ライフサイエンスコーパス: double-strand break

1 at two complexes are required to introduce a double strand break.

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

3 ficant role on the final number of simulated double strand breaks.

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

5 vity slows replication elongation and causes double-strand breaks.

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

7 toplasmic transport, and accumulation of DNA double-strand breaks.

8 omosome termini from being recognized as DNA double-strand breaks.

9 BP1 function by blocking its localization to double-strand breaks.

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

11 modulating pathway choice for the repair of double-strand breaks.

12 r plays a key role in limiting the levels of double-strand breaks.

13 rror-prone non-homologous end joining of DNA double-strand breaks.

14 ich induce massive DNA damage, including DNA double-strand breaks.

15 e removed without generation of highly toxic double-strand breaks.

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

17 ity and cell survival in the presence of DNA double-strand breaks.

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

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

20 gions expected to undergo DNA nicking and/or double-strand breaks.

21 lates in the nucleus and is recruited to DNA double-strand breaks.

22 egulation of homology-directed repair of DNA double-strand breaks.

23 he sensing, processing, and signaling of DNA double-strand breaks.

24 A2 to promote efficient RAD51 loading at DNA double-strand breaks.

25 econds after the induction of DNA single- or double-strand breaks.

26 nosine (8-OHdG), while ZMYND8 recruits it to double-strand breaks.

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

28 We present evidence that persistent DNA double-strand breaks act as silencing initiation sites.

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

30 n the mouse central nervous system increases double strand breaks and ATM defects and triggers neurod

31 These findings identify R-loops, double strand breaks and defective ATM-mediated repair a

32 methyltransferase activity, localize to DNA double strand breaks and mediate nucleosome accessibilit

33 addition, Mlh1-Mlh3 can generate religatable double-strand breaks and form an active nucleoprotein co

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

35 duced homologous recombination repair of DNA double-strand breaks and protein kinase B activation, le

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

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

38 deaminases to introduce changes (rather than double-stranded breaks and donor templates) and offers p

39 ed for only certain types of damage, such as double-stranded breaks and interstrand crosslinks.

40 ing foci of phosphorylated H2AX (a marker of double-strand breaks) and the DNA-repair enzyme RAD51.

41 ole in homology-directed repair (HDR) of DNA double strand breaks, and the repair defect of BRCA1-mut

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

43 sorders (eg, ataxia-telangiectasia), and DNA double-strand breaks are crucial to the modulation of ea

44 Because double-strand breaks are generally highly toxic, mechani

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

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

47 The RNA-guided endonuclease Cas9 generates a double-strand break at DNA target sites complementary to

48 These methods involve the induction of double-strand breaks at endogenous loci followed by the

49 ar intermediate during the repair of mitotic double-strand breaks by homologous recombination, but it

50 in promoting interhomolog repair of meiotic double-strand breaks by inhibiting intersister repair.

51 nvolved in DNA replication and repair of DNA double-strand breaks by the homologous recombination (HR

52 te ICL removal and repair of the ensuing DNA double-stranded break by homology-dependent repair (HDR)

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

54 internalized fractions) and the produced DNA double-strand breaks, by determining the number of p53 b

55 In response to double-strand breaks, chromatin is more mobile at large

56 XPG depletion causes DNA double-strand breaks, chromosomal abnormalities, cell-cy

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

58 Exo1 processing at DNA nicks and double-strand breaks creates long stretches of single-st

59 may be sites of selective susceptibility to double-strand-break damage due to high transcriptional a

60 accumulate in RNase H-deficient cells, while double-strand breaks do.

61 latory increase of p53 levels in response to double-strand breaks drives a counter-oscillatory decrea

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

63 end-joining (NHEJ) is the most prominent DNA double strand break (DSB) repair pathway in mammalian ce

64 he Muta1 ends and catalyzes excision through double strand breaks (DSB) and the joining of newly exci

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

66 siae mating-type switching is initiated by a double-strand break (DSB) at MATa, leaving one cut end p

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

68 profile associated with repair of a defined double-strand break (DSB) by the synthesis-dependent str

69 sover formation, regulating cessation of DNA double-strand break (DSB) formation following crossover

70 After DNA double-strand break (DSB) generation, Cdc14 is transient

71 motif associated with a meiosis-specific DNA double-strand break (DSB) in Saccharomyces cerevisiae fo

72 The frequency of TSI can be elevated by double-strand break (DSB) inducer and abolished by ATM/A

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

74 genotoxic damage or even a single unrepaired double-strand break (DSB) initiates a previously undescr

75 A DNA double-strand break (DSB) is the most critical type of g

76 Evidence exists for double-strand break (DSB) mediated recombination-depende

77 ce the ability of the HR pathway to complete double-strand break (DSB) repair by about 50%.

78 ual 53BP1 and RIF1 foci, suggesting that DNA double-strand break (DSB) repair by homologous recombina

79 Pathway choice within DNA double-strand break (DSB) repair is a tightly regulated

80 DNA double-strand break (DSB) repair is essential for mainta

81 non homologous end-joining (NHEJ) pathway of double-strand break (DSB) repair often requires DNA synt

82 Homologous recombination (HR) is a DNA double-strand break (DSB) repair pathway that protects t

83 us DNA end-joining (NHEJ) is the predominant double-strand break (DSB) repair pathway throughout the

84 ncy is constrained by competition from other double-strand break (DSB) repair pathways, including non

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

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

87 Namely, XAB2 is important for chromosomal double-strand break (DSB) repair via two pathways of HR

88 y proteins critical for genome integrity-DNA double-strand break (DSB) repair, DNA interstrand crossl

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

90 combination (HR), the error-free pathway for double-strand break (DSB) repair, is required during phy

91 or of homologous recombination (HR)-mediated double-strand break (DSB) repair, which is mediated thro

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

93 ACLY facilitates histone acetylation at double-strand break (DSB) sites, impairing 53BP1 localiz

94 ates FBXW7 at serine 26 to recruit it to DNA double-strand break (DSB) sites, whereas activated DNA-P

95 4me3 demethylation within chromatin near DNA double-strand break (DSB) sites.

96 research, the spatio-mechanical processes of double-strand break (DSB)-repair, especially the auxilia

97 ndogenous chromosomal locus containing a DNA double-strand break (DSB).

98 its repair proteins, including 53BP1, to DNA double-strand breaks (DSB) and undergoes dynamic acetyla

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

100 nd found that HsRAD52 supports repair of DNA double-strand breaks (DSB) by a mechanism of HR that con

101 DNA double-strand breaks (DSB) elicit a ubiquitylation casca

102 e, but due to their clustering the yields of double-strand breaks (DSB) increase, up to saturation ar

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

104 spontaneous occurrence of single-strand and double-strand breaks (DSB).

105 (ciCas9) and a droplet digital PCR assay for double-strand breaks (DSB-ddPCR) to investigate the kine

106 7 T) and the effect of contrast agent on DNA double-strand-break (DSB) formation in patients undergoi

107 s enhanced, and the complex was recruited to double-stranded break (DSB) sites in response to etoposi

108 It has been reported that double-stranded break (DSB)-induced small RNAs (diRNAs)

109 frequently during healing of induced nuclear double-stranded breaks (DSB) but the resulting nuclear i

110 k radiation showed a significant increase in double-stranded breaks (DSB) in the DNA of parotid saliv

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

112 s in more telomeric RNA:DNA hybrids and more double strand breaks (DSBs) at telomeres and subtelomere

113 DNA double strand breaks (DSBs) can be repaired by either re

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

115 ium histones are modified in response to DNA double strand breaks (DSBs) in vivo by the ARTs Adprt1a

116 Repair of DNA double strand breaks (DSBs) is key for maintenance of ge

117 tor (CTCF) and cohesin are vulnerable to DNA double strand breaks (DSBs) mediated by topoisomerase 2B

118 Double strand breaks (DSBs) represent highly deleterious

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

120 nome instability and sensitizes cells to DNA double strand breaks (DSBs), suggesting defects in DNA r

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

122 ltered chromatin dynamics in response to DNA double strand breaks (DSBs).

123 vels of radiation that cause hundreds of DNA double strand breaks (DSBs).

124 s ATM and DNA-PKcs through the generation of double stranded breaks (DSBs) in murine macrophage genom

125 measuring the location and frequency of DNA double-strand breaks (DSBs) along the genome is instrume

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

127 umulated reactive oxygen species-induced DNA double-strand breaks (DSBs) and were modestly sensitive

128 ncy and type of pathway chosen to repair DNA double-strand breaks (DSBs) are critically influenced by

129 DNA double-strand breaks (DSBs) are mainly repaired either b

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

131 DNA double-strand breaks (DSBs) are rare, but highly toxic,

132 We demonstrate that double-strand breaks (DSBs) are rate-limiting for germin

133 ic recombination, a subset of programmed DNA double-strand breaks (DSBs) are repaired as crossovers,

134 DNA double-strand breaks (DSBs) are repaired by either the n

135 Double-strand breaks (DSBs) are repaired through two maj

136 DNA double-strand breaks (DSBs) arise during physiological t

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

138 Induced double-strand breaks (DSBs) at the mutant paternal allel

139 NCJ has been implicated in the repair of DNA double-strand breaks (DSBs) by homologous recombination

140 nd is dependent upon repair of SPO11-induced double-strand breaks (DSBs) by homologous recombination.

141 nce-specific nuclease-induced DNA nicking or double-strand breaks (DSBs) by homology-directed repair

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

143 ion initiates following the formation of DNA double-strand breaks (DSBs) by the Spo11 endonuclease ea

144 de genetic and biochemical evidence that DNA double-strand breaks (DSBs) can be directly generated by

145 of IR survival and repair efficiency of DNA double-strand breaks (DSBs) caused by exposure to gamma

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

147 Double-strand breaks (DSBs) in DNA are recognized by the

148 nery responsible for detection and repair of double-strand breaks (DSBs) in DNA, although detail conc

149 fluorene functional groups and which induces double-strand breaks (DSBs) in DNA.

150 -homologous end joining (c-NHEJ) repairs DNA double-strand breaks (DSBs) in G1 cells with biphasic ki

151 ion (CSR) requires targeted formation of DNA double-strand breaks (DSBs) in repetitive switch region

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

153 DNA double-strand breaks (DSBs) induced by abortive topoisom

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

155 of histone H2A Lys13,15 (H2AK13,15ub) at DNA double-strand breaks (DSBs) is crucial for preventing ab

156 Nucleolytic resection of DNA double-strand breaks (DSBs) is essential for both checkp

157 Repairing double-strand breaks (DSBs) is particularly challenging

158 DNA double-strand breaks (DSBs) occurring within fragile zon

159 Double-strand breaks (DSBs) of DNA in eukaryotic cells a

160 Resection of double-strand breaks (DSBs) plays a critical role in the

161 DNA double-strand breaks (DSBs) prevent cells from entering

162 ombination (HR) repair of programmed meiotic double-strand breaks (DSBs) requires endonucleolytic cli

163 DNA double-strand breaks (DSBs) serve as obligatory intermed

164 uch as etoposide and then converted into DNA double-strand breaks (DSBs) that carry adducts at the 5'

165 The Spo11-generated double-strand breaks (DSBs) that initiate meiotic recomb

166 ed protein 80 (RAP80) helps recruit BRCA1 to double-strand breaks (DSBs) through the scaffold protein

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

168 tivating gene (RAG) endonuclease-induced DNA double-strand breaks (DSBs) transcend hazardous intermed

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

170 lating formation of recombination-initiating double-strand breaks (DSBs) via a feedback loop triggere

171 DNA double-strand breaks (DSBs) were assessed by immunofluor

172 x and displaced single-stranded DNA) and DNA double-strand breaks (DSBs) were monitored in multiple s

173 DNA double-strand breaks (DSBs) with 5' adducts are frequent

174 se (AID), the activity of which leads to DNA double-strand breaks (DSBs) within IgH switch (S) region

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

176 CS protein response to oxidative DNA damage, double-strand breaks (DSBs), angelicin monoadducts and t

177 n cancer therapy and is a main source of DNA double-strand breaks (DSBs), one of the most toxic forms

178 ns also promote the formation of meiotic DNA double-strand breaks (DSBs), the precursors of cross-ove

179 rly step in homology-dependent repair of DNA double-strand breaks (DSBs).

180 og segregation and arise from self-inflicted double-strand breaks (DSBs).

181 and bleomycin treatment, agents that induce double-strand breaks (DSBs).

182 al role in orchestrating the response to DNA double-strand breaks (DSBs).

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

184 ining (NHEJ), a major repair pathway for DNA double-strand breaks (DSBs).

185 ly of recombination-initiation complexes and double-strand breaks (DSBs).

186 iting systems generally rely on inducing DNA double-strand breaks (DSBs).

187 d conversion of stalled replication forks to double-strand breaks (DSBs).

188 tment of DNA repair proteins to sites of DNA double-strand breaks (DSBs).

189 f DNA strands is essential for repair of DNA double-strand breaks (DSBs).

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

191 ning the ends from two different chromosomal double-strand breaks (DSBs).

192 sruption strategies rely on Cas9-induced DNA double-strand breaks (DSBs).

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

194 -resistant cells regain RAD51 loading to DNA double-stranded breaks (DSBs) and stalled replication fo

195 rly remarkable in the examination of how DNA double-stranded breaks (DSBs) are repaired, with many co

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

197 Cas9 creates targeted double-stranded breaks (DSBs) in the genome.

198 emplate-driven repair pathway that mends DNA double-stranded breaks (DSBs), and thus helps to maintai

199 ion, PTEN-deficient cells fail to resect DNA double-strand breaks efficiently after irradiation and s

200 sive accumulation of DNA damage, genome-wide double-strand breaks enriched at Ssb-binding regions and

201 acts, which progress into R-gaps and then to double-strand breaks-explaining why R-tracts do not accu

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

203 A and especially TOP2B-DNA complexes and DNA double-strand break formation.

204 or formulation demonstrated significant DNA double-strand breaks (>/=5% gamma-H2A.X-positive cells).

205 mers to higher order oligomers to generate a double strand break in DNA.

206 this system, the endonuclease Cas9 generates double strand breaks in DNA upon RNA-guided recognition

207 on-homologous end joining (NHEJ) repairs DNA double strand breaks in non-cycling eukaryotic cells.

208 ated levels of DNA-RNA hybrids (R-loops) and double strand breaks in rat neurons, human cells and C9o

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

210 has been associated with the introduction of double-strand breaks in epithelial cells, triggering dam

211 172H to irradiation, we found persistent DNA double-strand breaks in p53R172H testes and the formatio

212 al for homology-directed repair (HDR) of DNA double-strand breaks in part through antagonism of the n

213 cells that overexpress Mdm2 have reduced DNA double-strand breaks in response to doxorubicin or etopo

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

215 onserved DNA repair apparatus processing DNA double-strand breaks in stationary phase.

216 ECQL5 associates longer at laser-induced DNA double-strand breaks in the absence of Werner syndrome (

217 ent of sperm by analyzing, (1) the levels of double-strand breaks in the DNA, and (2) oxidative damag

218 ntain genomic stability despite ever-present double-strand breaks in the DNA.

219 ttle overlap, however, with the locations of double-strand breaks in wild-derived house mouse strains

220 evidence of ATR inhibition and enhanced DNA double-stranded breaks in response to the combination.

221 gative plasmids by introducing site-specific double-stranded breaks in target DNA.

222 r removes an antioxidant barrier against DNA double strand breaks induced by TGFbeta expressed in the

223 cynin, a NOX inhibitor, protected cells from double-strand breaks induced by HDM.

224 plex mediates DNA repair pathways, including double-strand breaks induced by radiotherapy.

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

226 the nuclear-soluble fraction and alters the double-strand break-induced protein complex centring 53B

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

228 ternative end-joining (alt-EJ) repair of DNA double-strand breaks is associated with deletions, chrom

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

230 red by the CometChip and the staining of DNA double-strand break marker, gammaH2AX.

231 ds to the declined repair efficiency for DNA double-strand breaks on the GFP-Pem1 reporter gene by ho

232 here the mitochondrial DNA (mtDNA) undergoes double-strand breaks only in dopaminergic neurons.

233 Persistent induction of DNA double-strand breaks or mTORC1 inhibition by rapamycin r

234 by inhibiting cep-1/p53, endogenous meiotic double strand breaks, or the expression of MIRAGE1 DNA t

235 vity is required to relocate heterochromatic double-strand breaks outside the domain, as well as for

236 ice expressed high levels of a marker of DNA double-strand breaks, phosphorylated histone 2A, member

237 face is a potent environmental source of DNA double-strand breaks, potential drivers of genome struct

238 Resolution of DNA double-strand breaks proceeds through formation of S-S s

239 g frequency compared with treatment with DNA double strand-breaking reagents alone.

240 end-joining pathway plays a critical role in double strand break repair and is uniquely responsible f

241 cilitates histone H2A ubiquitination and DNA double strand break repair by homologous recombination.

242 ntageous in gap-filling synthesis during DNA double strand break repair by nonhomologous end joining,

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

244 vity to deoxycholate and was impaired in DNA double strand break repair.

245 Double-strand break repair and mismatch repair subtypes

246 les in homologous recombination-mediated DNA double-strand break repair and replication fork processi

247 BRCA1 is best known for its functions in double-strand break repair and resolution of DNA replica

248 DNA double-strand break repair by homologous recombination e

249 Twelve of 27 (45%) double-strand break repair cases lacked germline or soma

250 repair genes to irradiation and inefficient double-strand break repair correlated with severe late r

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

252 cN is a cohesin-like protein involved in DNA double-strand break repair in bacteria.

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

254 An early step in double-strand break repair is the recruitment of ataxia-

255 nd is required for timely pairing and proper double-strand break repair kinetics.

256 e not explicable by the simplest form of the double-strand break repair model of recombination.

257 rhang structure is a critical determinant of double-strand break repair pathway choice.

258 -homologous end joining (the predominant DNA double-strand break repair pathway in higher eukaryotes)

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

260 ht on structural attributes of this X-family double-strand break repair polymerase that impact its bi

261 ding protein 1 (53BP1) is a multi-functional double-strand break repair protein that is essential for

262 Efficient and accurate DNA double-strand break repair systems have been demonstrate

263 lates the DNA damage response as well as DNA double-strand break repair through homologous recombinat

264 dentify TIRR as a new factor that influences double-strand break repair using a unique mechanism of m

265 the Rad52 protein mediates RNA-dependent DNA double-strand break repair via inverse strand exchange.

266 malian proteins, SFPQ and NONO, promotes DNA double-strand break repair via the canonical nonhomologo

267 in X-chromosome inactivation, imprinting and double-strand break repair, and mutations in SMCHD1 cont

268 cting oxidative stress and affecting meiotic double-strand break repair, chromosome synapsis and cros

269 actors that control DNA end resection during double-strand break repair, including the Bloom syndrome

270 red PDAC into 4 major subtypes: age related, double-strand break repair, mismatch repair, and 1 with

271 w mutations appear to be caused by imprecise double-strand break repair, nucleotide misincorporation

272 Homologous recombination plays key roles in double-strand break repair, rescue, and repair of stalle

273 orks have identified the role of PTEN in DNA double-strand break repair, vulnerabilities of PTEN-defi

274 nce.DNA polymerase (pol) mu functions in DNA double-strand break repair.

275 in the non-homologous end-joining pathway of double-strand break repair.

276 ns or insertions-molecular signatures of DNA double-strand break repair.

277 53BP1 plays a central regulatory role in DNA double-strand break repair.

278 structure, thereby hiding telomere ends from double-stranded break repair and ATM signaling, whereas

279 enomic DNA to investigate the quality of the double-strand break repairs in the class-switch recombin

280 de of chromatin mobility induced by a single double-strand break requires active microtubule function

281 that differences between DNA sequences near double-strand breaks should alter repair outcomes in pre

282 e that cytoplasmic TRADD translocates to DNA double-strand break sites (DSBs) during the DNA damage r

283 al increase in the stability of RAD51 at DNA double-strand break sites and in the overall efficiency

284 In the past two decades, several double-strand break technologies have been developed.

285 leukemia cells accumulate highly lethal DNA double-strand breaks that are repaired by 2 major mechan

286 in at chromosomal loop anchors generates DNA double-strand breaks that drive multiple oncogenic trans

287 DNA double-strand breaks that initiate meiotic recombination

288 in meiotic prophase by the formation of DNA double-strand breaks that occur throughout the genome.

289 homologous end joining (NHEJ), repairing DNA double-strand breaks that would otherwise lead to apopto

290 complexes to allow error-free repair of DNA double-strand breaks, thereby conferring cellular resist

291 ZMYM3 is recruited to DNA double-strand breaks through bivalent interactions with

292 o all 53BP1 activities is its recruitment to double-strand breaks via the interaction of the tandem T

293 ed histone H2AX (gammaH2AX), a marker of DNA double-strand breaks, was increased in vitamin B12 deple

294 DNA double-strand breaks were determined in peripheral blood

295 DNA double-strand breaks were measured using anti-gamma-H2A.

296 at BMI1 is rapidly recruited to sites of DNA double strand breaks where it facilitates histone H2A ub

297 MRN binds DNA double-strand breaks, where it functions in repair and t

298 ulations are derived from programmed meiotic double strand breaks, which precede chromosomal crossove

299 in the DDR; ATM is engaged in the repair of double-strand breaks, while ATR deals mainly with single

300 s in fragile X syndrome, are also subject to double-strand breaks within the repetitive tract followe