ライフサイエンスコーパス: DNA break

1 e PARP-1 allostery to promote release from a DNA break.

2 gradation of the 5'-terminated strand of the DNA break.

3 mbination to repair the cleavage of a single DNA break.

4 ain rapidly unfolds when PARP-1 encounters a DNA break.

5 heir ability to trap PARP-1 at the site of a DNA break.

6 3' phosphate group on a single-stranded (ss)DNA break.

7 bitors drive allostery to retain PARP-1 on a DNA break.

8 signaling and accumulation of protein-linked DNA breaks.

9 to coordinate the repair of double-stranded DNA breaks.

10 le-stranded DNA lesions into double-stranded DNA breaks.

11 erates at low basal levels and is induced by DNA breaks.

12 erine 569 is required for its recruitment to DNA breaks.

13 required to recruit DNA repair complexes to DNA breaks.

14 A repair factors including 53BP and BRCA1 to DNA breaks.

15 topoisomerases and inducing double-stranded DNA breaks.

16 herefore plays a vital role in processing of DNA breaks.

17 rimentally induced telomeric double-stranded DNA breaks.

18 ction together to recruit PARP-2 to sites of DNA breaks.

19 stress caused by MMS and not to more direct DNA breaks.

20 lymerase Pol IV, overwhelms cells with toxic DNA breaks.

21 or pathway for the repair of double-stranded DNA breaks.

22 ricentromere to suppress crossovers, but not DNA breaks.

23 tions downstream of RAD18 to recruit REV1 to DNA breaks.

24 lications, and generation of double-stranded DNA breaks.

25 a cell lines, directly causing double-strand DNA breaks.

26 -out mice confirms an increase in unrepaired DNA breaks.

27 , is involved in the repair of double-strand DNA breaks.

28 f KP372-1 cause robust DNA damage, including DNA breaks.

29 factors organize to repair diverse types of DNA breaks.

30 in normal cells acts to repair double-strand DNA breaks.

31 51 homologous recombination repair factor at DNA breaks.

32 trand, leading to staggered instead of blunt DNA breaks.

33 guided nuclease that creates double-stranded DNA breaks.

34 topology by creating transient double-strand DNA breaks.

35 doses of agents that induce single-stranded DNA breaks.

36 (MRN) complex and other factors at sites of DNA breaks.

37 nce capture during repair of double-stranded DNA breaks.

38 d for the removal of DNA adducts at sites of DNA breaks.

39 e complexes (Top2cc), leading to Top2-linked DNA breaks.

40 nome maintenance by directing a remodeler to DNA breaks.

41 recombination and repair of double-stranded DNA breaks.

42 nucleoplasm and controls its accumulation at DNA breaks.

43 fect p53 function in response to physiologic DNA breaks.

44 A association at both telomeres and internal DNA breaks.

45 ion recruited RAD18 to ub-H2AX at HU-induced DNA breaks.

46 initial step in the repair of double-strand DNA breaks.

47 the PARP1-dependent recruitment of ZBTB24 to DNA breaks.

48 28 PIP mutant failed to suppress TRC-induced DNA breaks.

49 ops is associated with replication-dependent DNA breaks.

50 al basis for the function of CtIP at complex DNA breaks.

51 directed DNA repair (HDR) of double-stranded DNA breaks.

52 a cell lines, directly causing double strand DNA breaks.

53 istone H2AX, a known marker of double-strand DNA breaks.

54 MSH2-MSH6) proteins, and then processed into DNA breaks.

55 ternally derived and display double-stranded DNA breaks.

56 rdinates ATM activation with its exchange at DNA-breaks.

57 ignalling and repair factors to the sites of DNA breaks(2,11).

58 as non-self and introduces a double-stranded DNA break [3].

59 enotoxic molecule(s) causing double-stranded DNA breaks(4) and enhanced colorectal cancer development

60 h neurons has uncovered how sleep can repair DNA breaks accumulated during wake to maintain genome in

61 brogated PNKP activity results in persistent DNA break accumulation, preferentially in actively trans

62 Cipro-induced DNA breaks activate the Escherichia coli SOS DNA-damage

63 pendent recruitment of BRCA1 directly to the DNA break and is required for nonhomologous end-joining

64 tein A (RPA) to the RAD51 recombinase during DNA break and replication fork repair by homologous reco

65 ion mode: Ino80 deletion leads to unrepaired DNA breaks and apoptosis in symmetric NPC-NPC divisions,

66 lear entry by Dox, promoting double-stranded DNA breaks and apoptosis.

67 events replication fork collapse, a cause of DNA breaks and apoptosis.

68 down of ODC1, UC cells undergo double-strand DNA breaks and apoptosis.

69 study, we investigated topoisomerase-induced DNA breaks and chromatin structural alterations in conju

70 the formation of replication stress-induced DNA breaks and chromosomal aberrations in BRCA1/2-defici

71 Quantification of DNA breaks and clonogenic survival assays confirm a role

72 Here we report a significant role for DNA breaks and DDR signalling in the mechanisms of trans

73 tion of LINE-1 transcripts and double-strand DNA breaks and decreases viability in primary cultured u

74 DBAN is not mutagenic but causes DNA breaks and elevates sister chromatid exchange in mam

75 rrow hotspots, observed both at the level of DNA breaks and final crossovers.

76 ncies in unfolding GQ are known to result in DNA breaks and genomic instability, which are prominent

77 ng the loss of the endogenous centromere via DNA breaks and HP1-dependent epigenetic inactivation.

78 participates in the repair of double-strand DNA breaks and in base excision repair of oxidized guani

79 Moreover, meiotic DNA breaks and interhomolog crossovers preferentially fo

80 t not normal transcription complexes, induce DNA breaks and orientation-specific DNA damage responses

81 is involved in the repair of RAG1/2-mediated DNA breaks and prevents their propagation.

82 may indicate APOBEC3A-induced double-strand DNA breaks and pro-metastatic hypermutation.

83 Depletion of WRN induced double-stranded DNA breaks and promoted apoptosis and cell cycle arrest

84 s, such as for the repair of double-stranded DNA breaks and protein quality control, are also critica

85 se is involved in repairing damage caused by DNA breaks and stalled replication forks via homologous

86 h acts in both the repair of double-stranded DNA breaks and the degradation of bacteriophage DNA.

87 ality observed between topoisomerase-induced DNA breaks and the RecBCD gene products, suggesting a ne

88 ARG in coordinating the induction of meiotic DNA breaks and their homologous recombination-mediated r

89 -binding interface to detect and stably bind DNA breaks and to accumulate at sites of chromosome dama

90 single-strand DNA formation, RPA exhaustion, DNA breaks, and aberrant DNA repair intermediates.

91 to replication fork collapse, double-strand DNA breaks, and cell death.

92 g (NHEJ), causes accumulation of spontaneous DNA breaks, and delays recovery from radiation-induced c

93 s in the repair of single- and double-strand DNA breaks, and discusses the notion that the substrate

94 arcinoma NuMA prevents 53BP1 accumulation at DNA breaks, and high NuMA expression predicts better pat

95 orks, insufficient repair of double-stranded DNA breaks, and improper segregation of sister chromosom

96 can slow replication fork progression, cause DNA breaks, and increase mutagenesis.

97 hydrocarbon receptor, increase double-strand DNA breaks, and increase the expression of MMP-1, MMP-3,

98 ous recombination, repair of double stranded DNA breaks, and integron recombination.

99 zolid caused S-phase arrest, double-stranded DNA breaks, and p53 stabilization, leading to apoptosis.

100 study lends further support to a model where DNA breaks are generated by multiple random nicks due to

101 These DNA breaks are repaired by homologous recombination, whi

102 Double-strand DNA breaks are the most cytotoxic form of DNA damage and

103 In yeast, DNA breaks are usually repaired by homologous recombinat

104 display similar levels of alkylation-induced DNA breaks as wild type, PARP-1 activation is undetectab

105 double-stranded breaks using biotin-labeling DNA break assay, and End-seq analysis indicated that the

106 The creation of a DNA break at a specific locus by a designer endonuclease

107 ) is more active in creating double-stranded DNA breaks at 37 degrees C than at 22 degrees C, thus in

108 technologies introduce double-stranded (ds) DNA breaks at a target locus as the first step to gene c

109 te nuclease that generates two noncompatible DNA breaks at a target site, effectively deleting the ma

110 ive lymphomagenesis by generating off-target DNA breaks at loci that harbor highly active enhancers a

111 loping lymphocytes by generating "on-target" DNA breaks at matched pairs of bona fide recombination s

112 ily reprogrammed to induce sequence-specific DNA breaks at target loci, resulting in fixed mutations

113 (RAG) 1 and RAG2 protein complex introduces DNA breaks at Tcr and Ig gene segments that are required

114 in the frequencies of meiotic double-strand DNA breaks at the hotspot near the His4 locus, is found

115 Upon induction of DNA breaks, ATM activation leads to a cascade of local c

116 s were initially characterized as sensors of DNA breaks but are now known to play key roles not only

117 ion and reagents that induce double-stranded DNA breaks, but exhibit normal responses to chemicals th

118 ersists until sufficient modification of the DNA break by alternative NHEJ prevents further Cas9 cutt

119 role of BRCA1 in the repair of double-strand DNA breaks by homologous recombination (HR) is its best

120 n deficient in the repair of double-stranded DNA breaks by homologous recombination(8-13), and conseq

121 not required for the repair of double-strand DNA-breaks by homologous recombination.

122 at the expense of genome protection because DNA breaks cannot be repaired in dense heterochromatin.

123 ne marrow cells in response to double-strand DNA breaks caused by ionizing radiation and chemotherape

124 ore that histone eviction alone, rather than DNA breaks, contributes strongly to the overall cytotoxi

125 s limited as multiple nearby double-stranded DNA breaks created by Cas9 routinely result in the delet

126 olism; these lesions include double-stranded DNA breaks, daughter-strand gaps, and DNA cross-links.

127 and ATM-dependent responses to double-strand DNA breaks, demonstrate functional plasticity of introni

128 displayed significantly higher double-strand DNA break (DSB) accumulation and p53 activation than the

129 cell differentiation through double-stranded DNA break (DSB) and ASC-mediated inflammasome assembly i

130 int signalling at a persistent double-strand DNA break (DSB) and at uncapped telomeres.

131 uestions about the repair of a double-strand DNA break (DSB) concerns how the two free DNA ends are b

132 We focus on regulation of double-strand DNA break (DSB) repair via the non-homologous end joinin

133 h the role of DBHS proteins in double-strand DNA break (DSB) repair, elevated DSBs were observed in c

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

135 anization before and after a double-stranded DNA break (DSB), to estimate the level of chromatin deco

136 Recognition and repair of double-stranded DNA breaks (DSB) involves the targeted recruitment of BR

137 ctivator of ATM in response to double-strand DNA breaks (DSBs) and as a downstream effector of ATM ac

138 es, which respond primarily to double-strand DNA breaks (DSBs) and replication stress, respectively.

139 In mammalian cells, double-stranded DNA breaks (DSBs) are preferentially repaired through en

140 susceptible to formation of double-stranded DNA breaks (DSBs) arising from physiological and/or envi

141 Repair of double strand DNA breaks (DSBs) can result in gene disruption or gene

142 Double-strand DNA breaks (DSBs) continuously arise and cause mutations

143 inal centers (GCs) and IgH switch (S) region DNA breaks (DSBs) for class-switch recombination (CSR).

144 nomic sequences subjected to double-stranded DNA breaks (DSBs) made by programmable nucleases (e.g. C

145 it up to a 25-fold increase in double-strand DNA breaks (DSBs) throughout meiotic prophase I and a co

146 for recognizing and repairing double-strand DNA breaks (DSBs) via non-homologous end joining.

147 is activated in response to double stranded DNA breaks (DSBs) where it mono-ubiquitinates gammaH2AX

148 by the programmed induction of double-strand DNA breaks (DSBs), lesions that pose a potential threat

149 rmediates (TOP2ccs) that contain TOP2-linked DNA breaks (DSBs).

150 for the HMT MMSET in promoting AID-mediated DNA breaks during CSR.

151 on compete for the repair of double-stranded DNA breaks during the cell cycle.

152 ofactor and the generation of long staggered DNA breaks during transposition.

153 ion and avoids the creation of double-strand DNA breaks, enabling precise chromosome modifications at

154 e mutagenic potential of Lig3-mediated EJ by DNA break end protection involving p53 binding protein 1

155 zed role of the Dna2 translocase activity in DNA break end resection and in the imposition of the 5'

156 rand breaks by homologous recombination, the DNA break ends must first be processed into 3' single-st

157 In humans, Ku70/80 recognizes DNA broken ends and recruits the DNA-dependent protein k

158 ced DNA damage signaling and accumulation of DNA breaks ex vivo and in vivo.

159 cate both proteins as critical for repair of DNA breaks following transposase cleavage in vivo.

160 n both DNA strands to generate double-strand DNA breaks for efficient class switch recombination.

161 cterial cells, processing of double-stranded DNA breaks for repair by homologous recombination is cat

162 cterial cells, processing of double-stranded DNA breaks for repair by homologous recombination is dep

163 and report that simultaneous single-stranded DNA break formation at donor and acceptor DNA by CRISPR-

164 fork restart, prevention of double-stranded DNA break formation, and avoidance of replication catast

165 The Ctf19 complex prevents meiotic DNA break formation, the initiating event of recombinati

166 TMPRSS2 gene rearrangements occur at DNA breaks formed during androgen receptor-mediated tran

167 end-joining (NHEJ) repair of double-stranded DNA breaks generated by Cas9 are much less amenable to s

168 DNA breaks generated by topoisomerases are short-lived b

169 de that the pattern of mutation hotspots and DNA break generation is influenced by sequence-intrinsic

170 rovement in tumor cell damage (double strand DNA breaks), growth suppression, and overall survival un

171 cleaved complexes because of the presence of DNA breaks, have been crystallized and found to have the

172 ntinued to evaluate their capacity to induce DNA breaks, histone eviction, and relocated topoisomeras

173 donuclease-1), and repair of double-stranded DNA breaks (homologs of BRCA2, XRCC3, KU80 and WRNexo).

174 In both conditions, Holliday junctions at DNA break hotspots form more frequently between sister c

175 ng complex/cyclosome (APC/C), accumulates on DNA breaks in a BubR1 KEN box-dependent manner.

176 m and progenitor cells undergo very frequent DNA breaks in a very restricted set of genes involved in

177 urrence of RAG1/2-dependent and -independent DNA breaks in developing lymphocytes exposed to genotoxi

178 ibitor, whereas forced targeting of PALB2 to DNA breaks in mutant cells circumvents BRCA1 haploinsuff

179 to study the mechanistic impact of targeted DNA breaks in nearly any chromatin environment.

180 eplication origins and a higher frequency of DNA breaks in PSCs with incompletely reprogrammed DNA re

181 ssential factors for repair of single-strand DNA breaks in replication regions.

182 stent phosphorylation of H2AX-Y142 along the DNA breaks in stem cells, which promotes apoptosis while

183 ugh Cas9 efficiently induces double-stranded DNA breaks in the early embryo and male germline, these

184 can be reprogrammed to create double-strand DNA breaks in the genomes of a variety of organisms, fro

185 rogrammed to create specific double-stranded DNA breaks in the genomes of a variety of organisms, ran

186 loss results in progressive accumulation of DNA breaks in the nervous system, triggering hallmarks o

187 comprehensive chromosome end remodeling with DNA breaks in their subtelomeric regions and loss of dis

188 ad50 complex for the repair of double-strand DNA breaks in thermophilic archaea.

189 chromosome copy numbers is seen to increase DNA breaks in U2OS osteosarcoma cells without affecting

190 recruitment without affecting KU dynamics at DNA breaks in vivo.

191 s, we propose a model for M/R recognition at DNA breaks in which the Rad50 coiled coils aid movement

192 eting the Agouti locus induced site-directed DNA breaks in zygotes within 6 h of injection, an activi

193 that a RecQ helicase, RECQ2, acts to repair DNA breaks, including in the telomeric site of VSG expre

194 induced significant levels of single-strand DNA breaks, indicating a mechanism of action different f

195 absence, chromosomes mostly suffer one-ended DNA breaks, indicating disintegration of replication for

196 uivalent role at chromosomal double-stranded DNA breaks, indicating that tandem duplications form spe

197 sister chromatid exchanges and double strand DNA breaks, indicating the formation of mitotic recombin

198 A damage, including age-related DNA lesions, DNA breaks induced by several agents (bleomycin, doxorub

199 Here, we demonstrate that single-strand DNA breaks induced by the L1 endonuclease trigger the re

200 fragments that subsequently reintegrate into DNA breaks induced on a heterologous chromosome.

201 We show here that SSEs can spread via DNA break-induced homologous recombination, a process kn

202 Here we show that, upon DNA break induction, the budding yeast SUMO ligase Siz2

203 epair pathways in resolving nuclease-induced DNA breaks into genome editing outcomes, we previously d

204 Here we introduced double-stranded DNA breaks into the nuclear genome of tobacco through in

205 ays following the introduction of a targeted DNA break is essential to further advance the safety and

206 Resection of DNA breaks is impaired when either Sae2 activity is bloc

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

208 Histone ubiquitination at DNA breaks is required for activation of the DNA damage

209 t recruitment of BRCA1 to chromatin flanking DNA breaks is required for BRCA1 phosphorylation at seri

210 1-dependent, TOP2beta-mediated double-strand DNA breaks is required for efficient GR-stimulated trans

211 ectasia mutated (ATM), a kinase activated by DNA breaks, is a hallmark of the HCMV-induced DDR.

212 e activity generates aberrant protein-linked DNA breaks, jeopardising genome stability.

213 on through mitosis following double-stranded DNA breaks leads to the formation of micronuclei, which

214 iation induces more single and double strand DNA breaks, less H2AX phosphorylation, increased Chk2 ph

215 Using genome-wide DNA break mapping/sequencing techniques at single-nucleo

216 istone 3 lysine 9 (H3K9) at loci surrounding DNA breaks, masking a local H3K9 trimethylation signal t

217 However, DNA breaks may engage one of several competing repair pa

218 system couples a site-specific double-strand DNA break mediated by two Cas9 ribonucleoproteins with m

219 pairs were designed to induce double-strand DNA break near the starting codon of each gene that eith

220 redominant binding of PARP1 to single-strand DNA breaks, occluding its Erk binding sites, suppressed

221 viability following an induced double-strand DNA break, of a magnitude comparable with the defect mea

222 fragility and suggests potential impacts of DNA breaks on neurodevelopment and neural functions.

223 uces the DNA damage response without causing DNA breaks or allowing cellular dormancy.

224 The complexes failed to induce double-strand DNA breaks or DNA cross-linking but induced significant

225 oes not require formation of double-stranded DNA breaks or provision of a donor DNA template.

226 an be used to simultaneously create multiple DNA breaks or to target multiple transcriptional activat

227 I (TDP1); a key TOP1-mediated protein-linked DNA break (PDB) repair enzyme.

228 on DNA, generating cytotoxic protein-linked DNA breaks (PDBs).

229 uid component controls the rate of repair of DNA breaks per unit volume by repair factors, which are

230 rylation of EXO1 augments its recruitment to DNA breaks possibly via interactions with BRCA1.

231 Following its phosphorylation by ATM at DNA breaks, "primed" PIDD relocates to kinetochores via

232 '-phosphatase activities to modify ends of a DNA break prior to ligation.

233 Our results demonstrate that Cas9-induced DNA breaks promote efficient rearrangement between pairs

234 s TIP60-dependent mobilization of 53BP1 from DNA breaks, promoting HR.

235 DNA breaks recruit and activate PARP1/2, which deposit p

236 opose that DNA damage-elicited double-strand DNA breaks releases DNA fragments, which may either acti

237 of XRCC5/6 that is not directly involved in DNA break repair (NHEJ).

238 nation-mediated genetic engineering), single DNA break repair (SDBR, introduced by W.

239 vated levels of Mdmx-inhibited double-strand DNA break repair and induced chromosome and chromatid br

240 However, the interplay between DNA break repair and transcription processivity is uncle

241 gastric cancers have defective double-strand DNA break repair by homologous recombination and may ben

242 was associated with failure of double-strand DNA break repair by homologous recombination based on it

243 We have therefore probed DNA break repair containing a template 8-oxo-7,8-dihydro

244 arrangements, revealing an important role of DNA break repair pathway choice in the preservation of g

245 XRCC1) are key proteins in the single-strand DNA break repair pathway.

246 DNA break repair via homology-based mechanisms involves

247 ein kinase (DNA-PK) mediates double-stranded DNA break repair, V(D)J recombination and immunoglobulin

248 into nuclear genomes through double-stranded DNA break repair.

249 hese proteins in DNA replication rather than DNA break repair.

250 by the RAD51 recombinase enables error-free DNA break repair.

251 e/nuclease that functions in double-stranded DNA break repair.

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

253 ing of DNA ends is coordinated to facilitate DNA break repair.

254 eral-stress response, which allows mutagenic DNA-break repair.

255 n machine essential for the major pathway of DNA break-repair and recombination.

256 g the DSB, whereas BRCA1 binding directly to DNA breaks requires Nijmegen breakage syndrome 1 (NBS1).

257 valyl-tRNA synthetase (ValRS(ED)) activated DNA break-responsive H2AX and p53-responsive downstream

258 th topoisomerase I-generated single-stranded DNA breaks resulted in the generation of persistent doub

259 The double-strand DNA breaks resulting from replication fork collapse were

260 ISPRi/a, which do not induce double-stranded DNA breaks, revealed that a distinct set of off-targets

261 DNA breaks sharply elevate PARP-1 catalytic activity to

262 edicts the extent to which a double-stranded DNA break site will utilize the microhomology-mediated r

263 tranded oligonucleotide donor (ssODN) at the DNA break site.

264 imulates further chromatin relaxation around DNA break sites and brings in HDAC1/2 for localized chro

265 th resulted from the recruitment of 53BP1 to DNA break sites and inhibition of DNA end resection.

266 importance for normal retention of RAD51 at DNA break sites and regulation of HR.

267 ment module for the localization of 53BP1 to DNA break sites.

268 Both ROS-induced single- and double-strand DNA breaks (SSBs and DSBs) contribute to R-loop inductio

269 lesions, such as single- and double-stranded DNA breaks (SSBs and DSBs), and single-stranded gaps can

270 n situ detection of single- or double-strand DNA breaks (sSTRIDE or dSTRIDE), in nuclei of single cel

271 ology-directed repair that repairs one-ended DNA breaks, such as those formed at broken replication f

272 sensitivity and specificity of detection of DNA breaks than the commonly used terminal deoxynucleoti

273 ons differ in the density of double-stranded DNA breaks that are generated.

274 CRISPR/Cas9 causes double-stranded DNA breaks that can undergo DNA repair either via non-ho

275 It is suggested that for double-strand DNA breaks that have initially formed a complex with PAR

276 er chromatids bearing targeted double strand DNA breaks that is entirely uncoupled from its requisite

277 was observed, due to increased single-strand DNA breaks that likely occur due to heterodimers consist

278 amage, whole-chromosome aneuploidies lead to DNA breaks that persist into mitosis.

279 tidine deaminase protein induces genome-wide DNA breaks that, if not repaired through RAD51-mediated

280 h fluoroquinolones stabilize double-stranded DNA breaks, the antibacterial thiophenes stabilize gyras

281 endent assembly of the LIG4/XRCC4 complex at DNA breaks, thereby promoting error-free NHEJ.

282 mary mesenchymal stem cells (MSCs) increases DNA breaks throughout the nucleoplasm as assessed by end

283 iquitin-mediated degradation and to minimize DNA breaks, thus providing insights into the SUMO and ub

284 es in PARP2 that signal the recognition of a DNA break to the catalytic domain, which licenses HPF1 b

285 bp) to dimerise and produce a double-strand DNA break using just two strand-cleavage events.

286 AIRE has been shown to promote DNA breaks via its interaction with topoisomerase 2 (TOP

287 the generation of persistent double-stranded DNA breaks was found to be a primary cause of heat stres

288 Inhibition of DNA repair and accumulation of DNA breaks was functionally confirmed by the presence of

289 by staggered but not blunt, double-stranded DNA breaks was impaired by SAMHD1 depletion, which was a

290 preferentially integrates into double-strand DNA breaks, we adapted a CRISPR/Cas9 system to demonstra

291 echanisms underpinning topoisomerase-induced DNA breaks, we map Top2 DNA cleavage with strand-specifi

292 nblock significantly reduced double-stranded DNA breaks when compared with a commercial sunscreen for

293 e per unit volume due to naturally occurring DNA breaks, whereas the volume fraction of the fluid com

294 independent of Cas9-induced double-stranded DNA breaks (which causes substantial indel formation) an

295 ing apoptotic cell death via double-stranded DNA breaks while causing a remodeling of the tumor micro

296 3A itself is highly proficient at generating DNA breaks, whose repair can trigger the formation of si

297 G9a and GLP1 rapidly localizes to DNA breaks, with GLP1 localization being dependent on G9

298 al HDR factors, is substantially impaired at DNA breaks, with reduced end resection and diminished re

299 ar mechanism by which PARP enzymes recognize DNA breaks within chromatin, we determined the cryo-elec

300 Repairing DNA breaks within the complexity of the cell chromatin i