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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
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
14 n induced site-specific DSB in budding yeast is repaired by a 2-kb donor sequence inserted at differe
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
26 silonG is the only etheno lesion that cannot be repaired by AlkB, which partially explains its persis
30 ng frame of an out-of-frame DMD deletion can be repaired by antisense oligonucleotide (AO)-mediated e
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
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
47 For the extreme case of damage that cannot be repaired by conventional enzymes, there are proteins
49 nal or ablation injury to the corneal stroma is repaired by deposition of a fibrotic tissue produced
52 ar plasmid with a single defined fluorescein was repaired by efficient extracts from Xenopus oocyte n
55 uble-strand breaks (DSBs) in mammalian cells are repaired by either homology-directed repair (HDR), u
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
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
69 om cell cycle checkpoint arrest when the DSB is repaired by gene conversion is substantially defectiv
76 s programmed DNA double-strand breaks (DSBs) are repaired by homologous recombination using the siste
85 apse and chemical or physical damage and may be repaired by homologous recombination (HR) and non-hom
94 he mutated alleles in the Rag2(-/-) ES cells was repaired by homologous recombination, thereby restor
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
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.
108 base excision repair, we found that cyclo-dA is repaired by NER and not by base excision repair.
111 tion is prevented, most double-strand breaks are repaired by non-homologous end-joinings similar to t
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
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
120 aks (DSBs) activate checkpoint signaling and are repaired by nonhomologous end-joining (NHEJ) and hom
124 crosslink and the acetylaminofluorene lesion were repaired by normal cell extracts approximately 15-2
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
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
138 ed that RAG-generated chromosomal breaks can be repaired by pathways other than NHEJ in mouse embryon
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
148 S-phase damage in checkpoint mutants, which is repaired by recombination without activating checkpoi
150 response to severing, a finite gap forms and is repaired by recruitment of new material in an actin p
155 ated mutagenic adducts epsilonA and epsilonC are repaired by separate gene products; and (iii) APNG d
159 endonuclease-induced double-strand break can be repaired by single-strand annealing (SSA) between fla
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
166 lesions such as oxidized or alkylated bases are repaired by the base excision repair (BER) pathway.
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.
175 erase epsilon; that most of these mismatches are repaired by the MMR system; and that MMR repairs abo
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
181 cleotide runs, most frameshift intermediates are repaired by the postreplicative mismatch repair (MMR
184 ces cerevisiae), and mammals, these hydrates are repaired by the tandem action of an ADP- or ATP-depe
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
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
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.
199 -RO) and methionine S-sulfoxide (Met-SO) can be repaired by thioredoxin-dependent enzymes MsrB and Ms
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
206 In humans, DNA double-strand breaks (DSBs) are repaired by two mutually-exclusive mechanisms, homol
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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