ライフサイエンスコーパス: be repaired by

1 highly lethal DNA double-strand breaks that are repaired by 2 major mechanisms: BRCA-dependent homol

2 f DNA damage, 8-oxoG and abasic sites, which are repaired by 8-oxoguanine glycosylase (OGG1) and apur

3 ydro-8-oxo-2'-deoxyguanosine (8-oxoG), which is repaired by 8-oxoguanine DNA glycosylase1 (OGG1) duri

4 atson and Crick strands of the double helix, are repaired by a complex, replication-coupled pathway i

5 DNA double-strand breaks (DSBs) are repaired by a hierarchically regulated network of pa

6 efore, in high-grade tumours mismatched DSBs are repaired by a highly mutagenic, microhomology-mediat

7 Plasma membrane wounds are repaired by a mechanism involving Ca(2+)-regulated e

8 Genetic variants then result when breaks are repaired by a mutagenic mechanism involving recombin

9 lude that long resected chromosomal DSB ends are repaired by a single-strand DNA oligonucleotide thro

10 osely spaced lesions in opposing strands can be repaired by a combination of short and long-patch bas

11 ch causes double-stranded breaks that cannot be repaired by a haploid cell if induced before replicat

12 s analysis indicated that the DSBs appear to be repaired by a mechanism similar to nonhomologous end

13 during meiotic prophase become designated to be repaired by a pathway that specifically yields interh

14 ecombining with a template sequence, DNA can be repaired by a recombination-dependent DNA replication

15 The F167Y defect could also be repaired by a second, independent suppressor in the C

16 est that this complex strand break/ICL might be repaired by a simple mechanism in which the 3'-exonuc

17 Traditionally, these defects would have been repaired by a maxillofacial prosthesis but advances

18 n induced site-specific DSB in budding yeast is repaired by a 2-kb donor sequence inserted at differe

19 In humans this lesion is repaired by a mismatch-specific thymine DNA glycosyla

20 Mitochondrial DNA (mtDNA) is repaired by a mtBER pathway.

21 g agents, indicating that a cytotoxic lesion is repaired by a PCNA-dependent DNA repair pathway.

22 It is repaired by a radical SAM (S-adenosylmethionine) enzy

23 In A. aegypti, the midgut epithelium is repaired by a unique actin cone zipper mechanism that

24 Each of the resulting gingival defects was repaired by a distinct plastic surgery procedure, in

25 owed that RE was high because the cross-link was repaired by a pathway involving nucleotide excision

26 Twenty-one median or ulnar nerve lesions were repaired by a collagen nerve conduit or direct sutu

27 alysis established that DSBs occurring in G1 were repaired by a replicative mechanism, producing two

28 sylase acts on lesions previously thought to be repaired by Aag.

29 rves, indicating that the respective isomers are repaired by AlkB with different efficiencies.

30 erved that whereas 1,N (6)-ethenoadenine can be repaired by AlkB with similar efficiencies in both si

31 silonG is the only etheno lesion that cannot be repaired by AlkB, which partially explains its persis

32 genic analog 3,N4-ethenocytosine (eC), which is repaired by AlkB family enzymes in the direct reversa

33 This mutation was repaired by allelic replacement, resulting in restor

34 me VR implies that ancestral telomere damage was repaired by alternative lengthening of telomeres eve

35 Breaks are repaired by an end-joining reaction that requires DN

36 Previously studied [3Fe-4S] clusters are repaired by an Isc/Suf-independent pathway, so the r

37 At UIHC, almost all cases of OGI were repaired by anterior segment surgeons, with postope

38 ng frame of an out-of-frame DMD deletion can be repaired by antisense oligonucleotide (AO)-mediated e

39 A DNA double-strand break (DSB) can be repaired by any of several alternative and competing

40 Double-strand DNA breaks can be repaired by any of several alternative mechanisms tha

41 AP sites are repaired by AP endonucleases during the process of b

42 cision of damaged bases by DNA glycosylases, are repaired by AP-endonucleases (APEs).

43 nd breaks induced by reactive oxygen species are repaired by AP-endonucleases.

44 , such as uracil and abasic sites, appear to be repaired by at least two base excision repair (BER) s

45 endonuclease-induced double-strand break can be repaired by at least two pathways of nonhomologous en

46 ) are single strand breaks (SSBs) thought to be repaired by base excision repair enzymes.

47 These lesions cannot be repaired by base excision repair, but they are substr

48 DNA alkylation damage is repaired by base excision repair (BER) initiated by a

49 te of 5-fluorouracil, causes DNA damage that is repaired by base excision repair (BER).

50 These lesions are repaired by BCR/ABL-stimulated homologous recombinat

51 een the base and sugar moieties, they cannot be repaired by BER.

52 t cytotoxic lesions to eukaryotic genome and are repaired by both homologous recombination-dependent

53 A to form interstrand cross-links, which can be repaired by both nonmutagenic nucleotide excision rep

54 Nascent strand gaps can be repaired by BRCA-mediated homology repair.

55 seDSBs can be repaired by break-induced replication (BIR), which is

56 Because oxidized cysteine can be repaired by cellular reductants, the effect was to av

57 Function was "repaired" by charge reversal (E91R/R298E), implying

58 arise as intermediates of TOP2cc repair and are repaired by classical and alternative nonhomologous

59 For the extreme case of damage that cannot be repaired by conventional enzymes, there are proteins

60 The break is repaired by copying DNA from an extrachromosomal temp

61 nal or ablation injury to the corneal stroma is repaired by deposition of a fibrotic tissue produced

62 ctional telomeres are recognized as DSBs and are repaired by distinct DNA repair mechanisms.

63 aline-challenged rats were dysfunctional and were repaired by DIZE treatment.

64 only single-strand breaks in neurons, which are repaired by DNA ligase 3 with minimal toxicity.

65 g activity of the replicative DNA polymerase are repaired by DNA mismatch repair (MMR).

66 The fact that the oxidative damage can be repaired by DTT suggests that a cysteine or methionin

67 ar plasmid with a single defined fluorescein was repaired by efficient extracts from Xenopus oocyte n

68 DSBs are repaired by either error prone non-homologous end-jo

69 DNA double-strand breaks (DSBs) are repaired by either homologous recombination (HR) or

70 uble-strand breaks (DSBs) in mammalian cells are repaired by either homology-directed repair (HDR), u

71 DNA double-strand breaks (DSBs) are repaired by either the non-homologous end joining (N

72 hat arise through DNA replication errors can be repaired by either base excision repair or mismatch r

73 are potentially lethal DNA lesions that can be repaired by either homologous recombination (HR) or n

74 Chromosomal double-strand breaks (DSBs) can be repaired by either homology-dependent or homology-ind

75 DNA double strand breaks (DSBs) can be repaired by either recombination-based or direct liga

76 mine whether DNA double-strand breaks (DSBs) are repaired by end joining or homologous recombination.

77 gle-strand annealing and much less likely to be repaired by end joining compared with identical break

78 DSBs are repaired by endogenous cellular pathways such as non

79 In Escherichia coli, oxidative pyrimidines are repaired by endonuclease III (EndoIII) and endonucle

80 This 8-oxoG:A can be repaired by enzymes that remove Ade opposite to templ

81 Next, we found that stalled forks are repaired by error-prone pathways, such as microhomol

82 enotoxic DNA double-strand breaks (DSBs) can be repaired by error-free homologous recombination (HR)

83 eles formed when the drive-induced DNA break is repaired by error-prone pathways, which creates mutat

84 for the first time that this type of DPC can be repaired by Escherichia coli (E. coli) long-patch bas

85 tudy, it was found that the strand break can be repaired by Escherichia coli DNA polymerase I and E.

86 activates a checkpoint response, the damage is repaired by factors required for inter-sister homolog

87 crystallo isolation, suggested that epsilonA was repaired by formation of an epoxide (epsilonA-ep) th

88 ion does occur at the bulged guanine, but it is repaired by Fpg.

89 A DNA double-strand break (DSB) is repaired by gene conversion (GC) if both ends of the

90 om cell cycle checkpoint arrest when the DSB is repaired by gene conversion is substantially defectiv

91 by TCR whereas the lesions induced by 4-NQO are repaired by global genome repair.

92 PAH-DNA adducts may be repaired by global genomic nucleotide excision repair

93 d B lymphocytes, where nearly 70% of alleles were repaired by HDR and 7% by NHEJ.

94 ase mispairs, and all substrates tested that were repaired by hMutSbeta.

95 DNA double-strand breaks (DSBs) are repaired by homologous recombination (HR) and nonhom

96 DSBs are repaired by homologous recombination (HR) and nonhom

97 We also find that heterochromatic DSBs are repaired by homologous recombination (HR) but with s

98 gle-ended double-strand breaks (seDSBs) that are repaired by homologous recombination (HR).

99 Most double-strand breaks in flies are repaired by homologous recombination through the syn

100 s programmed DNA double-strand breaks (DSBs) are repaired by homologous recombination using the siste

101 In the absence of RNAi, stalled forks are repaired by homologous recombination without histone

102 When DSBs are repaired by homologous recombination, DNA ends can u

103 These DNA breaks are repaired by homologous recombination, which facilita

104 Double-strand breaks are repaired by homologous recombination.

105 ate repair: D10A but not N863A-induced nicks are repaired by homologous recombination.

106 lindromic DNA sequence by the SbcCD nuclease are repaired by homologous recombination.

107 ast are typically converted into deDSBs that are repaired by homologous recombination.

108 on of DNA double-strand breaks (DSBs), which are repaired by homologous recombination.

109 By contrast, AID-induced non-Igh DSBs are repaired by homologous recombination.

110 site-specific DNA double-strand breaks that are repaired by homologous recombination.

111 apse and chemical or physical damage and may be repaired by homologous recombination (HR) and non-hom

112 DNA DSBs can be repaired by homologous recombination (HR) and nonhomo

113 Double-strand breaks (DSBs) can be repaired by homologous recombination (HR) in mammalia

114 The break can be repaired by homologous recombination, an error-free m

115 ermediate in one sister chromatid, which can be repaired by homologous recombination, and a monoadduc

116 to instances of telomere damage that cannot be repaired by homologous recombination.

117 t of the palindrome-induced breaks appear to be repaired by homologous recombination.

118 that is processed to form breaks, which can be repaired by homologous recombination.

119 f DNA cleavage by the SbcCD complex that can be repaired by homologous recombination.

120 ground; the resulting cleavage of the genome is repaired by homologous recombination restoring the WT

121 ting a double-strand-break intermediate that is repaired by homologous recombination(2).

122 A DSB in MATa is repaired by homologous recombination--specifically, b

123 he mutated alleles in the Rag2(-/-) ES cells was repaired by homologous recombination, thereby restor

124 Double strand breaks (DSBs) can be repaired by homology independent nonhomologous end jo

125 DSBs can also be repaired by homology-dependent pathways (HDR), in whi

126 DSBs may also be repaired by homology-directed repair (HDR) using a DN

127 3'-PUA-protein DPCs, and found that they can be repaired by human tyrosyl-DNA phosphodiesterase 1 (TD

128 age product, 8-oxo-7,8-dihydroguanine (8oG), is repaired by human adenine DNA glycosylase homologue (

129 e misprocessed intermediates in ERCC1- cells are repaired by illegitimate recombination.

130 DNA double-strand breaks can be repaired by illegitimate recombination without extend

131 dues produced deleterious effects that could be repaired by increased temperature in combination with

132 ) and observed that a fraction of these DSBs were repaired by insertion of sequences, which we termed

133 The defect could be repaired by intergeneric complementation with E. coli

134 They can be repaired by ligation; however, if a nick occurs just

135 Paternal DNA double strand breaks were repaired by maternally provided error-prone polymer

136 Interstrand DNA cross-links (ICLs) are repaired by mechanisms using translesion DNA synthes

137 forms of methionine residues in proteins can be repaired by methionine-S-sulfoxide reductase (MsrA) a

138 is susceptible to oxidative inactivation and is repaired by methionine synthase reductase (MTRR) in t

139 s double-stranded DNA breaks (DSBs) that can be repaired by mitotic recombination with the homolog.

140 s will be converted to strand breaks if they are repaired by MMR.

141 DNA double-strand breaks (DSB) are repaired by multiple distinct pathways, with outcome

142 A3A-induced ssDNA gaps are repaired by multiple pathways involving ATR, RAD51,

143 DNA double-strand breaks are repaired by multiple pathways, including non-homolog

144 form long single-stranded overhangs that can be repaired by mutagenic pathways.

145 base excision repair, we found that cyclo-dA is repaired by NER and not by base excision repair.

146 In mammals, most DSBs are repaired by non-homologous end joining (NHEJ), which

147 noglobulin class switch recombination (CSR), are repaired by non-homologous end joining (NHEJ).

148 DSBs are repaired by non-homologous end-joining or homology d

149 tion is prevented, most double-strand breaks are repaired by non-homologous end-joinings similar to t

150 DNA double strand breaks (DSBs) can be repaired by non-homologous end joining (NHEJ) or homo

151 karyotic cells, DNA double-strand breaks can be repaired by non-homologous end-joining, a process dep

152 tabilize the PCC, allowing coding and SEs to be repaired by non-standard pathways, including alternat

153 asion steps, DSBs either are not repaired or are repaired by nonconservative single-strand annealing

154 DNA double-strand breaks (DSBs) are repaired by nonhomologous end joining (NHEJ) or homo

155 mologous template, as expected, Ac excisions are repaired by nonhomologous end joining (NHEJ) that ca

156 cleavage generates four broken DNA ends that are repaired by nonhomologous end joining forming coding

157 DNA strand breaks are repaired by nonhomologous end joining in mammalian c

158 both endogenous and exogenous in origin and are repaired by nonhomologous end joining or homologous

159 aks (DSBs) activate checkpoint signaling and are repaired by nonhomologous end-joining (NHEJ) and hom

160 DNA double strand breaks (DSB) are repaired by nonhomologous end-joining (NHEJ) or homo

161 by initiating DNA double strand breaks that are repaired by nonhomologous end-joining pathways.

162 n the remaining observed repair events, DSBs are repaired by nonhomologous processes.

163 crosslink and the acetylaminofluorene lesion were repaired by normal cell extracts approximately 15-2

164 There is evidence that these lesions are repaired by nucleotide excision repair (NER).

165 erally block replicative DNA polymerases and are repaired by nucleotide excision repair or bypassed b

166 produces cyclobutane pyrimidine dimers that are repaired by nucleotide excision repair, whereas DMS

167 8,5'-cyclopurine-2'-deoxynucleosides in DNA are repaired by nucleotide-excision repair, and act as s

168 The lesions can only be repaired by nucleotide excision repair with a low eff

169 hylcytosine and a neighboring guanine, which is repaired by nucleotide excision repair.

170 cts induced by tobacco-specific nitrosamines are repaired by O(6)-alkylguanine DNA alkyltransferase (

171 (O(6)-Me-dG) is highly mutagenic, and it can be repaired by O(6)-alkylguanine DNA alkyltransferase an

172 and mutagenic O6-alkylguanine adducts in DNA are repaired by O6-alkylguanine-DNA alkyltransferases (M

173 This lesion is repaired by O6-methylguanine-DNA methyltransferase (M

174 damage sustained by the OM of one population was repaired by OME with a healthy population.

175 They can be repaired by one of two pathways, homologous recombina

176 AAs were repaired by open surgical and endovascular techniqu

177 Repair of shorter deletions, however, are repaired by other mechanisms.

178 The remaining DSBs must be repaired by other mechanisms to restore genomic integ

179 resolved as crossovers with the homolog must be repaired by other pathways to ensure genome integrity

180 These SSBs are repaired by PARP1 and XRCC1-dependent mechanisms.

181 ed that RAG-generated chromosomal breaks can be repaired by pathways other than NHEJ in mouse embryon

182 This damage is repaired by photolyase and the nucleotide excision re

183 These cellular defects can be repaired by physiologic activation, transfection, or

184 henotype of pos5 and its arginine auxotrophy were repaired by plasmid-borne POS5 but not UTR1 or ADH1

185 The DSBs were repaired by POLD3/POLD4-dependent break-induced rep

186 tors or after exposure to ionizing radiation are repaired by proteins important for nonhomologous end

187 Ku: in lower eukaryotes such as yeast, DSBs are repaired by Rad52-dependent homologous recombination

188 ble-strand breaks (DSBs) made during meiosis are repaired by recombination with the homologous chromo

189 emonstrated that a DSB in one chromosome can be repaired by recombination with a homologous sequence

190 some forms of spontaneous S-phase damage can be repaired by recombination without activating checkpoi

191 In yeast, broken chromosomes can be repaired by recombination, resulting in nonreciprocal

192 Replication forks frequently break and must be repaired by recombination.

193 S-phase damage in checkpoint mutants, which is repaired by recombination without activating checkpoi

194 Once the fork is repaired by recombination, PriA is important for rest

195 response to severing, a finite gap forms and is repaired by recruitment of new material in an actin p

196 Damaged DNA can be repaired by removal and re-synthesis of up to 30 nucl

197 The demyelination can be repaired by remyelination in both humans and rodents,

198 This structural incompatibility was "repaired" by replacing the specific beta 2 TMD sequ

199 ctile dysfunction of myofibers from patients was repaired by replacing endogenous, mutant TnC with re

200 rks lacking Mrc1 create DNA damage that must be repaired by Rrm3.

201 ated mutagenic adducts epsilonA and epsilonC are repaired by separate gene products; and (iii) APNG d

202 Broken chromosomes can be repaired by several homologous recombination mechanis

203 DNA double-stranded breaks (DSBs) can be repaired by several mechanisms, including classical N

204 DNA double-strand breaks (DSBs) can be repaired by several pathways.

205 ismatches during T. brucei recombination may be repaired by short-patch mismatch repair.

206 damage found in the chromatinized genome and are repaired by single-strand break repair (SSBR) or bas

207 endonuclease-induced double-strand break can be repaired by single-strand annealing (SSA) between fla

208 o, lattice damage induced by wild-type KIF5C was repaired by soluble tubulin and resulted in increase

209 A total of 112 (56%) patients were repaired by specialist hepatobiliary surgeons [timi

210 s in DNA, e.g., unpaired/bulged nucleotides, are repaired by specific repair enzymes.

211 tablished that the kidney tubular epithelium is repaired by surviving epithelial cells.

212 cyclobutane pyrimidine dimers, are known to be repaired by TCR whereas the lesions induced by 4-NQO

213 idopsis thaliana and found that (6-4)PPs can be repaired by TCR; however, the main subpathway to remo

214 trated that in vitro 3'-PUA-protein DPCs can be repaired by TDP1, APE1, and TREX1 following proteolys

215 ther I-AniI or the CRISPR/Cas9(D10A) nickase are repaired by the alternative HDR pathway with little

216 Most of these small base modifications are repaired by the base excision repair (BER) pathway.

217 lesions such as oxidized or alkylated bases are repaired by the base excision repair (BER) pathway.

218 Although these lesions are repaired by the base excision repair pathway, they h

219 It has been inferred that these gaps are repaired by the cellular DNA repair machinery.

220 oduced in the G1 phase of the cell cycle and are repaired by the classical NHEJ machinery.

221 iously showed that acetaldehyde-induced ICLs are repaired by the FA pathway and a novel excision-inde

222 DNA crosslinks block DNA replication and are repaired by the Fanconi anaemia pathway.

223 In Escherichia coli, Fapy lesions are repaired by the Fapy-DNA glycosylase (Fpg) protein.

224 idatively generated DNA lesions, cdG and cdA are repaired by the human nucleotide excision repair (NE

225 experiments show that while DPCs from MEBAC are repaired by the metalloprotease SPRTN and the protea

226 igned structures that escape the exonuclease are repaired by the methyl-directed mismatch repair, alb

227 e DNA resulting from insertions or deletions are repaired by the mismatch repair (MMR) machinery.

228 In wild-type strains, these mismatches are repaired by the mismatch repair (MMR) system, produc

229 erase epsilon; that most of these mismatches are repaired by the MMR system; and that MMR repairs abo

230 In human cells, NMPs are repaired by the multi-step base excision repair path

231 ation induces DNA double-strand breaks which are repaired by the nonhomologous end joining (NHEJ) pat

232 ggest that some DSBs in mre-11(iow1) mutants are repaired by the nonhomologous end joining (NHEJ) pat

233 man cell nuclear extracts the HNE-dG adducts are repaired by the nucleotide excision repair (NER) pat

234 CPDs are repaired by the nucleotide excision repair pathway.

235 cleotide runs, most frameshift intermediates are repaired by the postreplicative mismatch repair (MMR

236 Intestinal mucosal defects are repaired by the process of intestinal restitution, d

237 s) introduced by the RAG1/2 nuclease complex are repaired by the process of nonhomologous end-joining

238 ces cerevisiae), and mammals, these hydrates are repaired by the tandem action of an ADP- or ATP-depe

239 generate a DNA double strand break that can be repaired by the DNA damage response machinery.

240 ICLs can be repaired by the Fanconi anemia (FA) pathway and throu

241 upt the brain microvasculature, which cannot be repaired by the hemostasis system because of its proc

242 mpression of the fate map does not appear to be repaired by the induction of new cell divisions.

243 Damage to peripheral nerves often cannot be repaired by the juxtaposition of the severed nerve en

244 ithin retroviral double-strand DNA could not be repaired by the mismatch-deficient cells.

245 an cells DNA double strand breaks (DSBs) can be repaired by the non-homologous end-joining (NHEJ) pat

246 lesions are highly toxic and are believed to be repaired by the sequential activity of nucleotide exc

247 the most cytotoxic forms of DNA damage, can be repaired by the tightly regulated nonhomologous end j

248 sed to determine whether the injured RPE was being repaired by the donor bone marrow.

249 8-oxoG is repaired by the 8-oxoguanine glycosylase 1 (OGG1)-ini

250 s high mutagenic and cytotoxic potential and is repaired by the alkyltransferase AGT.

251 DNA damage caused by reactive oxygen species is repaired by the base excision repair (BER) pathway wh

252 tive oxygen species (ROS)-induced DNA damage is repaired by the base excision repair pathway.

253 udies demonstrate that, although base damage is repaired by the BER pathway, incomplete BER intermedi

254 ystem that an ICL synthesized by this method is repaired by the FA pathway.

255 f several endogenously produced DNA adducts, is repaired by the nucleotide excision repair pathway.

256 pproximately 25% of the 8-oxoguanine lesions were repaired by the long patch repair pathway.

257 -RO) and methionine S-sulfoxide (Met-SO) can be repaired by thioredoxin-dependent enzymes MsrB and Ms

258 eaks, but it is unknown whether both strands are repaired by this pathway, and if one strand break's

259 DNA ends generated at a double strand break being repaired by this pathway.

260 ations suggest that psoralen cross-links can be repaired by three pathways: an error-free recombinati

261 oduce targeted chromosomal breaks, which can be repaired by transformation with a homologous DNA frag

262 n the oestrogen receptor target regions that are repaired by translocations, suggesting a role of oes

263 DNA replication-associated mutations are repaired by two components: polymerase proofreading

264 DNA double-strand breaks are repaired by two main pathways: nonhomologous end joi

265 Most DNA double-strand-breaks (DSBs) are repaired by two major mechanisms, homologous-recombi

266 DSBs are repaired by two major pathways, homologous recombina

267 In humans, DNA double-strand breaks (DSBs) are repaired by two mutually-exclusive mechanisms, homol

268 DNA double-strand breaks (DSBs) are repaired by two principal mechanisms: non-homologous

269 s presented here show that these defects can be repaired by unpairing short (3 or 5 bp) DNA segments

270 ation, gene function was previously shown to be repaired by unusual trans-splicing mediated by direct

271 s in most eukaryotic cells (including axons) are repaired by vesicles, at least some of which arise b

272 cal assay, we confirmed that tandem mispairs were repaired by wild-type cells but not by Pms2(-/-) hu