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1  highly lethal DNA double-strand breaks that are repaired by 2 major mechanisms: BRCA-dependent homol
2 ydro-8-oxo-2'-deoxyguanosine (8-oxoG), which is repaired by 8-oxoguanine DNA glycosylase1 (OGG1) duri
3 atson and Crick strands of the double helix, are repaired by a complex, replication-coupled pathway i
4 efore, in high-grade tumours mismatched DSBs are repaired by a highly mutagenic, microhomology-mediat
5                       Plasma membrane wounds are repaired by a mechanism involving Ca(2+)-regulated e
6     Genetic variants then result when breaks are repaired by a mutagenic mechanism involving recombin
7 lude that long resected chromosomal DSB ends are repaired by a single-strand DNA oligonucleotide thro
8 ch causes double-stranded breaks that cannot be repaired by a haploid cell if induced before replicat
9 s analysis indicated that the DSBs appear to be repaired by a mechanism similar to nonhomologous end
10 during meiotic prophase become designated to be repaired by a pathway that specifically yields interh
11 ecombining with a template sequence, DNA can be repaired by a recombination-dependent DNA replication
12                  The F167Y defect could also be repaired by a second, independent suppressor in the C
13      Traditionally, these defects would have been repaired by a maxillofacial prosthesis but advances
14 n induced site-specific DSB in budding yeast is repaired by a 2-kb donor sequence inserted at differe
15                        In humans this lesion is repaired by a mismatch-specific thymine DNA glycosyla
16                    Mitochondrial DNA (mtDNA) is repaired by a mtBER pathway.
17 g agents, indicating that a cytotoxic lesion is repaired by a PCNA-dependent DNA repair pathway.
18                                           It is repaired by a radical SAM (S-adenosylmethionine) enzy
19         In A. aegypti, the midgut epithelium is repaired by a unique actin cone zipper mechanism that
20       Each of the resulting gingival defects was repaired by a distinct plastic surgery procedure, in
21 owed that RE was high because the cross-link was repaired by a pathway involving nucleotide excision
22     Twenty-one median or ulnar nerve lesions were repaired by a collagen nerve conduit or direct sutu
23 alysis established that DSBs occurring in G1 were repaired by a replicative mechanism, producing two
24 sylase acts on lesions previously thought to be repaired by Aag.
25 rves, indicating that the respective isomers are repaired by AlkB with different efficiencies.
26 silonG is the only etheno lesion that cannot be repaired by AlkB, which partially explains its persis
27                                This mutation was repaired by allelic replacement, resulting in restor
28                                       Breaks are repaired by an end-joining reaction that requires DN
29         Previously studied [3Fe-4S] clusters are repaired by an Isc/Suf-independent pathway, so the r
30 ng frame of an out-of-frame DMD deletion can be repaired by antisense oligonucleotide (AO)-mediated e
31          A DNA double-strand break (DSB) can be repaired by any of several alternative and competing
32                 Double-strand DNA breaks can be repaired by any of several alternative mechanisms tha
33                                     AP sites are repaired by AP endonucleases during the process of b
34 cision of damaged bases by DNA glycosylases, are repaired by AP-endonucleases (APEs).
35 nd breaks induced by reactive oxygen species are repaired by AP-endonucleases.
36 , such as uracil and abasic sites, appear to be repaired by at least two base excision repair (BER) s
37 endonuclease-induced double-strand break can be repaired by at least two pathways of nonhomologous en
38 ) are single strand breaks (SSBs) thought to be repaired by base excision repair enzymes.
39                         These lesions cannot be repaired by base excision repair, but they are substr
40 te of 5-fluorouracil, causes DNA damage that is repaired by base excision repair (BER).
41                                These lesions are repaired by BCR/ABL-stimulated homologous recombinat
42 een the base and sugar moieties, they cannot be repaired by BER.
43 t cytotoxic lesions to eukaryotic genome and are repaired by both homologous recombination-dependent
44 A to form interstrand cross-links, which can be repaired by both nonmutagenic nucleotide excision rep
45                Because oxidized cysteine can be repaired by cellular reductants, the effect was to av
46                                     Function was "repaired" by charge reversal (E91R/R298E), implying
47   For the extreme case of damage that cannot be repaired by conventional enzymes, there are proteins
48                                    The break is repaired by copying DNA from an extrachromosomal temp
49 nal or ablation injury to the corneal stroma is repaired by deposition of a fibrotic tissue produced
50 aline-challenged rats were dysfunctional and were repaired by DIZE treatment.
51       The fact that the oxidative damage can be repaired by DTT suggests that a cysteine or methionin
52 ar plasmid with a single defined fluorescein was repaired by efficient extracts from Xenopus oocyte n
53                                         DSBs are repaired by either error prone non-homologous end-jo
54              DNA double-strand breaks (DSBs) are repaired by either homologous recombination (HR) or
55 uble-strand breaks (DSBs) in mammalian cells are repaired by either homology-directed repair (HDR), u
56              DNA double-strand breaks (DSBs) are repaired by either the non-homologous end joining (N
57 hat arise through DNA replication errors can be repaired by either base excision repair or mismatch r
58  are potentially lethal DNA lesions that can be repaired by either homologous recombination (HR) or n
59  Chromosomal double-strand breaks (DSBs) can be repaired by either homology-dependent or homology-ind
60  Chromosomal double-strand breaks (DSBs) can be repaired by either homology-dependent or homology-ind
61          DNA double strand breaks (DSBs) can be repaired by either recombination-based or direct liga
62 gle-strand annealing and much less likely to be repaired by end joining compared with identical break
63   In Escherichia coli, oxidative pyrimidines are repaired by endonuclease III (EndoIII) and endonucle
64 tudy, it was found that the strand break can be repaired by Escherichia coli DNA polymerase I and E.
65  activates a checkpoint response, the damage is repaired by factors required for inter-sister homolog
66 crystallo isolation, suggested that epsilonA was repaired by formation of an epoxide (epsilonA-ep) th
67 ion does occur at the bulged guanine, but it is repaired by Fpg.
68              A DNA double-strand break (DSB) is repaired by gene conversion (GC) if both ends of the
69 om cell cycle checkpoint arrest when the DSB is repaired by gene conversion is substantially defectiv
70  by TCR whereas the lesions induced by 4-NQO are repaired by global genome repair.
71 ase mispairs, and all substrates tested that were repaired by hMutSbeta.
72              DNA double-strand breaks (DSBs) are repaired by homologous recombination (HR) and nonhom
73                                         DSBs are repaired by homologous recombination (HR) and nonhom
74       We also find that heterochromatic DSBs are repaired by homologous recombination (HR) but with s
75           Most double-strand breaks in flies are repaired by homologous recombination through the syn
76 s programmed DNA double-strand breaks (DSBs) are repaired by homologous recombination using the siste
77        In the absence of RNAi, stalled forks are repaired by homologous recombination without histone
78                                    When DSBs are repaired by homologous recombination, DNA ends can u
79                         Double-strand breaks are repaired by homologous recombination.
80 lindromic DNA sequence by the SbcCD nuclease are repaired by homologous recombination.
81 ate repair: D10A but not N863A-induced nicks are repaired by homologous recombination.
82 on of DNA double-strand breaks (DSBs), which are repaired by homologous recombination.
83        By contrast, AID-induced non-Igh DSBs are repaired by homologous recombination.
84  site-specific DNA double-strand breaks that are repaired by homologous recombination.
85 apse and chemical or physical damage and may be repaired by homologous recombination (HR) and non-hom
86                                 DNA DSBs can be repaired by homologous recombination (HR) and nonhomo
87              Double-strand breaks (DSBs) can be repaired by homologous recombination (HR) in mammalia
88                                The break can be repaired by homologous recombination, an error-free m
89  to instances of telomere damage that cannot be repaired by homologous recombination.
90 t of the palindrome-induced breaks appear to be repaired by homologous recombination.
91  that is processed to form breaks, which can be repaired by homologous recombination.
92 f DNA cleavage by the SbcCD complex that can be repaired by homologous recombination.
93                                A DSB in MATa is repaired by homologous recombination--specifically, b
94 he mutated alleles in the Rag2(-/-) ES cells was repaired by homologous recombination, thereby restor
95              Double strand breaks (DSBs) can be repaired by homology independent nonhomologous end jo
96                                DSBs can also be repaired by homology-dependent pathways (HDR), in whi
97                                DSBs may also be repaired by homology-directed repair (HDR) using a DN
98 e misprocessed intermediates in ERCC1- cells are repaired by illegitimate recombination.
99                 DNA double-strand breaks can be repaired by illegitimate recombination without extend
100 dues produced deleterious effects that could be repaired by increased temperature in combination with
101 ) and observed that a fraction of these DSBs were repaired by insertion of sequences, which we termed
102                             The defect could be repaired by intergeneric complementation with E. coli
103           Interstrand DNA cross-links (ICLs) are repaired by mechanisms using translesion DNA synthes
104 forms of methionine residues in proteins can be repaired by methionine-S-sulfoxide reductase (MsrA) a
105 s double-stranded DNA breaks (DSBs) that can be repaired by mitotic recombination with the homolog.
106 s will be converted to strand breaks if they are repaired by MMR.
107 form long single-stranded overhangs that can be repaired by mutagenic pathways.
108 base excision repair, we found that cyclo-dA is repaired by NER and not by base excision repair.
109 noglobulin class switch recombination (CSR), are repaired by non-homologous end joining (NHEJ).
110                                         DSBs are repaired by non-homologous end-joining or homology d
111 tion is prevented, most double-strand breaks are repaired by non-homologous end-joinings similar to t
112          DNA double strand breaks (DSBs) can be repaired by non-homologous end joining (NHEJ) or homo
113 karyotic cells, DNA double-strand breaks can be repaired by non-homologous end-joining, a process dep
114 tabilize the PCC, allowing coding and SEs to be repaired by non-standard pathways, including alternat
115 asion steps, DSBs either are not repaired or are repaired by nonconservative single-strand annealing
116              DNA double-strand breaks (DSBs) are repaired by nonhomologous end joining (NHEJ) or homo
117 mologous template, as expected, Ac excisions are repaired by nonhomologous end joining (NHEJ) that ca
118 cleavage generates four broken DNA ends that are repaired by nonhomologous end joining forming coding
119                            DNA strand breaks are repaired by nonhomologous end joining in mammalian c
120 aks (DSBs) activate checkpoint signaling and are repaired by nonhomologous end-joining (NHEJ) and hom
121               DNA double strand breaks (DSB) are repaired by nonhomologous end-joining (NHEJ) or homo
122  by initiating DNA double strand breaks that are repaired by nonhomologous end-joining pathways.
123 n the remaining observed repair events, DSBs are repaired by nonhomologous processes.
124 crosslink and the acetylaminofluorene lesion were repaired by normal cell extracts approximately 15-2
125         There is evidence that these lesions are repaired by nucleotide excision repair (NER).
126 erally block replicative DNA polymerases and are repaired by nucleotide excision repair or bypassed b
127  produces cyclobutane pyrimidine dimers that are repaired by nucleotide excision repair, whereas DMS
128  8,5'-cyclopurine-2'-deoxynucleosides in DNA are repaired by nucleotide-excision repair, and act as s
129                         The lesions can only be repaired by nucleotide excision repair with a low eff
130 hylcytosine and a neighboring guanine, which is repaired by nucleotide excision repair.
131 cts induced by tobacco-specific nitrosamines are repaired by O(6)-alkylguanine DNA alkyltransferase (
132 and mutagenic O6-alkylguanine adducts in DNA are repaired by O6-alkylguanine-DNA alkyltransferases (M
133                                  This lesion is repaired by O6-methylguanine-DNA methyltransferase (M
134 damage sustained by the OM of one population was repaired by OME with a healthy population.
135                                     They can be repaired by one of two pathways, homologous recombina
136        Repair of shorter deletions, however, are repaired by other mechanisms.
137                      The remaining DSBs must be repaired by other mechanisms to restore genomic integ
138 ed that RAG-generated chromosomal breaks can be repaired by pathways other than NHEJ in mouse embryon
139                                  This damage is repaired by photolyase and the nucleotide excision re
140                   These cellular defects can be repaired by physiologic activation, transfection, or
141 henotype of pos5 and its arginine auxotrophy were repaired by plasmid-borne POS5 but not UTR1 or ADH1
142 tors or after exposure to ionizing radiation are repaired by proteins important for nonhomologous end
143  Ku: in lower eukaryotes such as yeast, DSBs are repaired by Rad52-dependent homologous recombination
144 emonstrated that a DSB in one chromosome can be repaired by recombination with a homologous sequence
145 some forms of spontaneous S-phase damage can be repaired by recombination without activating checkpoi
146             In yeast, broken chromosomes can be repaired by recombination, resulting in nonreciprocal
147  Replication forks frequently break and must be repaired by recombination.
148  S-phase damage in checkpoint mutants, which is repaired by recombination without activating checkpoi
149                                Once the fork is repaired by recombination, PriA is important for rest
150 response to severing, a finite gap forms and is repaired by recruitment of new material in an actin p
151                              Damaged DNA can be repaired by removal and re-synthesis of up to 30 nucl
152                        The demyelination can be repaired by remyelination in both humans and rodents,
153              This structural incompatibility was "repaired" by replacing the specific beta 2 TMD sequ
154 rks lacking Mrc1 create DNA damage that must be repaired by Rrm3.
155 ated mutagenic adducts epsilonA and epsilonC are repaired by separate gene products; and (iii) APNG d
156                       Broken chromosomes can be repaired by several homologous recombination mechanis
157        DNA double-stranded breaks (DSBs) can be repaired by several mechanisms, including classical N
158 ismatches during T. brucei recombination may be repaired by short-patch mismatch repair.
159 endonuclease-induced double-strand break can be repaired by single-strand annealing (SSA) between fla
160                A total of 112 (56%) patients were repaired by specialist hepatobiliary surgeons [timi
161 s in DNA, e.g., unpaired/bulged nucleotides, are repaired by specific repair enzymes.
162 tablished that the kidney tubular epithelium is repaired by surviving epithelial cells.
163  cyclobutane pyrimidine dimers, are known to be repaired by TCR whereas the lesions induced by 4-NQO
164 ther I-AniI or the CRISPR/Cas9(D10A) nickase are repaired by the alternative HDR pathway with little
165       Most of these small base modifications are repaired by the base excision repair (BER) pathway.
166  lesions such as oxidized or alkylated bases are repaired by the base excision repair (BER) pathway.
167                       Although these lesions are repaired by the base excision repair pathway, they h
168         It has been inferred that these gaps are repaired by the cellular DNA repair machinery.
169 oduced in the G1 phase of the cell cycle and are repaired by the classical NHEJ machinery.
170            In Escherichia coli, Fapy lesions are repaired by the Fapy-DNA glycosylase (Fpg) protein.
171 idatively generated DNA lesions, cdG and cdA are repaired by the human nucleotide excision repair (NE
172 igned structures that escape the exonuclease are repaired by the methyl-directed mismatch repair, alb
173 e DNA resulting from insertions or deletions are repaired by the mismatch repair (MMR) machinery.
174       In wild-type strains, these mismatches are repaired by the mismatch repair (MMR) system, produc
175 erase epsilon; that most of these mismatches are repaired by the MMR system; and that MMR repairs abo
176                         In human cells, NMPs are repaired by the multi-step base excision repair path
177 ggest that some DSBs in mre-11(iow1) mutants are repaired by the nonhomologous end joining (NHEJ) pat
178 ation induces DNA double-strand breaks which are repaired by the nonhomologous end joining (NHEJ) pat
179 man cell nuclear extracts the HNE-dG adducts are repaired by the nucleotide excision repair (NER) pat
180                                         CPDs are repaired by the nucleotide excision repair pathway.
181 cleotide runs, most frameshift intermediates are repaired by the postreplicative mismatch repair (MMR
182                   Intestinal mucosal defects are repaired by the process of intestinal restitution, d
183                   Intestinal mucosal defects are repaired by the process of intestinal restitution, d
184 ces cerevisiae), and mammals, these hydrates are repaired by the tandem action of an ADP- or ATP-depe
185  generate a DNA double strand break that can be repaired by the DNA damage response machinery.
186                                     ICLs can be repaired by the Fanconi anemia (FA) pathway and throu
187 upt the brain microvasculature, which cannot be repaired by the hemostasis system because of its proc
188 mpression of the fate map does not appear to be repaired by the induction of new cell divisions.
189     Damage to peripheral nerves often cannot be repaired by the juxtaposition of the severed nerve en
190 ithin retroviral double-strand DNA could not be repaired by the mismatch-deficient cells.
191 an cells DNA double strand breaks (DSBs) can be repaired by the non-homologous end-joining (NHEJ) pat
192 lesions are highly toxic and are believed to be repaired by the sequential activity of nucleotide exc
193 sed to determine whether the injured RPE was being repaired by the donor bone marrow.
194                                       8-oxoG is repaired by the 8-oxoguanine glycosylase 1 (OGG1)-ini
195 tive oxygen species (ROS)-induced DNA damage is repaired by the base excision repair pathway.
196 udies demonstrate that, although base damage is repaired by the BER pathway, incomplete BER intermedi
197 f several endogenously produced DNA adducts, is repaired by the nucleotide excision repair pathway.
198 pproximately 25% of the 8-oxoguanine lesions were repaired by the long patch repair pathway.
199 -RO) and methionine S-sulfoxide (Met-SO) can be repaired by thioredoxin-dependent enzymes MsrB and Ms
200  DNA ends generated at a double strand break being repaired by this pathway.
201 ations suggest that psoralen cross-links can be repaired by three pathways: an error-free recombinati
202 oduce targeted chromosomal breaks, which can be repaired by transformation with a homologous DNA frag
203         DNA replication-associated mutations are repaired by two components: polymerase proofreading
204                     DNA double-strand breaks are repaired by two main pathways: nonhomologous end joi
205         Most DNA double-strand-breaks (DSBs) are repaired by two major mechanisms, homologous-recombi
206   In humans, DNA double-strand breaks (DSBs) are repaired by two mutually-exclusive mechanisms, homol
207              DNA double-strand breaks (DSBs) are repaired by two principal mechanisms: non-homologous
208 s presented here show that these defects can be repaired by unpairing short (3 or 5 bp) DNA segments
209 s in most eukaryotic cells (including axons) are repaired by vesicles, at least some of which arise b
210 cal assay, we confirmed that tandem mispairs were repaired by wild-type cells but not by Pms2(-/-) hu

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