ライフサイエンスコーパス: DSB

1 DSB repair occurs in the context of chromatin, and multi

2 DSB unwinding by AdnAB in vitro is stringently dependent

3 DSB-ddPCR demonstrates time-resolved, highly quantitativ

4 DSBs are continuously formed throughout interphase, are

5 DSBs elicit a cascade of events controlled by the ubiqui

6 t the interplay between these complexes at a DSB remains unclear.

7 Among over 100 novel proteins enriched at a DSB were the phosphatase Sit4, the RNA pol II degradatio

8 tand this, we targeted bacterial Ku (bKu), a DSB binding protein, to the mitochondria of rho+ cells w

9 eplication, typically, is not initiated by a DSB.

10 In addition, DSB-induced nuclear enrichment or chromatin association

11 ctivation of the DNA damage checkpoint after DSB repair.

12 First, after DSB formation, Mer2 is required for pairing by mediating

13 y the ubiquitin-proteasome system soon after DSB induction in human cells.

14 into how PD-L1 expression is regulated after DSBs.

15 water-soluble distyrylbenzene-bis-aldehyde (DSB-3), and provided strong discrimination against the p

16 t the cell cycle and accounts for nearly all DSB repair outside of the S and G2 phases.

17 Rec10 is required for essentially all DSBs and recombination, and three others (Rec25, Rec27,

18 tone modification, chromatin remodelling and DSB-repair via HRR; effectively phenocopying loss of TIP

19 ow that Cdc14 promotes spindle stability and DSB-SPB tethering during DNA repair, and imply that meta

20 ntly, increased cellular load of R-loops and DSBs, which are normalized on RNaseH1-mediated suppressi

21 ation leads to decreased AID recruitment and DSBs at the upstream donor Smu region.

22 le- and double-stranded DNA breaks (SSBs and DSBs), and single-stranded gaps can block progression of

23 n increases 53BP1 and RIF1 colocalization at DSBs, which inhibits BRCA1 recruitment, and sensitizes c

24 assembly of PALB2-containing HR complexes at DSBs.

25 bromodomains to H4Ac, which is generated at DSBs by the Tip60/KAT5 acetyltransferase.

26 lly, PAXX promotes the accumulation of KU at DSBs, while XLF enhances LIG4 recruitment without affect

27 of TLC1 RNA depends on Cdc13 localization at DSBs and on the SUMO ligase Siz1, which is required for

28 Polmu to randomly incorporate nucleotides at DSBs.

29 deficiency reduces histone ubiquitination at DSBs, decreasing the recruitment of 53BP1, and decreases

30 terference influences the population-average DSB landscape but also demonstrate that locally inhibito

31 if1 activity defines a dividing line between DSBs and telomeres.

32 points to an intricate relationship between DSBs and transcription.

33 ein determinants of DSB hotspots - they bind DSB hotspots with high specificity and are required for

34 NA double-strand break (DSB) sites, blocking DSB repair, which led to DSB accumulation, DNA damage re

35 efore and after a double-stranded DNA break (DSB), to estimate the level of chromatin decompaction.

36 sive resection of a DNA double-strand break (DSB) by a multisubunit helicase-nuclease machine (e.g. R

37 ith repair of a defined double-strand break (DSB) by the synthesis-dependent strand-annealing (SDSA)

38 lating cessation of DNA double-strand break (DSB) formation following crossover designation, and ensu

39 After DNA double-strand break (DSB) generation, Cdc14 is transiently released from the

40 A DNA double-strand break (DSB) is the most critical type of genotoxic stress, but

41 HR pathway to complete double-strand break (DSB) repair by about 50%.

42 ci, suggesting that DNA double-strand break (DSB) repair by homologous recombination (HR) was comprom

43 thway choice within DNA double-strand break (DSB) repair is a tightly regulated process to maintain g

44 the most prominent DNA double strand break (DSB) repair pathway in mammalian cells.

45 mbination (HR) is a DNA double-strand break (DSB) repair pathway that protects the genome from chromo

46 HEJ) is the predominant double-strand break (DSB) repair pathway throughout the cell cycle and accoun

47 competition from other double-strand break (DSB) repair pathways, including non-homologous end-joini

48 pression of several DNA double-strand break (DSB) repair proteins and formation of repair complexes,

49 Improper DNA double-strand break (DSB) repair results in complex genomic rearrangements (C

50 r-prone pathway for DNA double-strand break (DSB) repair, is implicated in genomic rearrangement and

51 mbination (HR)-mediated double-strand break (DSB) repair, which is mediated through its ability to me

52 he progerin-induced DNA double-strand break (DSB) sites, blocking DSB repair, which led to DSB accumu

53 mechanical processes of double-strand break (DSB)-repair, especially the auxiliary factor(s) that can

54 locus containing a DNA double-strand break (DSB).

55 f contrast agent on DNA double-strand-break (DSB) formation in patients undergoing magnetic resonance

56 plex was recruited to double-stranded break (DSB) sites in response to etoposide treatment.

57 as been reported that double-stranded break (DSB)-induced small RNAs (diRNAs) are generated via the R

58 lyzes excision through double strand breaks (DSB) and the joining of newly excised transposon ends wi

59 ncluding 53BP1, to DNA double-strand breaks (DSB) and undergoes dynamic acetylation during DSB repair

60 DNA double-strand breaks (DSB) elicit a ubiquitylation cascade that controls DNA r

61 ity in the form of DNA double strand breaks (DSB) in cancer cells that lack the tumor suppressor gene

62 ustering the yields of double-strand breaks (DSB) increase, up to saturation around 300 keV/mum.

63 NA lesions (OCDL), DNA double-strand breaks (DSB), apoptosis, and the local and systemic immune respo

64 e of single-strand and double-strand breaks (DSB).

65 digital PCR assay for double-strand breaks (DSB-ddPCR) to investigate the kinetics of Cas9-mediated

66 g of induced nuclear double-stranded breaks (DSB) but the resulting nuclear integrants are often imme

67 en species-induced DNA double-strand breaks (DSBs) and were modestly sensitive to poly-ADP-ribose pol

68 y chosen to repair DNA double-strand breaks (DSBs) are critically influenced by the nucleosome packag

69 DNA double strand breaks (DSBs) are generally repaired through nonhomologous end j

70 DNA double-strand breaks (DSBs) are mainly repaired either by homologous recombina

71 pes of DNA damage, DNA double-strand breaks (DSBs) are probably the most deleterious.

72 bset of programmed DNA double-strand breaks (DSBs) are repaired as crossovers, with the remainder bec

73 Double-strand breaks (DSBs) are repaired through two major pathways, homology-

74 9, which generates DNA double-strand breaks (DSBs) at target loci, is a powerful tool for editing gen

75 d in the repair of DNA double-strand breaks (DSBs) by homologous recombination (HR), the molecular me

76 epair of SPO11-induced double-strand breaks (DSBs) by homologous recombination.

77 g the formation of DNA double-strand breaks (DSBs) by the Spo11 endonuclease early in prophase I, at

78 ical evidence that DNA double-strand breaks (DSBs) can be directly generated by Top1 at sites of geno

79 pair efficiency of DNA double-strand breaks (DSBs) caused by exposure to gamma radiation across archa

80 Double-strand breaks (DSBs) in DNA are recognized by the Ku70/80 heterodimer a

81 etection and repair of double-strand breaks (DSBs) in DNA, although detail concerning how Kaposi's sa

82 g (c-NHEJ) repairs DNA double-strand breaks (DSBs) in G1 cells with biphasic kinetics.

83 repair pathway for DNA double strand breaks (DSBs) in humans.

84 ied in response to DNA double strand breaks (DSBs) in vivo by the ARTs Adprt1a and Adprt2.

85 In pre-B cells, DNA double-strand breaks (DSBs) induced at Igkappa loci by the Rag1/Rag2 (RAG) end

86 d genome stability.DNA double-strand breaks (DSBs) induced by topoisomerase II (TOP2) are rejoined by

87 lytic resection of DNA double-strand breaks (DSBs) is essential for both checkpoint activation and ho

88 Repair of DNA double strand breaks (DSBs) is key for maintenance of genome integrity.

89 Repairing double-strand breaks (DSBs) is particularly challenging in pericentromeric het

90 are vulnerable to DNA double strand breaks (DSBs) mediated by topoisomerase 2B (TOP2B).

91 DNA double-strand breaks (DSBs) occurring within fragile zones of less than 200 ba

92 Resection of double-strand breaks (DSBs) plays a critical role in their detection and appro

93 DNA double-strand breaks (DSBs) prevent cells from entering mitosis allowing cells

94 Double strand breaks (DSBs) represent highly deleterious DNA damage and need t

95 helps recruit BRCA1 to double-strand breaks (DSBs) through the scaffold protein CCDC98 (Abraxas) and

96 End resection of DNA double-strand breaks (DSBs) to generate 3'-single-stranded DNA facilitates DSB

97 combination-initiating double-strand breaks (DSBs) via a feedback loop triggered by crossover designa

98 DNA double-strand breaks (DSBs) were assessed by immunofluorescence analysis of 53

99 of which leads to DNA double-strand breaks (DSBs) within IgH switch (S) regions.

100 s a main source of DNA double-strand breaks (DSBs), one of the most toxic forms of DNA damage.

101 ensitizes cells to DNA double strand breaks (DSBs), suggesting defects in DNA repair.

102 rmation of meiotic DNA double-strand breaks (DSBs), the precursors of cross-overs.

103 different chromosomal double-strand breaks (DSBs).

104 ly on Cas9-induced DNA double-strand breaks (DSBs).

105 echanism to repair DNA double-strand breaks (DSBs).

106 ependent repair of DNA double-strand breaks (DSBs).

107 ' end resection at DNA double-strand breaks (DSBs).

108 RAD51 loading to DNA double-stranded breaks (DSBs) and stalled replication forks, enabling two distin

109 amination of how DNA double-stranded breaks (DSBs) are repaired, with many components of the ubiquiti

110 ent that induces DNA double-stranded breaks (DSBs) does not affect the interaction between DDB2 and X

111 gh the generation of double stranded breaks (DSBs) in murine macrophage genomic DNA.

112 l therapies, as unwanted mutations caused by DSBs can have deleterious effects.

113 suggest that resection of blocked and clean DSBs is initiated via distinct mechanisms.

114 se directly initiates the resection of clean DSBs by cleaving the 5' strand DNA approximately 10-20 n

115 Also individual DSB tend to cluster; DSB clusters peak around 500 keV/mum, while DSB multipli

116 ed both NHEJ and HR and severely compromised DSB repair resulting in chromosomal instability.

117 sts that multiple mechanisms of conservative DSB repair may contribute to tumor suppression in human

118 e demonstrate that HR repair of conventional DSBs is severely compromised in DEK-deficient cells.

119 diated by the Mre11 complex and HR-dependent DSB repair.

120 sm of how Rad52 contributes to RNA-dependent DSB repair remained unknown.

121 vide evidence indicating that Tel1-dependent DSB interference influences the population-average DSB l

122 able strand exchange of crossover-designated DSBs.

123 ormal oscillatory SPB movements that disrupt DSB-SPB interactions.

124 bs1 (MRN) and Ku70-Ku80 (Ku) direct distinct DSB repair pathways, but the interplay between these com

125 eling complex in the repair of a defined DNA DSB.

126 s can be produced by a single engineered DNA DSB in H2ax knockout cells, and that the production of t

127 fined the function of this cross-talk in DNA DSB repair.

128 air, suggesting that Wwox contributes to DNA DSB repair pathway choice.

129 Furthermore, And-1 is recruited to DNA DSB sites in a manner dependent on MDC1, BRCA1 and ATM,

130 Thus, genomic DNA DSBs act as signaling intermediates in murine macrophage

131 f the three major pathways known to mend DNA DSBs, namely homologous recombination (HR), nonhomologou

132 To analyze the level of DNA DSBs, peripheral blood mononuclear cells were isolated f

133 with Ub, using the cellular response to DNA DSBs as the primary setting to compare these modificatio

134 SB) and undergoes dynamic acetylation during DSB repair.

135 t these pathways normally collaborate during DSB repair.

136 f PRMT5-mediated arginine methylation during DSB repair pathway choice through its ability to regulat

137 ly BLISS to profile endogenous and exogenous DSBs in low-input samples of cancer cells, embryonic ste

138 generate 3'-single-stranded DNA facilitates DSB repair via error-free homologous recombination (HR)

139 vironment surrounding DSBs which facilitates DSB repair and which is framed by extensive ZMYND8 domai

140 y immunofluorescence analysis of 53BP1 foci; DSB levels were determined by neutral comet assay; weste

141 ADP-ribosylation is also apparent following DSBs in vivo, by generating a strain with mutations at E

142 though tumor suppressor CtIP is critical for DSB end resection, a key initial event of HR repair, the

143 a high level of diRNAs is not necessary for DSB repair.

144 erved NHEJ to be the predominant pathway for DSB repair in our assay, MMEJ was significantly enhanced

145 s with high specificity and are required for DSB formation there.

146 NA damage response (DDR) and is required for DSB repair by homologous recombination (HR).

147 Yra1 and Def1 were required for DSB repair per se, while Sit4 was required for rapid ina

148 s work provides a comprehensive resource for DSB-free gene disruption by iSTOP.

149 The mislocalization of RAD51 away from DSBs in cells expressing HPV E6 and E7 hinders HR throug

150 on, which facilities 53BP1 displacement from DSBs.

151 king chromosomes less permissive for further DSB formation.

152 precise gene editing that does not generate DSBs.

153 be investigated at precisely mapped genomic DSBs is essential to study this relationship.

154 ction, and decreased HR repair in the DR-GFP DSB repair model.

155 sDNA), which serves as the template to guide DSB repair.

156 recombination (HR) repair of heterochromatic DSBs relies on the relocalization of DSBs to the nuclear

157 However, DSBs, which are the most deleterious type of DNA damage,

158 under most irradiation conditions; however, DSBs were elevated only after exposure to lower doses.

159 Furthermore, reduced OFD1 impaired DSB repair via homologous recombination repair (HRR).

160 This role of ASF1a in DSB repair cannot be provided by the closely related ASF

161 s, Tel1 absence causes widespread changes in DSB distributions across large chromosomal domains.

162 eat, which we show here to cause a defect in DSB repair in yeast.

163 ts that NMD pathway mutants are defective in DSB repair.

164 ate that ruxolitinib-induced deficiencies in DSB repair pathways sensitized MPN cells to synthetic le

165 n machinery now identified as key factors in DSB repair.

166 cted DNA methylation pathway and function in DSB repair in Arabidposis.

167 r Advanced Glycation End-products (nRAGE) in DSB-repair.

168 ment to DSBs, indicating that MLH1's role in DSB response/repair is important for suppressing TSI.

169 are prone to nuclease cleavage, resulting in DSBs.

170 It also facilitates a Ku-independent DSB repair, which favours intra-S region recombination a

171 Also individual DSB tend to cluster; DSB clusters peak around 500 keV/mu

172 itivity to bleomycin, a drug known to induce DSBs, further supports that NMD pathway mutants are defe

173 g Beclin 1 improved the repair of IR-induced DSB, but did not restore an autophagy response in cells

174 tribute to optimal resolution of AID-induced DSBs.

175 contribution to repair of radiation-induced DSBs has not been characterized.

176 ntaneously and in response to I-SceI-induced DSBs.

177 detected from CRISPR/Cas9- or TALEN-induced DSBs within the examined endogenous genes in Arabidopsis

178 a highlight the threat posed by TOP2-induced DSBs during transcription and demonstrate the importance

179 ak-induced replication in which the invading DSB end and its donor template share a 108-base-pair hom

180 to 8 are deleted in a switching B cell line, DSB formation is severely reduced and CSR frequency is i

181 ologous end joining (NHEJ) are the two major DSB repair pathways that are highly conserved from yeast

182 und-Thomson Syndrome, promotes the two major DSB repair pathways, non-homologous end joining (NHEJ) a

183 Preferential targeting of AID-mediated DSBs to S sequences is critical for allowing diversifica

184 ovokes increased R-loops and R-loop-mediated DSBs in TH1 cells relative to TH2 cells.

185 nome coined "hot spots." In mammals, meiotic DSB site selection is directed in part by sequence-speci

186 elated SCs of other species regulate meiotic DSB formation to form crossovers crucial for meiosis.

187 ed chromosomes, suggesting that many meiotic DSBs are normally repaired by intersister recombination

188 DNA repair pathways that essentially monitor DSB repair defects.

189 gh recruitment of the MRE11-RAD50-NBS1 (MRN) DSB-sensing complex to viral genomes and activation of t

190 is that bKu would bind persistently to mtDNA DSBs, thereby preventing mtDNA replication or repair.

191 GRs that originated from naturally occurring DSBs at (GAA)n microsatellites in Saccharomyces cerevisi

192 owever, illustrating homeostatic behavior of DSB regulatory systems.

193 11-oligonucleotide complexes, a byproduct of DSB formation, to reveal aspects of the contribution of

194 with conserved roles for Tel1 in control of DSB number and processing.

195 ec27, and Mug20) are protein determinants of DSB hotspots - they bind DSB hotspots with high specific

196 ysis of gammaH2AX foci showed no evidence of DSB induction after MR examination, independent of the a

197 Thus, our findings reveal the involvement of DSB repair in PD-L1 expression and provide mechanistic i

198 of genotoxic stress, but the involvement of DSB repair in PD-L1 expression has not been investigated

199 prehensive assessment of the localization of DSB repair proteins during KSHV replication, we have det

200 may allow the virus to evade localization of DSB repair proteins that would otherwise have a detrimen

201 us important insights into the mechanisms of DSB repair leading to CGRs.

202 53BP1 is a key regulator of DSB repair pathway choice in eukaryotic cells and functi

203 dy identifies nRAGE as a master regulator of DSB-repair, the absence of which orchestrates persistent

204 y decreased the IGF-1-mediated resolution of DSB.

205 The introduction of DSBs is initiated by activation-induced cytidine deamina

206 her IgH germline transcription or joining of DSBs within S regions by classical nonhomologous end joi

207 uring the following: (1) direct labelling of DSBs in fixed cells or tissue sections on a solid surfac

208 regation of chromosomes, but the majority of DSBs are processed toward a safer alternative, namely no

209 ly quantitative, and targeted measurement of DSBs.

210 In the presence of DSBs, TLC1 RNA remains nucleolar in most G2/M cells but

211 n vitro transcription; (3) quantification of DSBs through unique molecular identifiers; and (4) easy

212 romatic DSBs relies on the relocalization of DSBs to the nuclear periphery before Rad51 recruitment.

213 ired transcriptional silencing and repair of DSBs by homologous recombination.

214 propose a mechanism for iterative repair of DSBs by NHEJ.

215 cs of Cas9-mediated generation and repair of DSBs in cells.

216 genome by blocking the homologous repair of DSBs.

217 quired for efficient long-range resection of DSBs.

218 racts with MDC1 and is recruited to sites of DSBs to facilitate the interaction of phospho-ATM with M

219 n many possible junctional outcomes from one DSB.

220 the absence of which orchestrates persistent DSB signaling to senescence, tissue-fibrosis and oncogen

221 ized away from both transient and persistent DSBs, whereas HPV E7 is only capable of impairing RAD51

222 n compromised HR and misrejoining of S-phase DSBs, and increased the sensitivity to DNA-damaging agen

223 ed several phosphatase subunits as potential DSB-associated proteins.

224 n of Rag1 and Rag2 expression is a prevalent DSB response among immature lymphocytes.

225 However, how HR-deficient cells process DSBs is not clear.

226 We conclude that AdnAB's processive DSB unwinding activity suffices for AdnAB function in HR

227 of oocytes containing a synapsis-proficient, DSB repair-defective mutation in a gene (Trip13) require

228 We previously reported that RAG DSBs induced at one Igkappa allele signal through the at

229 X-ray-induced strand breaks, to recapitulate DSB repair via MMEJ or nonhomologous end-joining (NHEJ).

230 Down-regulation of BCCIP reduces DSB repair and disrupts BRCA2 and RAD51 foci formation.

231 petes with Ku70/Ku86 for binding to S-region DSB ends.

232 Atg7, suggesting that Beclin 1 may regulate DSB repair independent of autophagy in the cells exposed

233 f200 (Arid2) PBAF-defining subunit regulates DSB repair.

234 and is essential for HR repair by regulating DSB end resection.

235 shed that Polmu is the one adapted to repair DSBs with non-complementary ends, the most challenging s

236 h multiple enzymes at its disposal to repair DSBs, resulting in a diversity of repair outcomes.

237 o operate within damaged chromatin to repair DSBs.

238 Further, RAD51D-deficiency shifted DSB repair toward highly deleterious single-strand annea

239 segments associated with a meiosis-specific DSB site.

240 rich motifs associated with meiosis-specific DSBs fold into intramolecular G-quadruplex and i-motif s

241 romosomal segments surrounding site-specific DSBs at an exceptionally high frequency.

242 rming gammaH2AX immunofluorescence staining, DSBs were quantified with automated digital microscopy.

243 eric RNA:DNA hybrids, telomeric/subtelomeric DSBs and VSG switching frequency back to WT levels.

244 damage foci that Wwox expression suppresses DSB repair at the end-resection step of HDR.

245 restricted chromatin environment surrounding DSBs which facilitates DSB repair and which is framed by

246 equirement by linear amplification of tagged DSBs by in vitro transcription; (3) quantification of DS

247 nge plays an important role in RNA-templated DSB repair in vivo.

248 Therefore, this study provides evidence that DSB-mediated replication is the predominant form of mtDN

249 We also observed that DSB-induced H4K16 acetylation was abolished in cells upo

250 Finally, we demonstrate that DSBs induced in pre-B cells by etoposide or bleomycin in

251 In this article, we show that DSBs induced by ionizing radiation, etoposide, or bleomy

252 We show that DSBs repaired with slow kinetics, including those locali

253 Our results suggest that DSBs are necessary but not sufficient for efficient diRN

254 resection requires Exo1 exonuclease and the DSB-responsive kinase Tel1, but not Sgs1 helicase.

255 gions or harboring additional lesions at the DSB site, undergo resection prior to repair by c-NHEJ an

256 kedly lower indel frequency than that by the DSB-mediated approach.

257 flanking chromatin, but is excluded from the DSB region.

258 iencies and hyper-resection 0.15 kb from the DSB that was dependent on the nuclease activity of Dna2-

259 kinase activity and on the distance from the DSB.

260 patient cells have pronounced defects in the DSB-induced histone modification, chromatin remodelling

261 on enhancer, which tethers HMLalpha near the DSB.

262 In the process, the DSB forms hairpin intermediates on the flanking DNA side

263 the eviction of nucleosomes surrounding the DSB.

264 gly polar, favouring correction close to the DSB end.

265 panied by impaired recruitment of MRX to the DSB, and other functions of MRX in HR including the recr

266 OFD1 loss also adversely impacted upon the DSB-induced G2-M checkpoint, inducing a hypersensitive a

267 However, when the DSB end contains a 3' protruding nonhomologous tail, Msh

268 modulating the cell cycle stage at which the DSB was induced, we were able to avoid mosaicism in clea

269 e map genome-wide and at high resolution the DSBs induced by a restriction enzyme, and we characteriz

270 d the chromatin architecture surrounding the DSBs.

271 h viral oncogenes were shown to disrupt this DSB repair pathway.

272 hanism regulating the recruitment of CtIP to DSB sites remains largely unknown.

273 SB) sites, blocking DSB repair, which led to DSB accumulation, DNA damage responses, and early replic

274 or cancers susceptible to radiotherapy or to DSB-inducing chemotherapy.

275 s BRCA1 recruitment, and sensitizes cells to DSBs from IR or stalled replication forks that require H

276 Notably, artificial targeting of Fun30 to DSBs is sufficient to bypass the cell cycle regulation o

277 ) disrupt BRCA1-independent RAD51 loading to DSBs and stalled forks in PARPi-resistant BRCA1-deficien

278 In this study, the XPA mislocalization to DSBs occurred at stalled or collapsed replication forks,

279 the bromodomain protein BRD2 is recruited to DSBs.

280 pression of TSI requires MLH1 recruitment to DSBs, indicating that MLH1's role in DSB response/repair

281 RECQL4 interaction and RECQL4 recruitment to DSBs.

282 Little is known about the response to DSBs once cells have already committed to mitosis.

283 d DNA end resection and cellular response to DSBs.

284 ases NHEJ, rendering cells more sensitive to DSBs.

285 dings suggest that translocation of TRADD to DSBs into the nucleus contributes to cell survival in re

286 ere, we used CRISPR/Cas9- or TALEN-triggered DSBs to characterize diRNAs in Arabidopsis and rice.

287 arrangement that is formed by EJ between two DSBs induced by the Cas9 endonuclease.

288 n remodelling during resection is underlying DSB repair pathway choice.

289 to eliminate meiocytes containing unrepaired DSBs or unsynapsed chromosomes.

290 calizes with chromatin bound BRCA2, and upon DSB induction, RAD51 colocalizes with BRCA2-BCCIP foci.

291 pathway choice and resection regulation upon DSB formation.

292 d H4K16ac in cells after exposure to various DSB-inducing agents, including neocarzinostatin, gamma r

293 When DSBs are repaired by homologous recombination, DNA ends

294 Results Whereas DSBs in lymphocytes increased after CT exposure (before

295 DSB clusters peak around 500 keV/mum, while DSB multiplicities per cluster steadily increase with LE

296 nucleotide loss or addition, explaining why DSBs repaired by NHEJ are rarely restored to their origi

297 emonstrates that Tel1 shapes the genome-wide DSB landscape in unexpected ways.

298 ates in the nucleoplasm and colocalizes with DSBs in rad52Delta cells, leading to de novo telomere ad

299 ties with mechanisms in yeast that deal with DSBs in distinct sites that are difficult to repair, inc

300 CAG, CGA, and TGG) into STOP codons without DSB formation.