ライフサイエンスコーパス: DNA double-strand break

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

2 volved in repairing a subset of pathological DNA double strand breaks.

3 ng error-prone non-homologous end joining of DNA double-strand breaks.

4 , which induce massive DNA damage, including DNA double-strand breaks.

5 tegrity and cell survival in the presence of DNA double-strand breaks.

6 wild-type cells are not due to the repair of DNA double-strand breaks.

7 it may erroneously add telomeric repeats to DNA double-strand breaks.

8 cumulates in the nucleus and is recruited to DNA double-strand breaks.

9 er regulation of homology-directed repair of DNA double-strand breaks.

10 or the sensing, processing, and signaling of DNA double-strand breaks.

11 Mutation of Dicer-2 led to an increase in DNA double-strand breaks.

12 of radiation damage and, more specifically, DNA double-strand breaks.

13 abolish assembly of DDR factors at sites of DNA double-strand breaks.

14 ssisting the loading of RAD51 recombinase at DNA double-strand breaks.

15 ival by limiting nuclear envelope damage and DNA double-strand breaks.

16 ntaining genome integrity in the presence of DNA double-strand breaks.

17 tively, and for jointly generating staggered DNA double-strand breaks.

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

19 des an important mechanism for the repair of DNA double-strand breaks.

20 H2AX (gamma-H2A.X), a marker associated with DNA double-strand breaks.

21 eocytoplasmic transport, and accumulation of DNA double-strand breaks.

22 chromosome termini from being recognized as DNA double-strand breaks.

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

24 hase I exit to repair any persisting meiotic DNA double-strand breaks.

25 cin (CPT), PIAS3 contributes to formation of DNA double-stranded breaks.

26 hout the requirement for prior generation of DNA double-stranded breaks.

27 We present evidence that persistent DNA double-strand breaks act as silencing initiation sit

28 NA damage strongly promoted the formation of DNA double-strand breaks, activation of the ATM-CHK2 pat

29 5; 10; 20 MeV) and the results, in terms of DNA double strand breaks, agree with experimental data f

30 W-CIN induced DNA double strand breaks and elevated oxidative stress,

31 PRC2 methyltransferase activity, localize to DNA double strand breaks and mediate nucleosome accessib

32 cline targets topoisomerase II beta to cause DNA double-strand breaks and a profound change in the tr

33 C5-8 can efficiently repair nuclease-induced DNA double-strand breaks and accelerate the assembly of

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

35 d reduced homologous recombination repair of DNA double-strand breaks and protein kinase B activation

36 D50-NBS1) complex is essential for repair of DNA double-strand breaks and stalled replication forks.

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

38 al role in homology-directed repair (HDR) of DNA double strand breaks, and the repair defect of BRCA1

39 and BRCA2 have essential roles in repairing DNA double-strand breaks, and a deficiency of BRCA prote

40 ns, reduced doxorubicin-induced formation of DNA double-strand breaks, and mitigated synaptic and neu

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

42 process of homologous recombination, whereby DNA double-strand breaks are introduced into the genome

43 TOP2-induced DNA double-strand breaks are rejoined in part by tyrosyl

44 joining (NHEJ) is the major pathway by which DNA double-strand breaks are repaired.

45 Brca2 genes have reduced capacity to repair DNA double-strand breaks by homologous recombination and

46 gene promoters and to promote the repair of DNA double-strand breaks by homologous recombination.

47 is involved in DNA replication and repair of DNA double-strand breaks by the homologous recombination

48 dinate ICL removal and repair of the ensuing DNA double-stranded break by homology-dependent repair (

49 mplex BRCA1-BARD1 functions in the repair of DNA double-stranded breaks by homologous recombination.

50 and internalized fractions) and the produced DNA double-strand breaks, by determining the number of p

51 ombe cells induced misrepair and irreparable DNA double strand breaks causing chromosome fragmentatio

52 XPG depletion causes DNA double-strand breaks, chromosomal abnormalities, cel

53 here or in particular situations can lead to DNA double-strand breaks, chromosome rearrangements, and

54 ies of Nanog, which include the induction of DNA double-stranded break damage.

55 y and currently the most sensitive method of DNA double strand break (DSB) quantification (based on g

56 ions and phleomycin, attesting to a probable DNA double strand break (dsb) repair defect.

57 DNA double strand break (DSB) repair is critical for gen

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

59 DNA double strand break (DSB) responses depend on the se

60 ch initiation through direct generation of a DNA double strand break (DSB).

61 promotes genomic instability in the form of DNA double strand breaks (DSB) in cancer cells that lack

62 Mating-type switching is induced by a DNA double-strand break (DSB) at the MAT locus on chromo

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

64 The aim of the study was to investigate DNA double-strand break (DSB) formation and its correlat

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

66 After DNA double-strand break (DSB) generation, Cdc14 is trans

67 ich motif associated with a meiosis-specific DNA double-strand break (DSB) in Saccharomyces cerevisia

68 rough which H3K36me3 stimulates H4K16ac upon DNA double-strand break (DSB) induction in human cells.

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

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

71 DNA double-strand break (DSB) repair by homologous recom

72 C1/2/3 inhibition resulted in suppression of DNA double-strand break (DSB) repair by homologous recom

73 DNA double-strand break (DSB) repair by non-homologous e

74 The cell achieves DNA double-strand break (DSB) repair in the context of c

75 Pathway choice within DNA double-strand break (DSB) repair is a tightly regula

76 DNA double-strand break (DSB) repair is essential for ma

77 Non-homologous end joining (NHEJ) is a major DNA double-strand break (DSB) repair mechanism.

78 onhomologous end-joining (NHEJ) is the major DNA double-strand break (DSB) repair pathway in mammals

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

80 Single-strand annealing (SSA) is a DNA double-strand break (DSB) repair pathway that uses h

81 us end joining (C-NHEJ) is a major mammalian DNA double-strand break (DSB) repair pathway.

82 Multiple DNA double-strand break (DSB) repair pathways are active

83 ogous recombination (HR) is one of the major DNA double-strand break (DSB) repair pathways in mammali

84 n deacetylases facilitate the switch between DNA double-strand break (DSB) repair pathways, how SIRTs

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

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

87 BRCA1 plays an important role in DNA double-strand break (DSB) repair via homologous reco

88 h key proteins critical for genome integrity-DNA double-strand break (DSB) repair, DNA interstrand cr

89 d joining (MMEJ), an error-prone pathway for DNA double-strand break (DSB) repair, is implicated in g

90 During DNA double-strand break (DSB) repair, the ring-shaped Ku

91 ressor protein 53BP1, a pivotal regulator of DNA double-strand break (DSB) repair, was first identifi

92 alt)-nonhomologous end joining (NHEJ) during DNA double-strand break (DSB) repair.

93 ize p53 mediated apoptosis, but also promote DNA double-strand break (DSB) repair.

94 atrial arrhythmia, are potent inhibitors of DNA double-strand break (DSB) repair.

95 n about how the developmental changes impact DNA double-strand break (DSB) repair.

96 They are considered by-products of DNA double-strand break (DSB) repair: the homologous rec

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

98 orylates FBXW7 at serine 26 to recruit it to DNA double-strand break (DSB) sites, whereas activated D

99 H3K4me3 demethylation within chromatin near DNA double-strand break (DSB) sites.

100 Recent reports have demonstrated that DNA double-strand break (DSB)-induced small RNAs (diRNA)

101 as9 to any location in the genome, causing a DNA double-strand break (DSB).

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

103 ecruits repair proteins, including 53BP1, to DNA double-strand breaks (DSB) and undergoes dynamic ace

104 Unrepaired DNA double-strand breaks (DSB) are the most destructive

105 ne and found that HsRAD52 supports repair of DNA double-strand breaks (DSB) by a mechanism of HR that

106 amage-responsive kinase ATM and formation of DNA double-strand breaks (DSB) by formaldehyde (FA) that

107 DNA double-strand breaks (DSB) elicit a ubiquitylation c

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

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

110 are implicated in replication fork stalling, DNA double strand breaks (DSBs) and human disease.

111 DNA double strand breaks (DSBs) are generally repaired t

112 DNA double strand breaks (DSBs) can be repaired by eithe

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

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

115 Repair of DNA double strand breaks (DSBs) is key for maintenance o

116 factor (CTCF) and cohesin are vulnerable to DNA double strand breaks (DSBs) mediated by topoisomeras

117 is released during bacterial lysis, induces DNA double strand breaks (DSBs), as indicated by ataxia

118 s genome instability and sensitizes cells to DNA double strand breaks (DSBs), suggesting defects in D

119 DUB activity contributes to its function at DNA double strand breaks (DSBs), we used RNAi and genome

120 GCRs are thought to be triggered by DNA double strand breaks (DSBs), which in turn can be sp

121 nd altered chromatin dynamics in response to DNA double strand breaks (DSBs).

122 e levels of radiation that cause hundreds of DNA double strand breaks (DSBs).

123 mbination (HR)-mediated repair of programmed DNA double strand breaks (DSBs).

124 g persistent R-loops and promoting repair of DNA double strand breaks (DSBs).

125 DNA double-strand breaks (DSBs) activate a canonical DNA

126 sely measuring the location and frequency of DNA double-strand breaks (DSBs) along the genome is inst

127 DNA double-strand breaks (DSBs) and short telomeres are

128 DNA double-strand breaks (DSBs) and their repair can cau

129 ive immune responses that naturally generate DNA double-strand breaks (DSBs) and trigger a DNA repair

130 accumulated reactive oxygen species-induced DNA double-strand breaks (DSBs) and were modestly sensit

131 iciency and type of pathway chosen to repair DNA double-strand breaks (DSBs) are critically influence

132 DNA double-strand breaks (DSBs) are known to be powerful

133 DNA double-strand breaks (DSBs) are mainly repaired eith

134 DNA double-strand breaks (DSBs) are one of the most cyto

135 Of the many types of DNA damage, DNA double-strand breaks (DSBs) are probably the most de

136 DNA double-strand breaks (DSBs) are rare, but highly tox

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

138 DNA double-strand breaks (DSBs) are repaired by either t

139 DNA double-strand breaks (DSBs) are toxic lesions, which

140 DNA double-strand breaks (DSBs) arise during physiologic

141 ogous recombination (HR), which also repairs DNA double-strand breaks (DSBs) arising at collapsed for

142 CRISPR/Cas9, which generates DNA double-strand breaks (DSBs) at target loci, is a pow

143 Mechanistically, UHRF1 is recruited to DNA double-strand breaks (DSBs) by BRCA1 in S phase, whi

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

145 Repair of DNA double-strand breaks (DSBs) by non-homologous end jo

146 that facilitates homologous recombination of DNA double-strand breaks (DSBs) by promoting recruitment

147 Repair of DNA double-strand breaks (DSBs) by the nonhomologous end

148 ination initiates following the formation of DNA double-strand breaks (DSBs) by the Spo11 endonucleas

149 rovide genetic and biochemical evidence that DNA double-strand breaks (DSBs) can be directly generate

150 dies of activated B cells have revealed that DNA double-strand breaks (DSBs) capable of translocating

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

152 Here we show that RB also localizes to DNA double-strand breaks (DSBs) dependent on E2F1 and AT

153 nsposable elements (TEs), template or bridge DNA double-strand breaks (DSBs) during repair, and direc

154 The repair outcomes at site-specific DNA double-strand breaks (DSBs) generated by the RNA-gui

155 (cNHEJ) but is dispensable for the repair of DNA double-strand breaks (DSBs) generated during V(D)J r

156 omologous end-joining (NHEJ) pathway repairs DNA double-strand breaks (DSBs) in all domains of life.

157 oining (NHEJ) is the main repair pathway for DNA double-strand breaks (DSBs) in cells with limited 5'

158 non-homologous end joining (c-NHEJ) repairs DNA double-strand breaks (DSBs) in G1 cells with biphasi

159 only is Artemis important for the repair of DNA double-strand breaks (DSBs) in NHEJ, it is essential

160 ination (CSR) requires targeted formation of DNA double-strand breaks (DSBs) in repetitive switch reg

161 In pre-B cells, DNA double-strand breaks (DSBs) induced at Igkappa loci

162 DNA double-strand breaks (DSBs) induced by abortive topo

163 both gene transcription and genome stability.DNA double-strand breaks (DSBs) induced by topoisomerase

164 ion of histone H2A Lys13,15 (H2AK13,15ub) at DNA double-strand breaks (DSBs) is crucial for preventin

165 The ability of cells to detect and repair DNA double-strand breaks (DSBs) is dependent on reorgani

166 Nucleolytic resection of DNA double-strand breaks (DSBs) is essential for both ch

167 Repair of DNA double-strand breaks (DSBs) is essential for genomic

168 The cellular response to DNA double-strand breaks (DSBs) is initiated by the MRX/

169 y event in the choice of repair pathways for DNA double-strand breaks (DSBs) is the initial processin

170 DNA double-strand breaks (DSBs) leading to loss of nucle

171 Repair of DNA double-strand breaks (DSBs) must be properly orchest

172 DNA double-strand breaks (DSBs) occurring within fragile

173 DNA double-strand breaks (DSBs) pose a threat to genome

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

175 DNA double-strand breaks (DSBs) serve as obligatory inte

176 gs such as etoposide and then converted into DNA double-strand breaks (DSBs) that carry adducts at th

177 In most mammals, the DNA double-strand breaks (DSBs) that initiate meiotic re

178 erference of Rad51 Rad51 knockdown increases DNA double-strand breaks (DSBs) throughout the body, but

179 End resection of DNA double-strand breaks (DSBs) to generate 3'-single-st

180 n-activating gene (RAG) endonuclease-induced DNA double-strand breaks (DSBs) transcend hazardous inte

181 When programmed meiotic DNA double-strand breaks (DSBs) undergo recombinational

182 DNA double-strand breaks (DSBs) were assessed by immunof

183 uplex and displaced single-stranded DNA) and DNA double-strand breaks (DSBs) were monitored in multip

184 DNA double-strand breaks (DSBs) with 5' adducts are freq

185 Repair of DNA double-strand breaks (DSBs) with complex ends poses

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

187 Telomerase can generate a novel telomere at DNA double-strand breaks (DSBs), an event called de novo

188 evidenced by elevated DNA damage, primarily DNA double-strand breaks (DSBs), and activation of DNA d

189 We measured DNA double-strand breaks (DSBs), DNA repair proteins, an

190 ed in cancer therapy and is a main source of DNA double-strand breaks (DSBs), one of the most toxic f

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

192 tment of the damage response factor 53BP1 to DNA double-strand breaks (DSBs), thereby influencing the

193 nd Rad51 cannot be recruited to the sites of DNA double-strand breaks (DSBs), which impairs DSB repai

194 entral role in orchestrating the response to DNA double-strand breaks (DSBs).

195 to serve as a template during the repair of DNA double-strand breaks (DSBs).

196 d joining (NHEJ), a major repair pathway for DNA double-strand breaks (DSBs).

197 e-editing systems generally rely on inducing DNA double-strand breaks (DSBs).

198 cruitment of DNA repair proteins to sites of DNA double-strand breaks (DSBs).

199 ng of DNA strands is essential for repair of DNA double-strand breaks (DSBs).

200 action from DNA, leading to the formation of DNA double-strand breaks (DSBs).

201 bination, which is initiated via hundreds of DNA double-strand breaks (DSBs).

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

203 ion of a novel environment leads to neuronal DNA double-strand breaks (DSBs).

204 uch gross rearrangements is the formation of DNA double-strand breaks (DSBs).

205 e disruption strategies rely on Cas9-induced DNA double-strand breaks (DSBs).

206 bination (HR) is a major mechanism to repair DNA double-strand breaks (DSBs).

207 l early step in homology-dependent repair of DNA double-strand breaks (DSBs).

208 Most DNA double-strand-breaks (DSBs) are repaired by two majo

209 hat chromatin destabilization by clusters of DNA double-strand-breaks (DSBs) generated by the I-SceI

210 oughput assays for detecting and quantifying DNA double-stranded breaks (DSBs) across the genome in m

211 ARPi-resistant cells regain RAD51 loading to DNA double-stranded breaks (DSBs) and stalled replicatio

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

213 A DNA-damaging agent that induces DNA double-stranded breaks (DSBs) does not affect the in

214 a template-driven repair pathway that mends DNA double-stranded breaks (DSBs), and thus helps to mai

215 To allow for sufficient time to repair DNA double-stranded breaks (DSBs), eukaryotic cells acti

216 gle strand breaks (SSBs) can be converted to DNA double strand breaks during replication thus trigger

217 unction, PTEN-deficient cells fail to resect DNA double-strand breaks efficiently after irradiation a

218 DNA double-strand breaks enact nascent telomere synthesi

219 ich initiates a cascade of events leading to DNA double-strand break formation in switch (S) regions.

220 TOP2A and especially TOP2B-DNA complexes and DNA double-strand break formation.

221 vity or formulation demonstrated significant DNA double-strand breaks (>/=5% gamma-H2A.X-positive cel

222 Targeted DNA double-strand breaks have been shown to significantl

223 Non-homologous end joining (NHEJ) repairs DNA double strand breaks in non-cycling eukaryotic cells

224 SK2 promotes DNA double-strand breaks in cultured primary neurons.

225 clb(+) E. coli induce megalocytosis and DNA double-strand breaks in eukaryotic cells, but parado

226 clb(+) E. coli induce DNA double-strand breaks in mammalian cells in vitro and

227 p53R172H to irradiation, we found persistent DNA double-strand breaks in p53R172H testes and the form

228 ential for homology-directed repair (HDR) of DNA double-strand breaks in part through antagonism of t

229 The drug promoted the formation of DNA double-strand breaks in primary neurons and reduced

230 mor cells that overexpress Mdm2 have reduced DNA double-strand breaks in response to doxorubicin or e

231 Sae2 promotes the repair of DNA double-strand breaks in Saccharomyces cerevisiae The

232 a conserved DNA repair apparatus processing DNA double-strand breaks in stationary phase.

233 at RECQL5 associates longer at laser-induced DNA double-strand breaks in the absence of Werner syndro

234 nary evidence of ATR inhibition and enhanced DNA double-stranded breaks in response to the combinatio

235 MDNP treatment also increased apoptosis and DNA double strand breaks, increasing median host surviva

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

237 The O-GlcNAcylation negatively regulates DNA double-strand break-induced phosphorylation of H2AX

238 To estimate DNA double-strand-break induction at breast-tissue level

239 -induced cytidine deaminase (AID)-instigated DNA double-strand breaks into the IgH loci.

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

241 Repair of DNA double-strand breaks is crucial for maintaining geno

242 e that ATM affects resolution of RAG-induced DNA double-strand breaks is profuse and unequivocal; mor

243 Nucleolytic resection of DNA double-strand breaks is the crucial first step in th

244 mosomal DNA, which is used for the repair of DNA double-strand breaks, is exchanged.

245 MTHFR c. 1298A > C AC genotype with reduced DNA double-strand breaks levels.

246 o radiation during CT angiography to compare DNA double-strand-break levels by gamma-H2AX immunofluor

247 Results Breast shielding had no effect on DNA double-strand-break levels from ex vivo radiation of

248 giography, breast shielding had no effect on DNA double-strand-break levels in blood lymphocytes expo

249 Predictors of increased DNA double-strand-break levels included total radiation

250 g on blood lymphocyte deoxyribonucleic acid (DNA) double-strand-break levels resulting from in vivo r

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

252 AX and Rad51 suggests that topotecan-induced DNA double-strand breaks occur at sites distinct from st

253 leads to the declined repair efficiency for DNA double-strand breaks on the GFP-Pem1 reporter gene b

254 Persistent induction of DNA double-strand breaks or mTORC1 inhibition by rapamyc

255 wn mice expressed high levels of a marker of DNA double-strand breaks, phosphorylated histone 2A, mem

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

257 Resolution of DNA double-strand breaks proceeds through formation of S

258 e genome edits at DNA strand lesions made by DNA double strand break reagents.

259 iting frequency compared with treatment with DNA double strand-breaking reagents alone.

260 t facilitates histone H2A ubiquitination and DNA double strand break repair by homologous recombinati

261 advantageous in gap-filling synthesis during DNA double strand break repair by nonhomologous end join

262 to deoxycholate, as well as function of the DNA double strand break repair system.

263 sitivity to deoxycholate and was impaired in DNA double strand break repair.

264 g roles in homologous recombination-mediated DNA double-strand break repair and replication fork proc

265 DNA double-strand break repair by homologous recombinati

266 of gamma-H2AX foci and reduced induction of DNA double-strand break repair genes.

267 RecN is a cohesin-like protein involved in DNA double-strand break repair in bacteria.

268 RNA can serve as a template for DNA double-strand break repair in yeast cells, and Rad52

269 Homologous recombination (HR)-mediated DNA double-strand break repair is important for tumor su

270 nct and separable from 53BP1's regulation of DNA double-strand break repair pathway choice.

271 non-homologous end joining (the predominant DNA double-strand break repair pathway in higher eukaryo

272 Break-induced replication (BIR) is a DNA double-strand break repair pathway that leads to gen

273 Efficient and accurate DNA double-strand break repair systems have been demonst

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

275 how the Rad52 protein mediates RNA-dependent DNA double-strand break repair via inverse strand exchan

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

277 We find that LIG4, a DNA ligase in DNA double-strand break repair, is a direct target of be

278 us works have identified the role of PTEN in DNA double-strand break repair, vulnerabilities of PTEN-

279 etions or insertions-molecular signatures of DNA double-strand break repair.

280 f BLM and KU70, which are both essential for DNA double-strand break repair.

281 functions of the Mre11/Rad50 (MR) complex in DNA double-strand break repair.

282 ein 53BP1 plays a central regulatory role in DNA double-strand break repair.

283 tenance.DNA polymerase (pol) mu functions in DNA double-strand break repair.

284 Repair of single-ended DNA double-strand breaks (seDSBs) by homologous recombin

285 trate that cytoplasmic TRADD translocates to DNA double-strand break sites (DSBs) during the DNA dama

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

287 ting leukemia cells accumulate highly lethal DNA double-strand breaks that are repaired by 2 major me

288 strain at chromosomal loop anchors generates DNA double-strand breaks that drive multiple oncogenic t

289 DNA double-strand breaks that initiate meiotic recombina

290 ated in meiotic prophase by the formation of DNA double-strand breaks that occur throughout the genom

291 nonhomologous end joining (NHEJ), repairing DNA double-strand breaks that would otherwise lead to ap

292 apid oocyte elimination in response to a few DNA double strand breaks thereby acting as the key quali

293 vage complexes to allow error-free repair of DNA double-strand breaks, thereby conferring cellular re

294 alyzes homologous recombination triggered by DNA double strand breaks through the exchange of parenta

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

296 ylated histone H2AX (gammaH2AX), a marker of DNA double-strand breaks, was increased in vitamin B12 d

297 DNA double-strand breaks were determined in peripheral b

298 DNA double-strand breaks were measured using anti-gamma-

299 s that BMI1 is rapidly recruited to sites of DNA double strand breaks where it facilitates histone H2

300 MRN binds DNA double-strand breaks, where it functions in repair a