by homologous reco

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

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

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

196 ferent repair-deficient genetic backgrounds, double-strand DNA breaks generated by topoisomerase II a

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 e fact that there are two scissile bonds per double-stranded DNA break implies that there are two sit

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

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

204 molog of ATRIP, is specifically recruited to double-strand DNA breaks in an RPA-dependent manner.

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

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

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

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

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

210 recombination is important for the repair of double-stranded DNA breaks in all organisms.

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

212 e analyzed the repair of transposase-induced double-stranded DNA breaks in cells deficient in either

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

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

215 20 are colocalized at the gamma-H2AX foci of double-stranded DNA breaks in the nucleus.

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

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

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

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

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

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

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

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

224 The loading of Ku onto a DNA end in a double-strand DNA break is thought to be one of the firs

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

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

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

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

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

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

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

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

233 In herpes simplex virus 1, double-strand DNA breaks may arise as a consequence of r

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

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

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

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

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

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

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

241 on at Ser(92) in response to the presence of double-stranded DNA breaks or DNA replication blocks in

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

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

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

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

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

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

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

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

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

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

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

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

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

255 These results further implicate double-strand DNA break repair machinery as important co

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

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

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

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

260 Double-stranded DNA break repair by homologous recombina

261 5%) breakpoint junctions are consistent with double-stranded DNA break repair by nonhomologous end-jo

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

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

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

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

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

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

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

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

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

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

272 The double-strand DNA breaks resulting from replication fork

273 overexpression of MYC disrupts the repair of double-strand DNA breaks, resulting in a several-magnitu

274 icin is a potent cytotoxic agent that causes double-strand DNA breaks, resulting in cell death.

275 component of, or in close proximity to, the double-stranded DNA break-sensing machinery.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

298 Selective detection of double-strand DNA breaks with blunt ends was performed b

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