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1 entral mediator of response for cellular DNA double-strand break.
2 how the second strand is cut to complete the double-strand break.
3 al carcinogen Helicobacter pylori causes DNA double strand breaks.
4 ic survival, and increases resolution of DNA double strand breaks.
5 d break repair by promoting 53BP1 binding to double-strand breaks.
6 of DNA damage, such as bulky lesions and DNA double-strand breaks.
7 s or to produce 3' overhangs at telomeres or double-strand breaks.
8 for processing a subset of pathological DNA double-strand breaks.
9 Radiation kills cancer cells by inducing DNA double-strand breaks.
10 ons in genomic target sites without inducing double-strand breaks.
11 ng in replication from fewer origins and DNA double-strand breaks.
12 ads to replication fork regression and mtDNA double-strand breaks.
13 nsively characterized as staggered and blunt double-strand breaks.
14 roteins often enables accurate repair of DNA double-strand breaks.
15 genomic deletions are not the consequence of double-strand breaks.
16 iption factor Cap1, and the formation of DNA double-strand breaks.
17 that would otherwise generate mutations and double-strand breaks.
18 cing small clusters or individual single- or double-strand breaks.
19 esponse to genotoxic stresses that cause DNA double-strand breaks.
20 , insufficient mismatch repair and increased double-strand breaks.
21 es created after formation of programmed DNA double-strand breaks.
22 ases in mammalian cells without donor DNA or double-strand breaks.
23 er of the DNA damage response (DDR) upon DNA double-strand breaks.
24 ited biomarkers of DNA replication stress or double-strand breaks.
25 -Jun activation show cell activation and DNA double-strand breaks.
26 HR-dependent repair of directly induced DNA double-stranded breaks.
28 on, might contribute to the formation of DNA double strand breaks and activation of DNA damage respon
29 ivity and results in enhanced numbers of DNA double-strand breaks and a pronounced S/G2-phase arrest
30 ent and expansion can ultimately promote DNA double-strand breaks and androgen receptor activation in
33 inase that is recruited and activated by DNA double-strand breaks and functions as an important senso
34 Mre11-Rad50-Nbs1 complex that recognizes DNA double-strand breaks and has exonuclease and endonucleas
35 ic instability manifested by DNA single- and double-strand breaks and induction of p21 that was syner
36 teins that facilitate accurate repair of DNA double-strand breaks and prevent chromosomal rearrangeme
37 l of Il10 mRNA, and increased markers of DNA double-strand breaks and proliferation were observed in
38 ucible Cas9 was used for generating targeted double-strand breaks and simultaneous mobilization of th
40 homologous template to accurately repair DNA double-strand breaks and stalled replication forks to ma
41 ve sertraline-treated tissues accumulate DNA double-strand breaks and undergo apoptosis at increased
42 a DNA helicase protecting against G4 induced double-stranded breaks and concomitant loss of cohesion,
44 ed meiotic gene transcription, impairment of double-stranded breaks and pairing between homologous ch
49 show that naturally occurring background DNA double-strand breaks are associated with open chromatin,
50 ADP-ribosyl)ation in the germline, where DNA double-strand breaks are introduced by a regulated progr
53 inhibitor, talazoparib led to increased DNA double strand breaks, as assessed by gamma-H2AX foci for
54 epresented by Cas9 efficiently generates DNA double strand breaks at the target locus, followed by re
55 s with different isotypes by joining two DNA double-strand breaks at different switching regions via
56 nactive mutant blocked 53BP1 localization to double-strand breaks because (i) the mutant binding to T
57 terleukin (IL) 6 and IL8, and markers of DNA double-strand breaks but reduced markers of DNA repair,
60 dly respond to gamma-irradiation-induced DNA double-strand breaks by activating Ataxia Telangiectasia
64 ion, high-level transcription, and repair of double-strand breaks coalesce into foci, although the si
65 stribution does not reflect the abundance of double-strand breaks, detected by proxy as RAD51 foci at
70 le Strand Break (SSB) yields for plasmid and Double Strand Break (DSB) yields for plasmid/human cell.
71 nsive intrachromosomal mutations at a single double-strand break (DSB) and more frequent translocatio
73 dominant repair mechanism of any type of DNA double-strand break (DSB) during most of the cell cycle
74 uclear protein that negatively regulates DNA double-strand break (DSB) end resection and CCF formatio
75 y, HLTF-deficient cells also exhibit reduced double-strand break (DSB) formation and increased surviv
76 ibility that the minimal requirement for DNA double-strand break (DSB) formation is as low as even on
77 le telomeres in BLM-deficient cells involved double-strand break (DSB) formation, in this case by the
79 NA through the induction of an enzyme-linked double-strand break (DSB) in one DNA molecule and passag
80 e evaluate repair outcomes of a Cas9-induced double-strand break (DSB) introduced on the paternal chr
81 uclein in human cells leads to increased DNA double-strand break (DSB) levels after bleomycin treatme
85 estimated to inflict fewer than a single DNA double-strand break (DSB) per hour per cell, they still
86 XRCC4 plus p53, a genotype that enhances DNA double-strand break (DSB) persistence to enhance detecti
88 susceptibility protein (BRCA1) promotes DNA double-strand break (DSB) repair by homologous recombina
89 tional BRCA1 protein leads to defects in DNA double-strand break (DSB) repair by homologous recombina
92 P-seq) analysis showed the directionality of double-strand break (DSB) repair in the E. coli genome.
97 an BRD proteins for genome stability and DNA double-strand break (DSB) repair using several cell-base
98 erse lifespans, we show that more robust DNA double-strand break (DSB) repair, but not nucleotide exc
99 hat human DNA ligase IV, a key enzyme in DNA double-strand break (DSB) repair, is able to use NAD+ as
100 no80 deletion from cortical NPCs impairs DNA double-strand break (DSB) repair, triggering p53-depende
112 homologous recombination (HR) repair of DNA double-strand breaks (DSB); however, its precise role an
113 retrotransposition assay that identified the double-stranded break (DSB) repair and Fanconi anemia (F
120 to a large spectrum of DNA damage, including double strand breaks (DSBs) that interfere with replicat
125 ges the recruitment of DNA repair factors to double-strand breaks (DSBs) after genome editing with CR
126 -loops cause more telomeric and subtelomeric double-strand breaks (DSBs) and increase VSG switching r
127 mouse cells altered the repair of telomeric double-strand breaks (DSBs) and induced ALT-like phenoty
136 To generate a crossover, hundreds of DNA double-strand breaks (DSBs) are introduced in the genome
144 combination starts with the formation of DNA double-strand breaks (DSBs) at specific genomic location
145 d to as very fast CRISPR (vfCRISPR), creates double-strand breaks (DSBs) at the submicrometer and sec
146 ought to mediate homology-directed repair of double-strand breaks (DSBs) between two repeats, causing
147 A proper balance between the repair of DNA double-strand breaks (DSBs) by homologous recombination
148 Mechanistically, USP15 is recruited to DNA double-strand breaks (DSBs) by MDC1, which requires the
149 Mechanistically, BGL3 is recruited to DNA double-strand breaks (DSBs) by PARP1 at an early time po
150 t cancer cells to A3B-mediated mutations and double-strand breaks (DSBs) by perturbing canonical base
151 Exonucleolytic resection, critical to repair double-strand breaks (DSBs) by recombination, is not wel
152 rom the CUP1 locus through processing of DNA double-strand breaks (DSBs) by Sae2, Mre11 and Mus81, an
153 ologous end joining (NHEJ) for the repair of double-strand breaks (DSBs) caused by reactive oxygen sp
156 hybrids, replication stress markers and DNA double-strand breaks (DSBs) in cells depleted for Topois
157 replication origins (cSDR) and repair of DNA double-strand breaks (DSBs) in E. coli share a commonali
158 We were surprised to observe increased DNA double-strand breaks (DSBs) in mitochondria after exposu
160 Precise genome editing/correction of DNA double-strand breaks (DSBs) induced by CRISPR-Cas9 by ho
168 ment of the repair protein RAD51 to sites of double-strand breaks (DSBs) or the abundance of proteins
170 homologue-templated repair of programmed DNA double-strand breaks (DSBs) produces relatively few cros
171 Chromosome movements and programmed DNA double-strand breaks (DSBs) promote homologue pairing an
174 recombination were randomly distributed, the double-strand breaks (DSBs) that initiate recombination
175 an efficient, scalable method for analyzing double-strand breaks (DSBs) that we apply in parallel to
176 es of DNA repair counteract highly toxic DNA double-strand breaks (DSBs) to maintain genome stability
177 ves topological stress in DNA by introducing double-strand breaks (DSBs) via a transient, covalently
179 DNA-replication-fork associated single-ended double-strand breaks (DSBs), allowing some to be subject
180 ential step for homology-dependent repair of double-strand breaks (DSBs), and by attenuating DNA dama
181 AR-mediated, dose-dependent induction of DNA double-strand breaks (DSBs), G0/G1 cell cycle arrest and
182 single-strand breaks (SSBs), but not direct double-strand breaks (DSBs), in the genome during gene a
183 omal region (PAR), in which the formation of double-strand breaks (DSBs), pairing and crossing over m
184 se spo-11 mutants, which lack endogenous DNA double-strand breaks (DSBs), to induce a single DSB by M
185 way repairs psoralen-ICLs without generating double-strand breaks (DSBs), unlike the FA/BRCA pathway.
186 most deleterious types of DNA damage are DNA double-strand breaks (DSBs), which can cause cell lethal
187 mic integrity is threatened by cytotoxic DNA double-strand breaks (DSBs), which must be resolved effi
205 both DNA single-strand breaks (SSBs) and DNA double-strand breaks (DSBs); lesions that can trigger ne
208 e achieved upon repair of CRISPR-induced DNA double-stranded breaks (DSBs) by homology-directed repai
209 tenance of telomeres and rDNA, and repair of double-stranded breaks (DSBs) induced by genotoxins with
211 plex) are similarly deficient in joining DNA double-stranded breaks (DSBs) with hairpinned termini.
214 utations during somatic hypermutation or DNA double-strand breaks during class switch recombination (
215 y central roles in CCL as SPO11 mediates DNA double-strand break formation while both SPO11 and REC8
224 that this could be explained by reduced DNA double-strand breaks in female meiosis, paralleling the
225 s) were associated with the formation of DNA double-strand breaks in genomes of wheat, maize (Zea may
226 Depletion of WRN induces widespread DNA double-strand breaks in MSI cells, leading to cell cycle
227 that ASD-derived NPCs harbored elevated DNA double-strand breaks in replication stress-susceptible g
231 isomerases regulate DNA topology by making a double-stranded break in one DNA duplex, transporting an
233 knowledge about the fate of mtDNA following double-strand breaks, including the molecular players wh
234 cule microscopy measurements indicating that double-strand breaks induced by antibiotics strongly sti
235 iveFISH tracks the real-time movement of DNA double-strand breaks induced by CRISPR-Cas9-mediated edi
236 ly occurred during and immediately after DNA double-strand breaks induced by either doxorubicin or io
237 T cells exhibit improved expansion and lack double strand break-induced translocations observed in T
241 17 protein is recruited at nuclear foci upon double-strand break induction and colocalizes with gamma
243 BRCA1 protein degradation in response to DNA double-strand breaks is regulated by prolyl isomerase Pi
245 hromosomes of these bacteria was achieved by double-stranded breaks made by heterologous I-CeuI endon
246 ated during the repair of programmed meiotic double-strand breaks must be tightly regulated to promot
247 f microbial DNA with CRISPR-Cas9 to generate double-stranded breaks near the targeted sequences great
248 ion-induced foci (TIFs), indicating that DNA double-strand breaks occurred exclusively in telomeres a
249 > G as a mutagenic signature of male meiotic double-strand breaks on the X, which may result from lat
250 RNA-guided nuclease Cas9, we induced two DNA double-strand breaks, one each in the GAPDH and CD4 gene
253 eactive oxygen species (ROS), DNA single and double strand breaks, PFG, and apoptosis in umbilical co
254 er repair of deleterious DNA lesions such as double strand breaks prevents genomic instability and ca
255 tes 53BP1 stability and 53BP1 recruitment at double-strand breaks, providing yet another mechanism of
257 ination (HR) is important for error-free DNA double strand break repair and maintenance of genomic st
258 y restore HR, whereas KAT5 depletion rewires double strand break repair by promoting 53BP1 binding to
259 ubstantiation of a direct role for pol IV in double strand break repair in cells treated with double
262 SIRT6 stabilizes the genome by promoting DNA double strand break repair, thereby acting as a tumor su
263 ding of the mechanisms and regulation of DNA double strand break repair, we attempted to confirm that
264 xonuclease 5 (EXO5) gene in androgen-induced double strand breaks repair via homology-directed repair
265 tral role in homologous recombination during double-strand break repair and in replication fork dynam
267 in the paralog USP11, a key regulator of DNA double-strand break repair by homologous recombination.
268 the function of 53BP1, a key factor for DNA double-strand break repair by non-homologous end joining
270 tential functions: as a component of the DNA double-strand break repair machinery and as a ribonuclea
273 , these simple modifications of the original double-strand break repair model-asymmetry in recombinat
275 repair of transcribed genes, and error-free double-strand break repair of a 3'-phosphate-containing
276 nature associated with a backup, error-prone double-strand break repair pathway known as microhomolog
278 BRCA-deficient human cells and promotes DNA double-strand break repair through two pathways: homolog
279 tudies indicating the role of R-loops in DNA double-strand break repair with an updated view of much-
280 The contribution of remodelling factors to double-strand break repair within heterochromatin during
281 in completing replication is independent of double-strand break repair, and likely promotes joining
282 (DNA-PKcs) has well-established roles in DNA double-strand break repair, and recently, nonrepair func
283 ors of DNA fidelity through diverse roles in double-strand break repair, replication stress, and meio
284 I3K pathway activation and also hindered DNA double-strand break repair, which both led to improved r
286 ethylation at meiotic hotspots, impaired DNA double-strand-break repair, and reduced crossover number
287 iction to male germ cells elicits autonomous double-strand-break repair, consequently creating offspr
288 gulatable CRISPR/Cas9 strategy to induce DNA double strand breaks specifically in the telomeres, ChIP
289 which leads to the accumulation of toxic DNA double-strand breaks specifically in cancer cells with D
290 R) is a mechanism used to heal one-ended DNA double-strand breaks, such as those formed at collapsed
291 is highly mutagenic because Cas9 creates DNA double strand breaks, targeting of dead Cas9 (dCas9) is
292 ucleosomal DNA to designate the sites of DNA double-strand breaks that initiate meiotic recombination
293 itted high-energy alpha particles induce DNA double-strand breaks that might be irreparable and lead
294 n (HR) mediates the error-free repair of DNA double-strand breaks to maintain genomic stability.
296 NSD2 have been found to be recruited to DNA double strand breaks upon damage and H3K36me2 marks are
298 ysis of germline transcripts, examination of double-stranded breaks using biotin-labeling DNA break a
299 MRN has been shown to promote R-loops at DNA double-strand breaks, we show that it suppresses R-loops