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1 double helix and generate an enzyme-mediated double-stranded DNA break.
2 resent at both scissile bonds to stabilize a double-stranded DNA break.
3 ilizing a strand-specific nick rather than a double-stranded DNA break.
4 leading to further processing of the initial double-stranded DNA break.
5 role in determining the response of cells to double stranded DNA breaks.
6 Mre11 and Rad50 to coordinate the repair of double-stranded DNA breaks.
7 ad3-related (ATR) kinase to induce transient double-stranded DNA breaks.
8 tivity and might prevent DME from generating double-stranded DNA breaks.
9 nation, which is essential for the repair of double-stranded DNA breaks.
10 e that initiates homologous recombination at double-stranded DNA breaks.
11 nonhomologous end-joining pathways to repair double-stranded DNA breaks.
12 rays and ultraviolet light that can lead to double-stranded DNA breaks.
13 nation, an important mechanism for repair of double-stranded DNA breaks.
14 l DNA replication in egg extracts containing double-stranded DNA breaks.
15 is, which leads to excessive accumulation of double-stranded DNA breaks.
16 with, 53BP1 after exposure to agents causing double-stranded DNA breaks.
17 e that initiates homologous recombination at double-stranded DNA breaks.
18 equired in order to increase enzyme-mediated double-stranded DNA breaks.
19 ily by the enzyme and can generate permanent double-stranded DNA breaks.
20 ert processed BER intermediates to permanent double-stranded DNA breaks.
21 ls by inhibiting topoisomerases and inducing double-stranded DNA breaks.
22 uring mitosis, meiosis, and in the repair of double-stranded DNA breaks.
23 re deficient in genes required for repair of double-stranded DNA breaks.
24 due to the involvement of ATM in monitoring double-stranded DNA breaks.
25 that are secondary to aberrant responses to double-stranded DNA breaks.
26 athway allows immature thymocytes to survive double-stranded DNA breaks.
27 A2, BRCA1 does not function in the repair of double-stranded DNA breaks.
28 important cellular pathway for the repair of double-stranded DNA breaks.
29 mologous recombination and for the repair of double-stranded DNA breaks.
30 ells revealed the presence of site-specific, double-stranded DNA breaks.
31 gether with experimentally induced telomeric double-stranded DNA breaks.
32 on, and is a major pathway for the repair of double-stranded DNA breaks.
33 sions, small duplications, and generation of double-stranded DNA breaks.
34 Cas9 as an RNA-guided nuclease that creates double-stranded DNA breaks.
35 , suggests sequence capture during repair of double-stranded DNA breaks.
36 ed in homologous recombination and repair of double-stranded DNA breaks.
37 forms distinct foci, and can associate with double-stranded DNA breaks.
38 defective lentiviruses into nuclease-induced double-stranded DNA breaks.
39 converting single-stranded DNA lesions into double-stranded DNA breaks.
40 ved in the early recognition and response to double-stranded DNA breaks.
41 with other telomeric loci, or non-telomeric double-stranded DNA breaks.
42 ase/nuclease that initiates recombination at double-stranded DNA breaks.
43 ferred DNA and protecting the genome against double-stranded DNA breaks.
44 maximal activity and induced a high ratio of double-stranded DNA breaks.
45 identify SMARCAL1 as a protein recruited to double-stranded DNA breaks.
46 cells through an accumulation of persistent double-stranded DNA breaks.
47 es responsible for homology-driven repair of double-stranded DNA breaks.
48 phosphorylated histone H2AX, an indicator of double-stranded DNA breaks.
49 ation of Rad50 foci, which are formed around double-stranded-DNA breaks.
51 colibactin, a genotoxic molecule(s) causing double-stranded DNA breaks(4) and enhanced colorectal ca
52 mit capture of the second processed end of a double-stranded DNA break, a step which is required for
53 Myc or GpIb alpha overexpression and include double-stranded DNA breaks, altered nuclear size and mor
54 s, probably due to the dramatic induction of double-stranded DNA breaks and chromosomal fragmentation
55 urthermore, these tumors were aneuploid with double-stranded DNA breaks and end-to-end telomere fusio
57 usly we have shown that HCV infection causes double-stranded DNA breaks and enhances the mutation fre
58 sophila, a meiotic checkpoint which monitors double-stranded DNA breaks and involves Drosophila ATR a
59 various stressors, such as for the repair of double-stranded DNA breaks and protein quality control,
60 that has primarily evolved for the repair of double-stranded DNA breaks and stalled replication forks
61 CD complex, which acts in both the repair of double-stranded DNA breaks and the degradation of bacter
62 t during homologous recombination, repair of double stranded DNA breaks, and integron recombination.
63 ed replication forks, insufficient repair of double-stranded DNA breaks, and improper segregation of
65 etabolism, archazolid caused S-phase arrest, double-stranded DNA breaks, and p53 stabilization, leadi
70 pyogenes (SpCas9) is more active in creating double-stranded DNA breaks at 37 degrees C than at 22 de
72 germline transcripts and increased levels of double-stranded DNA breaks at the recombination signal s
73 eplacement "footprints" in IgH sequences and double-stranded DNA breaks at V(H) cRSS sites in immatur
74 et (UV)-C radiation and reagents that induce double-stranded DNA breaks, but exhibit normal responses
75 s sufficient to stimulate the formation of a double-stranded DNA break by human topoisomerase IIalpha
77 d51 are important proteins for the repair of double-stranded DNA breaks by homologous recombination i
80 o prevent telomeres from being recognized as double-stranded DNA breaks by sequestering the 3' single
81 s initiated by introduction of site-specific double-stranded DNA breaks by the RAG-1 and RAG-2 protei
83 air pathway is required to prevent or repair double-stranded DNA breaks caused by defective DNA repli
84 found that some cells within biofilms incur double-stranded DNA breaks caused by endogenous oxidativ
85 g cellular metabolism; these lesions include double-stranded DNA breaks, daughter-strand gaps, and DN
87 ted T helper 17 cell differentiation through double-stranded DNA break (DSB) and ASC-mediated inflamm
88 ern expected as a consequence of repair of a double-stranded DNA break (DSB) of an unreplicated chrom
91 ressing cells during the early stages of the double-stranded DNA break (DSB) response, accelerating a
92 al chromatin organization before and after a double-stranded DNA break (DSB), to estimate the level o
93 he RAG-1 and RAG-2 proteins, which introduce double-stranded DNA breaks (DSB) adjacent to the Ig and
94 ) are ancient selfish elements that catalyze double-stranded DNA breaks (DSB) in a highly specific ma
98 amages mitochondria, leading to induction of double-stranded DNA breaks (DSBs) and accumulation of ox
99 by ATR (ATM and Rad3-related) in response to double-stranded DNA breaks (DSBs) but not to DNA replica
101 The activation of ATR-ATRIP in response to double-stranded DNA breaks (DSBs) depends upon ATM in hu
102 J) and homologous recombination (HR), repair double-stranded DNA breaks (DSBs) in all eukaryotes.
103 cent reports show it is enriched at sites of double-stranded DNA breaks (DSBs) in mammalian cells.
104 tein essential for recombinational repair of double-stranded DNA breaks (DSBs) in somatic cells and d
106 functionally dicentric chromosome undergoes double-stranded DNA breaks (DSBs) that can be repaired b
107 a heterodimer of Ku70 and Ku86 that binds to double-stranded DNA breaks (DSBs), activates the catalyt
113 topoisomerase II generates a protein-linked double-stranded DNA break during its catalytic cycle, it
114 eveloped a new approach to study single- and double-stranded DNA breaks during chronic, moderate exci
118 utant was shown to have a capacity to repair double-stranded DNA breaks equivalent to wild-type.
122 AddAB is a helicase-nuclease that processes double-stranded DNA breaks for repair by homologous reco
123 and replication fork restart, prevention of double-stranded DNA break formation, and avoidance of re
124 s recombination events that are initiated by double-stranded DNA breaks formed prior to replication.
125 non-homologous end-joining (NHEJ) repair of double-stranded DNA breaks generated by Cas9 are much le
126 F, XPC and AP-endonuclease-1), and repair of double-stranded DNA breaks (homologs of BRCA2, XRCC3, KU
127 because AID(+) dividing cells exhibited more double-stranded DNA breaks, IGH class switching, and new
128 e fact that there are two scissile bonds per double-stranded DNA break implies that there are two sit
131 nstrate that DNA intercalating agents induce double-stranded DNA breaks in both immature thymocytes a
132 e analyzed the repair of transposase-induced double-stranded DNA breaks in cells deficient in either
136 Cas9 can be reprogrammed to create specific double-stranded DNA breaks in the genomes of a variety o
138 point mutations in the Ig variable region or double-stranded DNA breaks in the switch region DNA.
140 ions, and H2AX phosphorylation, a marker for double-stranded DNA breaks, in Hus1(neo/neo) and Hus1(ne
141 BRCA1 has no equivalent role at chromosomal double-stranded DNA breaks, indicating that tandem dupli
142 initiate recombination between homologs are double-stranded DNA breaks induced during S or G2 of the
146 rejoining of DNA ends at single-stranded or double-stranded DNA breaks is catalyzed by DNA ligases.
148 e are two scissile bonds per enzyme-mediated double-stranded DNA break, it has been assumed that ther
149 cycle progression through mitosis following double-stranded DNA breaks leads to the formation of mic
151 at large-scale, yet previously unrecognized, double-stranded DNA breaks occur normally in early postm
152 oksani et al. examine the impact of a single double-stranded DNA break on replication in the budding
153 e scissile bond is sufficient to stabilize a double-stranded DNA break or whether both drug sites nee
154 on at Ser(92) in response to the presence of double-stranded DNA breaks or DNA replication blocks in
155 antage that it does not require formation of double-stranded DNA breaks or provision of a donor DNA t
156 reaction of topoisomerase II, which creates double-stranded DNA breaks, plays a central role in both
157 (D)J recombinase directly, by monitoring the double-stranded DNA breaks produced in the process of V(
160 critical role in sister chromatid cohesion, double-stranded DNA break repair and regulation of gene
162 5%) breakpoint junctions are consistent with double-stranded DNA break repair by nonhomologous end-jo
163 a crucial role in genetic recombination and double-stranded DNA break repair in Archaea, Bacteria, a
165 s a key regulator of DNA replication timing, double-stranded DNA break repair, and replication fork r
166 n to their implications for the mechanism of double-stranded DNA break repair, these observations may
167 A-dependent protein kinase (DNA-PK) mediates double-stranded DNA break repair, V(D)J recombination an
172 coli, homologous recombination initiated at double-stranded DNA breaks requires the RecBCD enzyme, a
174 merase I and II create transient single- and double-stranded DNA breaks, respectively, it has been as
177 Unrepaired DNA lesions, such as single- and double-stranded DNA breaks (SSBs and DSBs), and single-s
180 ingle-stranded DNA breaks frequently lead to double-stranded DNA breaks that are not rapidly repaired
181 whether cells die via apoptosis by detecting double-stranded DNA breaks that are the result of endonu
182 omosome throughout the genome and can induce double-stranded DNA breaks that lead to chromosome trans
183 enesis is secondary to aberrant responses to double-stranded DNA breaks that occur during V(D)J recom
184 rcalating agents reflects their tolerance of double-stranded DNA breaks that occur normally during an
185 nocytes within psoriatic plaques do not have double-stranded DNA breaks, that they have a prolonged c
187 ough BRCA2 functions to help the cell repair double-stranded DNA breaks, the function of BRCA1 remain
188 horylated H2AX is a characteristic marker of double-stranded DNA breaks, this modification was widely
189 II topoisomerases (TOP2) introduce transient double-stranded DNA breaks through a covalent TOP2-DNA i
190 In all domains of life, the resection of double-stranded DNA breaks to form long 3'-ssDNA overhan
191 e ability of a single 1 Gy exposure to cause double stranded DNA breaks (TUNEL assay) was enhanced at
192 aks resulted in the generation of persistent double-stranded DNA breaks was found to be a primary cau
193 the BNP-based sunblock significantly reduced double-stranded DNA breaks when compared with a commerci
194 r growth by causing apoptotic cell death via double-stranded DNA breaks while causing a remodeling of
195 fork stalling, we suggest that formation of double-stranded DNA breaks within the Ytel sequences mig
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