ライフサイエンスコーパス: DNA double-strand break

1 a central mediator of response for cellular DNA double-strand break.

2 ve enabled genome editing without generating DNA double strand breaks.

3 is critical for the repair and signaling of DNA double strand breaks.

4 terial carcinogen Helicobacter pylori causes DNA double strand breaks.

5 ogenic survival, and increases resolution of DNA double strand breaks.

6 and for processing a subset of pathological DNA double-strand breaks.

7 Radiation kills cancer cells by inducing DNA double-strand breaks.

8 ulting in replication from fewer origins and DNA double-strand breaks.

9 CD proteins often enables accurate repair of DNA double-strand breaks.

10 nscription factor Cap1, and the formation of DNA double-strand breaks.

11 a corroborating that exposure to Al leads to DNA double-strand breaks.

12 in response to genotoxic stresses that cause DNA double-strand breaks.

13 a-mutated (ATM), is activated in response to DNA double-strand breaks.

14 activity, driven by the induction of complex DNA double-strand breaks.

15 trates created after formation of programmed DNA double-strand breaks.

16 t complexes in cells, which are converted to DNA double-strand breaks.

17 BRCA2 to promote efficient RAD51 loading at DNA double-strand breaks.

18 ilizer of the DNA damage response (DDR) upon DNA double-strand breaks.

19 th c-Jun activation show cell activation and DNA double-strand breaks.

20 pes of DNA damage, such as bulky lesions and DNA double-strand breaks.

21 tability through the resection of endogenous DNA double-stranded breaks.

22 gemcitabine-induced, replication-associated DNA double-stranded breaks.

23 the HR-dependent repair of directly induced DNA double-stranded breaks.

24 ard chromosome ends from being recognized as DNA double-strand breaks(2).

25 lesion, might contribute to the formation of DNA double strand breaks and activation of DNA damage re

26 nsitivity and results in enhanced numbers of DNA double-strand breaks and a pronounced S/G2-phase arr

27 uitment and expansion can ultimately promote DNA double-strand breaks and androgen receptor activatio

28 llular level of FA can trigger mitochondrial DNA double-strand breaks and dysfunction.

29 in kinase that is recruited and activated by DNA double-strand breaks and functions as an important s

30 the Mre11-Rad50-Nbs1 complex that recognizes DNA double-strand breaks and has exonuclease and endonuc

31 Homologous recombination repairs DNA double-strand breaks and must function even on activ

32 blocks MUC1-C nuclear localization, induced DNA double-strand breaks and potentiated cisplatin (CDDP

33 proteins that facilitate accurate repair of DNA double-strand breaks and prevent chromosomal rearran

34 level of Il10 mRNA, and increased markers of DNA double-strand breaks and proliferation were observed

35 Chromatin marks induced by DNA double-strand breaks and recognized by 53BP1 enable

36 by overcoming the cell death associated with DNA double-strand breaks and single-strand breaks.

37 s a homologous template to accurately repair DNA double-strand breaks and stalled replication forks t

38 DNA in PARP3(-/-) cells leads to widespread DNA double-strand breaks and synthetic lethality.

39 active sertraline-treated tissues accumulate DNA double-strand breaks and undergo apoptosis at increa

40 nterferes with replication forks, leading to DNA double-stranded breaks and genomic instability.

41 is critical for proper DNA repair following DNA double-strand breaks, and accumulate high numbers of

42 Temozolomide induced growth delay, DNA double-strand breaks, and G(2)-M cell-cycle arrest,

43 DNA double strand breaks are detected and processed in p

44 and show that naturally occurring background DNA double-strand breaks are associated with open chroma

45 e disorders (eg, ataxia-telangiectasia), and DNA double-strand breaks are crucial to the modulation o

46 oly(ADP-ribosyl)ation in the germline, where DNA double-strand breaks are introduced by a regulated p

47 DNA double-strand breaks are the most dangerous type of

48 ersistent and less reversible Top1cc-induced DNA double-strand breaks as detected by gammaH2AX foci i

49 ARP) inhibitor, talazoparib led to increased DNA double strand breaks, as assessed by gamma-H2AX foci

50 se represented by Cas9 efficiently generates DNA double strand breaks at the target locus, followed b

51 odies with different isotypes by joining two DNA double-strand breaks at different switching regions

52 hromosomal loci become mobile in response to DNA double-strand breaks both at the break site (local m

53 f interleukin (IL) 6 and IL8, and markers of DNA double-strand breaks but reduced markers of DNA repa

54 To repair a DNA double-strand break by homologous recombination, 5'-

55 rapidly respond to gamma-irradiation-induced DNA double-strand breaks by activating Ataxia Telangiect

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

57 In the repair of DNA double-strand breaks by homologous recombination, th

58 To repair DNA double-strand breaks by homologous recombination, th

59 Repair of DNA double-strand breaks by the nonhomologous end joinin

60 aled mechanisms of recognition and repair of DNA double-strand breaks, DNA interstrand crosslinks and

61 Previously, XRN2 was implicated in DNA double strand break (DSB) repair and in resolving re

62 Tracking DNA double strand break (DSB) repair is paramount for th

63 We studied DNA double strand break (DSB) repair kinetics using the

64 ous end-joining (NHEJ) is the most prominent DNA double strand break (DSB) repair pathway in mammalia

65 f homologous recombination (HR), a universal DNA double strand break (DSB) repair pathway.

66 DNA double strand break (DSB) repair through homologous

67 ion (HR) posit that extensive resection of a DNA double-strand break (DSB) by a multisubunit helicase

68 predominant repair mechanism of any type of DNA double-strand break (DSB) during most of the cell cy

69 a nuclear protein that negatively regulates DNA double-strand break (DSB) end resection and CCF form

70 crossover formation, regulating cessation of DNA double-strand break (DSB) formation following crosso

71 possibility that the minimal requirement for DNA double-strand break (DSB) formation is as low as eve

72 DNA double-strand break (DSB) formation is the initiatin

73 se macroH2A1.2 during acute RS to facilitate DNA double-strand break (DSB) formation, a process that

74 A DNA double-strand break (DSB) is the most critical type

75 -synuclein in human cells leads to increased DNA double-strand break (DSB) levels after bleomycin tre

76 atin at hot spots and provide access for the DNA double-strand break (DSB) machinery.

77 f higher levels of DNA strand breaks and the DNA double-strand break (DSB) marker gammaH2AX, compared

78 on tumor cell-autonomous gradual buildup of DNA double-strand break (DSB) misrepair.

79 are estimated to inflict fewer than a single DNA double-strand break (DSB) per hour per cell, they st

80 for XRCC4 plus p53, a genotype that enhances DNA double-strand break (DSB) persistence to enhance det

81 n Schizosaccharomyces pombe is essential for DNA double-strand break (DSB) repair by homologous recom

82 esidual 53BP1 and RIF1 foci, suggesting that DNA double-strand break (DSB) repair by homologous recom

83 pe 1 susceptibility protein (BRCA1) promotes DNA double-strand break (DSB) repair by homologous recom

84 functional BRCA1 protein leads to defects in DNA double-strand break (DSB) repair by homologous recom

85 Homologous recombination (HR)-directed DNA double-strand break (DSB) repair enables template-di

86 Chromatin responses during DNA double-strand break (DSB) repair have been studied w

87 The early steps of DNA double-strand break (DSB) repair in human cells invo

88 Deficiency in DNA double-strand break (DSB) repair mechanisms has been

89 ere homeostasis, DNA replication timing, and DNA double-strand break (DSB) repair pathway choice from

90 Homologous recombination (HR) is a DNA double-strand break (DSB) repair pathway that protec

91 he nonhomologous end joining (NHEJ)-mediated DNA double-strand break (DSB) repair pathway.

92 This perspective will highlight DNA double-strand break (DSB) repair pathways in human c

93 In mitosis, cells inactivate DNA double-strand break (DSB) repair pathways to preserv

94 se, but attenuated the expression of several DNA double-strand break (DSB) repair proteins and format

95 Improper DNA double-strand break (DSB) repair results in complex

96 human BRD proteins for genome stability and DNA double-strand break (DSB) repair using several cell-

97 diverse lifespans, we show that more robust DNA double-strand break (DSB) repair, but not nucleotide

98 rt that human DNA ligase IV, a key enzyme in DNA double-strand break (DSB) repair, is able to use NAD

99 al Ino80 deletion from cortical NPCs impairs DNA double-strand break (DSB) repair, triggering p53-dep

100 s including actin cytoskeletal signaling and DNA double-strand break (DSB) repair.

101 sensitivity to genotoxic stress and delayed DNA double-strand break (DSB) repair.

102 to ionizing radiation (IR) and a decrease in DNA double-strand break (DSB) repair.

103 ation, DNA replication fork progression, and DNA double-strand break (DSB) repair.

104 Germline mutations of DNA double-strand break (DSB) response and repair genes

105 e and erroneously causes the accumulation of DNA double-strand break (DSB) response factors.

106 ation (small ubiquitin-like modifier) in the DNA double-strand break (DSB) response regulates recruit

107 Creating access to DNA double-strand break (DSB) sites in the chromatin con

108 hat XPA mislocalized to the progerin-induced DNA double-strand break (DSB) sites, blocking DSB repair

109 -2.55 angstrom resolutions, including a full DNA double-strand break (DSB) synapsis.

110 cortex (PLPFC) through its interaction with DNA double-strand break (DSB)-mediated changes in DNA me

111 py endogenous chromosomal locus containing a DNA double-strand break (DSB).

112 phorylated histone H2A (gamma-H2AX) around a DNA double-strand break (DSB).

113 DNA double-strand breaks (DSB) are the most deleterious

114 The efficient site-specific DNA double-strand breaks (DSB) created by CRISPR/Cas9 ha

115 ys, in accordance with the irreparability of DNA double-strand breaks (DSB) induced by high-LET radia

116 Repair of DNA double-strand breaks (DSB) is performed by two major

117 tively induced clustered DNA lesions (OCDL), DNA double-strand breaks (DSB), apoptosis, and the local

118 RAD51 recombinase in HR repair of programmed DNA double-strand breaks (DSB).

119 RCA-deficient tumors, do not initially cause DNA double-strand breaks (DSB).

120 e in homologous recombination (HR) repair of DNA double-strand breaks (DSB); however, its precise rol

121 and 7 T) and the effect of contrast agent on DNA double-strand-break (DSB) formation in patients unde

122 Best studied in the context of DNA double-stranded break (DSB) repair, recombination en

123 J) pathway is the primary repair pathway for DNA double strand breaks (DSBs) in humans.

124 stelium histones are modified in response to DNA double strand breaks (DSBs) in vivo by the ARTs Adpr

125 The repair of DNA double strand breaks (DSBs) that arise from external

126 ed histone H2AX phosphorylation, a marker of DNA double strand breaks (DSBs), in human cervix cancer

127 OTUD5 localizes to DNA double strand breaks (DSBs), interacts with UBR5 and

128 the homologous recombination (HR) repair of DNA double strand breaks (DSBs).

129 rom errors in the repair processes following DNA double strand breaks (DSBs).

130 Using targeted DNA double-strand breaks (DSBs) and long-read whole-geno

131 ZPET binds ssDNA and localizes to DNA double-strand breaks (DSBs) and stalled replication

132 DNA double-strand breaks (DSBs) are among the most letha

133 DNA double-strand breaks (DSBs) are common genome lesion

134 DNA double-strand breaks (DSBs) are highly cytotoxic les

135 DNA double-strand breaks (DSBs) are highly toxic lesions

136 DNA double-strand breaks (DSBs) are implicated in variou

137 During meiosis, DNA double-strand breaks (DSBs) are induced as part of t

138 In mice and humans, DNA double-strand breaks (DSBs) are initiated by SPO11 a

139 To generate a crossover, hundreds of DNA double-strand breaks (DSBs) are introduced in the ge

140 DNA double-strand breaks (DSBs) are particularly dangero

141 Ionizing radiation (IR)-induced DNA double-strand breaks (DSBs) are predominantly repair

142 eiotic recombination, a subset of programmed DNA double-strand breaks (DSBs) are repaired as crossove

143 DNA double-strand breaks (DSBs) are repaired through hom

144 DNA double-strand breaks (DSBs) are serious genomic insu

145 DNA double-strand breaks (DSBs) are the most toxic DNA l

146 DNA double-strand breaks (DSBs) are toxic to mammalian c

147 nts are mediated by the repair of programmed DNA double-strand breaks (DSBs) as genetic crossovers be

148 c recombination starts with the formation of DNA double-strand breaks (DSBs) at specific genomic loca

149 ered oxidative base damage is converted into DNA double-strand breaks (DSBs) by base excision repair

150 A proper balance between the repair of DNA double-strand breaks (DSBs) by homologous recombinat

151 h FANCJ has been implicated in the repair of DNA double-strand breaks (DSBs) by homologous recombinat

152 Mechanistically, USP15 is recruited to DNA double-strand breaks (DSBs) by MDC1, which requires

153 Mechanistically, BGL3 is recruited to DNA double-strand breaks (DSBs) by PARP1 at an early tim

154 ng non-coding RNAs (dilncRNA) synthesized at DNA double-strand breaks (DSBs) by RNA polymerase II are

155 vo from the CUP1 locus through processing of DNA double-strand breaks (DSBs) by Sae2, Mre11 and Mus81

156 protein 53BP1 plays key roles in response to DNA double-strand breaks (DSBs) by serving as a master s

157 Genotoxic DNA double-strand breaks (DSBs) can be repaired by error

158 stic of IR survival and repair efficiency of DNA double-strand breaks (DSBs) caused by exposure to ga

159 During meiosis, DNA double-strand breaks (DSBs) enter interhomolog repai

160 Because DNA double-strand breaks (DSBs) facilitate transcription

161 It is not clear how spontaneous DNA double-strand breaks (DSBs) form and are processed i

162 istinguishing sites likely to form canonical DNA double-strand breaks (DSBs) from those predisposed t

163 A damage response RNAs (DDRNAs) generated at DNA double-strand breaks (DSBs) in a DROSHA- and DICER-d

164 :DNA hybrids, replication stress markers and DNA double-strand breaks (DSBs) in cells depleted for To

165 new replication origins (cSDR) and repair of DNA double-strand breaks (DSBs) in E. coli share a commo

166 We were surprised to observe increased DNA double-strand breaks (DSBs) in mitochondria after ex

167 Induction of DNA double-strand breaks (DSBs) in ribosomal DNA (rDNA)

168 Precise genome editing/correction of DNA double-strand breaks (DSBs) induced by CRISPR-Cas9 b

169 Programmed DNA double-strand breaks (DSBs) initiate meiotic recombi

170 The number of DNA double-strand breaks (DSBs) initiating meiotic recom

171 Timely repair of DNA double-strand breaks (DSBs) is essential to maintain

172 Efficient repair of DNA double-strand breaks (DSBs) is of critical importanc

173 We demonstrate that endogenous DNA double-strand breaks (DSBs) mediated by Topoisomeras

174 Repair of DNA double-strand breaks (DSBs) must be orchestrated pro

175 When DNA double-strand breaks (DSBs) occur, H2AX is phosphory

176 When DNA double-strand breaks (DSBs) occur, MRN is quickly re

177 DNA double-strand breaks (DSBs) pose an everyday threat

178 DNA double-strand breaks (DSBs) prevent cells from enter

179 Malaria parasites repair DNA double-strand breaks (DSBs) primarily through homolo

180 on, homologue-templated repair of programmed DNA double-strand breaks (DSBs) produces relatively few

181 Chromosome movements and programmed DNA double-strand breaks (DSBs) promote homologue pairin

182 Efficient repair of DNA double-strand breaks (DSBs) requires a coordinated D

183 DNA double-strand breaks (DSBs) resulting from reactive

184 types of DNA repair counteract highly toxic DNA double-strand breaks (DSBs) to maintain genome stabi

185 for cell proliferation, but also localize to DNA double-strand breaks (DSBs) to promote repair.

186 In this study, multiple DNA double-strand breaks (DSBs) were generated via the C

187 minase (AID), the activity of which leads to DNA double-strand breaks (DSBs) within IgH switch (S) re

188 an AR-mediated, dose-dependent induction of DNA double-strand breaks (DSBs), G0/G1 cell cycle arrest

189 To safeguard genome integrity in response to DNA double-strand breaks (DSBs), mammalian cells mobiliz

190 oteins also promote the formation of meiotic DNA double-strand breaks (DSBs), the precursors of cross

191 we use spo-11 mutants, which lack endogenous DNA double-strand breaks (DSBs), to induce a single DSB

192 t ZIKV, but not dengue virus (DENV), induces DNA double-strand breaks (DSBs), triggering the DNA dama

193 the most deleterious types of DNA damage are DNA double-strand breaks (DSBs), which can cause cell le

194 plicing factories, and (3) the clustering of DNA double-strand breaks (DSBs), which concentrates dama

195 Genomic integrity is threatened by cytotoxic DNA double-strand breaks (DSBs), which must be resolved

196 eiosis, BRCA2 binds to MEILB2 to localize to DNA double-strand breaks (DSBs).

197 rs to the DNA repair process particularly at DNA double-strand breaks (DSBs).

198 ch mediates HRR through the end resection of DNA double-strand breaks (DSBs).

199 ovo telomere addition (dnTA) is regulated at DNA double-strand breaks (DSBs).

200 vers result from homology-directed repair of DNA double-strand breaks (DSBs).

201 nthesis in response to replication stress or DNA double-strand breaks (DSBs).

202 ion (HR) is an important route for repairing DNA double-strand breaks (DSBs).

203 tiates homologous recombination by resecting DNA double-strand breaks (DSBs).

204 esin is required to repress transcription at DNA double-strand breaks (DSBs).

205 microhomology-mediated end-joining (MMEJ) of DNA double-strand breaks (DSBs).

206 generation of genetic diversity to repair of DNA double-strand breaks (DSBs).

207 ing pathway (NHEJ) used to detect and repair DNA double-strand breaks (DSBs).

208 PARP-1 is rapidly recruited and activated by DNA double-strand breaks (DSBs).

209 sover recombination by potentially genotoxic DNA double-strand breaks (DSBs).

210 ain finger 11 (PHF11) in 5' end resection at DNA double-strand breaks (DSBs).

211 n (HR) and increases cellular sensitivity to DNA double-strand breaks (DSBs).

212 eorganized at multiple levels in response to DNA double-strand breaks (DSBs).

213 ulator of the cellular damage response after DNA double-strand breaks (DSBs).

214 response to local DNA damage, specifically, DNA double-strand breaks (DSBs).

215 recombination-mediated repair of programmed DNA double-strand breaks (DSBs).

216 protein (CRISPR/Cas) system, used to target DNA double-strand breaks (DSBs).

217 via cellular senescence and death induced by DNA double-strand breaks (DSBs); however, the chemical b

218 of both DNA single-strand breaks (SSBs) and DNA double-strand breaks (DSBs); lesions that can trigge

219 DNA double-stranded breaks (DSBs) are dangerous lesions

220 cularly remarkable in the examination of how DNA double-stranded breaks (DSBs) are repaired, with man

221 DNA double-stranded breaks (DSBs) are strongly associate

222 an be achieved upon repair of CRISPR-induced DNA double-stranded breaks (DSBs) by homology-directed r

223 for the formation, of SPO11-induced meiotic DNA double-stranded breaks (DSBs) in Arabidopsis.

224 DNA double-stranded breaks (DSBs) trigger human genome i

225 complex) are similarly deficient in joining DNA double-stranded breaks (DSBs) with hairpinned termin

226 e (DDR) encompasses the cellular response to DNA double-stranded breaks (DSBs), and includes recognit

227 ogous recombination-mediated repair (HRR) of DNA double-stranded breaks (DSBs).

228 ed mutations during somatic hypermutation or DNA double-strand breaks during class switch recombinati

229 n even earlier function in HR in restricting DNA double-stranded break ends resection that generates

230 en shown to play a crucial role in repair of DNA double-strand breaks, facilitating nonhomologous end

231 play central roles in CCL as SPO11 mediates DNA double-strand break formation while both SPO11 and R

232 Repair of DNA double-strand breaks have been shown to enable "shuf

233 We investigated telomere length and DNA double-strand breaks (histone variant pgamma-H2AX) a

234 Introduction of a DNA double strand break in the model UBE2T locus in vivo

235 s recombination repair (HRR) pathway repairs DNA double-strand breaks in an error-free manner.

236 DNA double-strand breaks in cells of radionuclide-treate

237 and that this could be explained by reduced DNA double-strand breaks in female meiosis, paralleling

238 lleys) were associated with the formation of DNA double-strand breaks in genomes of wheat, maize (Zea

239 Depletion of WRN induces widespread DNA double-strand breaks in MSI cells, leading to cell c

240 ates that ASD-derived NPCs harbored elevated DNA double-strand breaks in replication stress-susceptib

241 HEJ) is the predominant pathway that repairs DNA double-strand breaks in vertebrates.

242 and accumulation of gammaH2AX, a marker for DNA double-strand breaks, in mammalian cells.

243 DDIAS knockdown results in DNA double-strand breaks, indicated by ATM kinase activa

244 ancer removes an antioxidant barrier against DNA double strand breaks induced by TGFbeta expressed in

245 n, LiveFISH tracks the real-time movement of DNA double-strand breaks induced by CRISPR-Cas9-mediated

246 rently occurred during and immediately after DNA double-strand breaks induced by either doxorubicin o

247 und that fbl17 mutants are hypersensitive to DNA double-strand break-induced genotoxic stress.

248 nk-inducing agents (e.g., platinum drugs) or DNA double-strand break-inducing agents.

249 Alternative end-joining (alt-EJ) repair of DNA double-strand breaks is associated with deletions, c

250 ich BRCA1 protein degradation in response to DNA double-strand breaks is regulated by prolyl isomeras

251 In response to DNA double-strand breaks, MAD2L2-containing shieldin com

252 easured by the CometChip and the staining of DNA double-strand break marker, gammaH2AX.

253 he wild-type sequence simply by generating a DNA double-stranded break near the centre of the duplica

254 unction-induced foci (TIFs), indicating that DNA double-strand breaks occurred exclusively in telomer

255 the RNA-guided nuclease Cas9, we induced two DNA double-strand breaks, one each in the GAPDH and CD4

256 ies face is a potent environmental source of DNA double-strand breaks, potential drivers of genome st

257 ch HPV E7 subverts the function of RNF168 at DNA double-strand breaks, providing a rationale for incr

258 combination (HR) is important for error-free DNA double strand break repair and maintenance of genomi

259 ted DNA methylation that utilizes endogenous DNA double strand break repair pathways.

260 (XLF) is a non-homologous end joining (NHEJ) DNA double strand break repair protein.

261 orts indicate that lamin A/C plays a role in DNA double strand break repair, but a role in DNA base e

262 ase SIRT6 stabilizes the genome by promoting DNA double strand break repair, thereby acting as a tumo

263 standing of the mechanisms and regulation of DNA double strand break repair, we attempted to confirm

264 The BRCA1-A and BRISC complexes serve in DNA double-strand break repair and immune signaling and

265 ins in the paralog USP11, a key regulator of DNA double-strand break repair by homologous recombinati

266 an ideal therapeutic target, as it regulates DNA double-strand break repair by homologous recombinati

267 DNA double-strand break repair by homologous recombinati

268 DNA double-strand break repair by homologous recombinati

269 ting the function of 53BP1, a key factor for DNA double-strand break repair by non-homologous end joi

270 G2 mutation confers synthetic lethality with DNA double-strand break repair genes and increased sensi

271 o potential functions: as a component of the DNA double-strand break repair machinery and as a ribonu

272 ogous end-joining (cNHEJ) pathway is a major DNA double-strand break repair pathway in mammalian cell

273 d activator of ATM signaling, which promotes DNA double-strand break repair through homologous recomb

274 regulates the DNA damage response as well as DNA double-strand break repair through homologous recomb

275 HMCES specifically enables DNA double-strand break repair through the microhomology

276 e in BRCA-deficient human cells and promotes DNA double-strand break repair through two pathways: hom

277 mammalian proteins, SFPQ and NONO, promotes DNA double-strand break repair via the canonical nonhomo

278 nt studies indicating the role of R-loops in DNA double-strand break repair with an updated view of m

279 nit (DNA-PKcs) has well-established roles in DNA double-strand break repair, and recently, nonrepair

280 ed genomic patterns reflective of defects in DNA double-strand break repair, comparing HPV-associated

281 am PI3K pathway activation and also hindered DNA double-strand break repair, which both led to improv

282 , base excision repair, mismatch repair, and DNA double-strand break repair.

283 me in the HR pathway that mediates efficient DNA double-strand break repair.

284 trimethylation at meiotic hotspots, impaired DNA double-strand-break repair, and reduced crossover nu

285 antial increase in the stability of RAD51 at DNA double-strand break sites and in the overall efficie

286 y regulatable CRISPR/Cas9 strategy to induce DNA double strand breaks specifically in the telomeres,

287 ir, which leads to the accumulation of toxic DNA double-strand breaks specifically in cancer cells wi

288 (BIR) is a mechanism used to heal one-ended DNA double-strand breaks, such as those formed at collap

289 cus is highly mutagenic because Cas9 creates DNA double strand breaks, targeting of dead Cas9 (dCas9)

290 es nucleosomal DNA to designate the sites of DNA double-strand breaks that initiate meiotic recombina

291 e emitted high-energy alpha particles induce DNA double-strand breaks that might be irreparable and l

292 ZMYM3 is recruited to DNA double-strand breaks through bivalent interactions w

293 organisms that allows the faithful repair of DNA double strand breaks, through the exchange of DNA st

294 e time for sites of recombination-initiating DNA double-strand breaks to find and engage their homolo

295 ation (HR) mediates the error-free repair of DNA double-strand breaks to maintain genomic stability.

296 During meiosis, DNA double-strand breaks undergo interhomolog repair to

297 and NSD2 have been found to be recruited to DNA double strand breaks upon damage and H3K36me2 marks

298 In bacteria, repair of DNA double-strand breaks uses a highly conserved helicas

299 ile MRN has been shown to promote R-loops at DNA double-strand breaks, we show that it suppresses R-l

300 DNA double-strand breaks were determined in peripheral b