ライフサイエンスコーパス: DNA lesion

1 erms of sequence context and the presence of DNA lesions).

2 polymerase with an incoming rNTP opposite a DNA lesion.

3 ymerase correctly and incorrectly bypasses a DNA lesion.

4 hpol eta bypass of the most common oxidative DNA lesion.

5 transcriptional induction in the absence of DNA lesion.

6 tion of pol delta from PCNA on stalling at a DNA lesion.

7 genic role for pol eta when replicating this DNA lesion.

8 DNA damage response to replication-blocking DNA lesions.

9 well as fork progression through UV-induced DNA lesions.

10 mulation at challenged replication forks and DNA lesions.

11 oduce cytotoxic O(6)-methylguanine (O(6)-mG) DNA lesions.

12 cially in the major groove) and tolerance of DNA lesions.

13 chanisms to bypass nuclear and mitochondrial DNA lesions.

14 he biological significance of this family of DNA lesions.

15 proliferating cell nuclear antigen (PCNA) to DNA lesions.

16 l of a large variety of structurally diverse DNA lesions.

17 ted DNA substrates, such as those containing DNA lesions.

18 rand cross-links are exceptionally bioactive DNA lesions.

19 for maintaining replication bypass of these DNA lesions.

20 nisms to detect and repair multiple types of DNA lesions.

21 ures of transcription across different bulky DNA lesions.

22 by recruiting the SMC5/6 cohesion complex to DNA lesions.

23 etic modification products of 5caC behave as DNA lesions.

24 y) represent an important class of ethylated DNA lesions.

25 ven DNA photolyases, which remove UV-induced DNA lesions.

26 cally adducted, toxic 5'-adenylated (5'-AMP) DNA lesions.

27 ses needed to carry out error-free bypass of DNA lesions.

28 es to promote error-prone replication across DNA lesions.

29 it to efficiently attend to large numbers of DNA lesions.

30 to enzymes or agents that cause longer-lived DNA lesions.

31 ttenuates TCR but enhances cell tolerance to DNA lesions.

32 consistent with replication fork stalling at DNA lesions.

33 ity, cells have evolved mechanisms to repair DNA lesions.

34 ctive site can accommodate highly distorting DNA lesions.

35 se important for repairing multiple types of DNA lesions.

36 g the early stage of NER of UV light-induced DNA lesions.

37 lation vertex, creating spatially correlated DNA lesions.

38 the idea that toxicity arose from oxidative DNA lesions.

39 ensable for repairing TOP1 inhibitor-induced DNA lesions.

40 s (DSBs), a ubiquitination cascade occurs at DNA lesions.

41 prevents the persistence and propagation of DNA lesions.

42 s the misreplication of structurally diverse DNA lesions.

43 ER pathway, i.e. recognition and excision of DNA lesions.

44 hereby preventing the removal of UVB-induced DNA lesions.

45 ants need to prevent irreversible UV-induced DNA lesions.

46 s at the inner surface of PCNA is induced by DNA lesions.

47 A phosphorylation modes during the repair of DNA lesions.

48 nosine (8-oxoG), is one of the most abundant DNA lesions.

49 ub, cells exhibit accumulation of unrepaired DNA lesions.

50 the regulation of susceptibility to acquire DNA lesions.

51 d DNA to promote the signaling and repair of DNA lesions.

52 uffer from genomic instability and increased DNA lesions.

53 cts of radiation and to explain formation of DNA lesions.

54 the stabilization and exclusion of Rad9 from DNA lesions.

55 n Mre11/Rad50 nuclease activities on protein-DNA lesions.

56 The oxidative DNA lesion 7,8-dihydro-2'-deoxyguanine (8-oxoG) often oc

57 orating rNTPs opposite undamaged DNA and the DNA lesions 7,8-dihydro-8-oxo-2'-deoxyguanosine and cycl

58 In human cells, the oxidative DNA lesion 8,5'-cyclo-2'-deoxyadenosine (CydA) induces p

59 c D2 mice manifested increased mitochondrial DNA lesions (8-oxoguanine) exclusively localized to glom

60 One common oxidative DNA lesion, 8-oxo-7,8-dihydro-2'-deoxyguanine (8-oxoG),

61 rt that discrimination between the oxidative DNA lesion, 8-oxoguanine (oxoG) and its normal counterpa

62 to investigate how the most common oxidative DNA lesions, 8-oxoguanine (8oxoG) and thymine glycol (Tg

63 ut whether Rad18 mediates tolerance of bulky DNA lesions acquired outside S-phase is unclear.

64 These oncogenic DNA lesions, acquired through errors in DNA replication,

65 gest that whereas DNA polymerase stalling at DNA lesions activates ATR to protect cell viability and

66 ecialized TLS DNA polymerases to replicate a DNA lesion, allowing stringent DNA synthesis to resume b

67 DNA repair in response to different types of DNA lesions allows for a better understanding of the eff

68 Because appropriate DNA lesions also interact with base excision repair prot

69 thways that originates endogenously from the DNA lesion and activates intrinsic DNA repair mechanisms

70 Both a DNA lesion and an intermediate for antibody maturation,

71 ns about the repair of the carboxymethylated DNA lesions and about the implications of these lesions

72 specialized ways opposite a diverse array of DNA lesions and act in a predominantly error-free manner

73 treated DNA due to an ability to bypass both DNA lesions and bisulfite intermediates, allowing signif

74 an be trapped by carcinogenic and endogenous DNA lesions and by camptothecin, resulting in transcript

75 ever, there was no efficient protection from DNA lesions and cell death induced by UVA radiation or n

76 mercial sunscreens, in terms of induction of DNA lesions and cell death.

77 y component PCNA and promotes replication of DNA lesions and common fragile sites.

78 omplex in the repair of specific MMS-induced DNA lesions and elucidate the interplay between HR and t

79 DNA damage response factors to the sites of DNA lesions and facilitates DNA damage repair.

80 t the way in which repair enzymes search for DNA lesions and form protein complexes that act in DNA r

81 ting cells cope with accumulating endogenous DNA lesions and how these ultimately affect the physiolo

82 f ATM signalling as evidenced by accumulated DNA lesions and increased cell sensitivity to irradiatio

83 conserved role in the initial processing of DNA lesions and influencing their subsequent repair path

84 nition factor that binds to helix-distorting DNA lesions and initiates NER.

85 lular activities that prevent duplication of DNA lesions and maintain genomic integrity, which is cri

86 possible role(s) in the repair of endogenous DNA lesions and neuroprotection.

87 nce shows that BRCA1 is quickly recruited to DNA lesions and plays an important role in the DNA damag

88 UNG2-dependent repair of floxuridine-induced DNA lesions and promotes tumor cell survival following e

89 eckpoint pathway is activated in response to DNA lesions and replication stress to preserve genome in

90 cur for DNA repair factors to gain access to DNA lesions and restore original chromatin configuration

91 n part by regulating ISWI factors loading at DNA lesions and supporting transcriptional programs requ

92 nfers an enhanced ability on cells to repair DNA lesions and survive insult.

93 DNA-PK binds DNA ends that result from many DNA lesions and that blocking ABCDE phosphorylation sequ

94 to and significantly overlaps with PARP1 at DNA lesions and that the interaction between Sam68 and P

95 Also, leakiness in repairing DNA lesions and uncapped telomeres imposes genomic stres

96 l IV recruitment is dependent on the type of DNA lesion, and that interactions with proteins other th

97 g translesion DNA synthesis (TLS) on certain DNA lesions, and accumulating data suggest that Pol IV m

98 ion elongation, including DNA strand breaks, DNA lesions, and nucleosomes.

99 Unrepaired DNA lesions are a potent block to replication, leading t

100 The most common DNA lesions are base, sugar, and single-strand break dam

101 UV-induced DNA lesions are important contributors to mutagenesis an

102 DNA lesions are initially detected by NER factors XPC an

103 Underreplicated DNA lesions are known to be transmitted through mitosis

104 Thus, potentially oncogenic DNA lesions are likely to also trigger apoptosis through

105 After fertilization, unrepaired sperm DNA lesions are mis-repaired into CSA by the egg's DNA r

106 These gammaH2AX-labelled DNA lesions are more dispersedly occupied by the conserv

107 different amounts and/or different types of DNA lesions are produced in the presence or absence of o

108 int monitors the cohesin-dependent repair of DNA lesions arising from DNA demethylation, which preven

109 How cells distinguish DNA lesion-arrested Pol II from other forms of arrested

110 es for the two proteins in the processing of DNA lesions, as BRCA2 mutants contained more short delet

111 In addition, this enzyme produces DNA lesions at off-target sites that lead to mutations a

112 enome engineering that can introduce various DNA lesions at specific genomic locations.

113 ropose that poleta's ability to bypass bulky DNA lesions at telomeres is critical for proper telomere

114 wing metabolic activation, PhIP causes bulky DNA lesions at the C8-position of guanine.

115 es nucleotide excision repair by recognizing DNA lesions before recruiting downstream factors.

116 By repairing these DNA lesions before they can cause cell death, UNG2 promo

117 ability to respond properly to an unrepaired DNA lesion blocking replication promote genomic instabil

118 ability which is not triggered by endogenous DNA lesions but by a dysregulation in the DNA polymerase

119 enotypes are not a simple result of a single DNA lesion, but are instead due to interactions of the f

120 tolerance of replication fork-stalling bulky DNA lesions, but whether Rad18 mediates tolerance of bul

121 for cells deficient in repair of endogenous DNA lesions by BER.

122 hat WRAP53beta targets the E3 ligase RNF8 to DNA lesions by facilitating the interaction between RNF8

123 trinsic capacity for transcription bypass of DNA lesions by incorporation or misincorporation of nucl

124 f oxidative stress- and inflammation-induced DNA lesions by the base excision repair (BER) pathway pr

125 The bypass of DNA lesions by the replication fork requires a switch be

126 DNA lesion bypass is mediated by DNA damage tolerance (D

127 les to replisome progression by facilitating DNA lesion bypass, extension of D-loops, or excision rep

128 Endogenous and carcinogenic DNA lesions can also trap Top1cc.

129 data suggest that acrolein-induced exocyclic DNA lesions can be bypassed by mitochondrial DNA polymer

130 a genuine repair mechanism in which complex DNA lesions can be removed without generation of highly

131 Bulky DNA lesions can cause DSBs if they block DNA replication

132 f homologous recombination and the repair of DNA lesions, can partially replace RTEL1 in the processi

133 RNS-induced DNA lesions cause genomic instability in the absence of

134 The major DNA repair pathway removing DNA lesions caused by exposure to UV light is nucleotide

135 Unlike some other oxidatively generated DNA lesions, cdG and cdA are repaired by the human nucle

136 DSBs) are one of the most cytotoxic types of DNA lesion challenging genome integrity.

137 important insights into how these alkylated DNA lesions compromise the flow of genetic information,

138 Quantification of DNA lesions constitutes one of the main tasks in toxicol

139 X-X-Arg motif is located within the proposed DNA lesion contact site of PhrB.

140 ion of damaged nucleotides opposite oxidized DNA lesions created by reactive oxygen species.

141 ranslesion synthesis opposite the UV-induced DNA lesion cyclobutane pyrimidine dimer and was recently

142 platin derivatives can form various types of DNA lesions (DNA-Pt) and trigger pleiotropic DNA damage

143 Furthermore, there was evidence for oxidized DNA lesions, double-strand DNA strand breaks, and pronou

144 are important for the removal of MMS-induced DNA lesions due to their role in regulating the basal an

145 g agent widely used in chemotherapy, induces DNA lesions during male mouse meiosis that persist unrep

146 damage tolerance (DDT) enables bypassing of DNA lesions during replication, thereby preventing fork

147 of apoptosis caused by potentially oncogenic DNA lesions elicited by RAG1/2-induced gene rearrangemen

148 t of chemically stable analogues of unstable DNA lesions enables accurate study of polymerase bypass.

149 DNA lesions encountered by replicative polymerases threa

150 Deoxyribonucleic acid (DNA) lesions encountered during replication are often by

151 DNA lesions exist in low levels, and cannot be amplified

152 xo-guanine (8-oxo-G), a highly pro-mutagenic DNA lesion formed by reactive oxygen species.

153 icient, and high-fidelity process that mends DNA lesions formed during cellular metabolism; these les

154 2'-deoxyguanosine (O(6)-MeG) is a ubiquitous DNA lesion, formed not only by xenobiotic carcinogens bu

155 In eukaryotes, diverse DNA lesions from environmental sources are recognized by

156 excision repair that preferentially removes DNA lesions from the template strand that block transloc

157 r its inactivation during the induction of a DNA lesion, generate abnormal oscillatory SPB movements

158 and selectively inhibits the replication of DNA lesions generated by temozolomide.

159 genic outcomes derived from these unrepaired DNA lesions has been hindered by the low throughput of e

160 one of the most commonly occurring types of DNA lesion, have been associated with three neuropatholo

161 lymerases (Pols) promote replication through DNA lesions; however, little is known about the protein

162 H2A) formed by Rad3/ATR checkpoint kinase at DNA lesions; however, the putative scaffold interactions

163 Carcinogens induce malignancies by creating DNA lesions (i.e., adducts) that can result in mutations

164 igated the effects of five carboxymethylated DNA lesions, i.e. O6-CMdG, N6-CMdA, N4-CMdC, N3-CMdT and

165 lex with PARP-1 in cells and is recruited to DNA lesions in a PARP-1-dependent manner, but independen

166 overcome this blockade by synthesizing past DNA lesions in a process called translesion synthesis (T

167 sion repair (NER) removes chemically diverse DNA lesions in all domains of life.

168 owing to the difficulty of inducing defined DNA lesions in cells and tissues without simultaneously

169 cetylation modulates base excision repair of DNA lesions in chromatin.

170 NA polymerases, leading to the most abundant DNA lesions in genomes.

171 ogical consequences of the carboxymethylated DNA lesions in living cells.

172 neous analysis of TLS and HDR across defined DNA lesions in mammalian genomes.

173 ive to immunoglobulin loci; it can instigate DNA lesions in non-immunoglobulin genes and thus stringe

174 ights into how DNA repair factors search for DNA lesions in the context of chromatin.

175 dinic (AP) sites, the most frequently formed DNA lesions in the genome, inhibit transcription and blo

176 guanosine (8-oxoG), one of the most abundant DNA lesions in the genome.

177 chromosome scale map of ultraviolet-induced DNA lesions in the human genome, and reveal the sequence

178 extracts or purified enzymes, we found that DNA lesions in the nucleosome core are preferentially re

179 n of low, physiologically relevant levels of DNA lesions in the respective strands of defined nucleot

180 n repair (NER) dedicated to rapid removal of DNA lesions in the transcribed strand of actively transc

181 red to determine whether BPA induces similar DNA lesions in vivo at environmentally relevant doses; h

182 radical is a powerful oxidant that generates DNA lesions including the stereoisomeric R and S 5',8-cy

183 In cells, these compounds form a mixture of DNA lesions, including nucleobase monoadducts, interstra

184 ep is employed during repair of a variety of DNA lesions, including oxidative and alkylation damage.

185 -rate/reactive oxygen species cause dramatic DNA lesion increases that are not repaired due to PARP i

186 served pathway that removes helix-distorting DNA lesions induced by a plethora of mutagens, including

187 y and quantified the spatial distribution of DNA lesions induced by charged particles in a mouse mode

188 cleotide excision repair (NER) excises bulky DNA lesions induced by mutagens and carcinogens.

189 first quantitative human genome-wide map of DNA lesions induced by ultraviolet (UV) radiation, the u

190 n repair (NER) is critical for the repair of DNA lesions induced by UV radiation, but its contributio

191 Potentially mutagenic DNA lesions induced by UVB (wavelengths 280-320 nm) are

192 types of DSBs and reveal that the density of DNA lesions influences the choice of DSB repair pathway

193 equence, the burden of unrepaired endogenous DNA lesions intensifies, progressively leading to genomi

194 tribute to TLD by converting single-stranded DNA lesions into double-stranded DNA breaks.

195 n of plasmids carrying defined site-specific DNA lesions into mammalian chromosomes, using phage inte

196 ounter of a replication fork with a blocking DNA lesion is a common event that cells need to address

197 the hindrance presented by the location of a DNA lesion is dependent on the structural requirements f

198 One of the best characterized oxidative DNA lesions is 7,8-dihydro-8-oxoguanine (8-oxo-G).

199 difficult to replicate or contain endogenous DNA lesions is a hallmark of BRCA2 deficiency.

200 nal DNA repair proteome for removing harmful DNA lesions is a prerequisite for an appropriate DNA dam

201 Our results indicate that removal of DNA lesions is greatly dependent on their rotational and

202 orgonarius (Tgo-Pol), able to replicate past DNA lesions, is described.

203 se polymerases are specialized for different DNA lesions, it is unclear if they interact differently

204 analysis and evaluated chromatin structure, DNA lesion load, glutathione content, and intracellular

205 Unrepaired DNA lesions may compromise genomic integrity by inhibiti

206 DNA lesions may reduce the electron density at the nucle

207 DNA lesion measurement remains one of the core tasks in

208 -family Pols) capable of traversing blocking DNA lesions, most archaea lack these enzymes.

209 Repair of DNA lesions must occur within the chromatin landscape an

210 hich are synthetic derivatives of UV-induced DNA lesions, namely, thymidine (6-4) photoproducts.

211 This sensitized cells to the cytotoxic DNA lesion O(6)-methylguanine and caused a synthetic let

212 Among the alkylated DNA lesions, O(4)-alkylthymidine (O(4)-alkyldT) are know

213 r (MMR) and the repair of the chemosensitive DNA lesion, O6-methylguanine (O6-MeG), by O6-methylguani

214 , we monitored oxidatively induced clustered DNA lesions (OCDL), DNA double-strand breaks (DSB), apop

215 ts into the impacts of the carboxymethylated DNA lesions on DNA replication in human cells, revealed

216 he quantitative assessment of the effects of DNA lesions on the efficiency and fidelity of transcript

217 However, this DNA lesion "opening" is slow ( 5-10 ms) compared with ty

218 wind substrates with site-specific oxidative DNA lesions or bound by the mitochondrial transcription

219 damage response proteins (DDR) activated by DNA lesions or chromatin alterations recruit the DNA rep

220 ility, since replisomes invariably encounter DNA lesions or other structures that stall or collapse r

221 s affinity for factors recognizing different DNA lesions or telomeres, helping to direct the SLX4 com

222 ded genome and suggest how Msh2-Msh3 locates DNA lesions outside of replication-coupled repair.

223 xcision repair (BER) removes at least 20,000 DNA lesions per human cell per day and is critical for t

224 iously known about how the carboxymethylated DNA lesions perturb DNA replication in human cells.

225 ns acting as repair enzymes for UV-B-induced DNA lesions (photolyases) or as UV-A/blue light photorec

226 ly, suggesting accumulation of rN-containing DNA lesions (R-lesions).

227 UV light to introduce transcription-blocking DNA lesions randomly in the genome prior to bromouridine

228 ur work elucidates essential aspects of FAN1-DNA lesion recognition and a unique mechanism of incisio

229 cific endonuclease that processes UV-induced DNA lesions, recombination intermediates, and inter-stra

230 mechanisms that control their recruitment to DNA lesions remain unclear.

231 on on leukemia development in mice harboring DNA lesions resembling those acquired during human stem

232 purines (cdPus) are common forms of oxidized DNA lesions resulting from endogenous and environmental

233 studies on TLS in eukaryotes have focused on DNA lesions resulting from ultraviolet (UV) radiation ex

234 Bs, but is not released from the MMC-induced DNA lesions, resulting in a defect in homologous recombi

235 A variety of DNA lesions, secondary DNA structures or topological str

236 which likely involves Gln(41) and Leu(81) as DNA lesion sensors.

237 However, despite the persistence of DNA lesions, SETD2-deficient cells failed to activate p5

238 By inducing backtracking, UvrD exposes DNA lesions shielded by blocked RNA polymerase, allowing

239 oxidant tempol to suppress RNS, not only are DNA lesions significantly reduced, but also the onset of

240 ions (Pig-a gene mutation of RBC(CD24-)) and DNA lesions (single strand breaks/alkali labile sites) w

241 ut it enhances the recruitment of XPC to the DNA lesion site after irradiation.

242 ng of this E3 ligase complex directly at the DNA lesion site, causing the assembly of the UV-DDB-CUL4

243 nt capacity to identify and stabilize at the DNA lesion sites, and this function is facilitated in th

244 enetic and DNA repair recognition factors at DNA lesion sites.

245 enzyme in base excision DNA repair (BER) of DNA lesions, specifically interacts with NPM1 within nuc

246 Measurement of oxidative DNA lesions such as 8-oxo-2'-deoxyguanosine (8-oxo-dG) a

247 ime bacteria to effectively cope with severe DNA lesions such as double strand DNA breaks.

248 rting dNMPs opposite unmodified templates or DNA lesions, such as 8-oxo-2'-deoxyguanosine or cyclobut

249 Archaeal Pri S can bypass common oxidative DNA lesions, such as 8-Oxo-2'-deoxyguanosines and UV lig

250 Unrepaired DNA lesions, such as single- and double-stranded DNA bre

251 esses helix-destabilizing and/or -distorting DNA lesions, such as UV-induced photoproducts.

252 NER activities co-exist and excise Gh and Sp DNA lesions, suggesting that the relative NER/BER produc

253 ne-DNA glycosylase (Fpg)-sensitive oxidative DNA lesions suppressible by antioxidant cotreatment.

254 rent, early replicating, and AID-independent DNA lesions, termed early replication fragile sites (ERF

255 Abasic sites are ubiquitous DNA lesions that are mutagenic and cytotoxic but are rem

256 f nucleotides during DNA replication or from DNA lesions that arise between replication cycles and ar

257 heckpoint, and it functions in the repair of DNA lesions that arise during replication.

258 cell cycle phase transitions in response to DNA lesions that block DNA polymerase movement.

259 rand cross-links (ICLs) are highly cytotoxic DNA lesions that block DNA replication and transcription

260 DNA lesions that block transcription may cause cell deat

261 Interstrand crosslinks (ICLs) are toxic DNA lesions that cause severe genomic damage during repl

262 trand cross-links (ICLs) are extremely toxic DNA lesions that create an impassable roadblock to DNA r

263 , we have identified a source of spontaneous DNA lesions that drives instability at preferred genomic

264 ts the specific classes of radiation-induced DNA lesions that evade repair and result in germline mut

265 DNA-protein cross-links (DPCs) are bulky DNA lesions that form both endogenously and following ex

266 DNA lesions that have escaped DNA repair can induce repl

267 d with cross-overs suggests that most of the DNA lesions that initiate recombination between homologs

268 lent DNA-protein crosslinks (DPCs) are toxic DNA lesions that interfere with essential chromatin tran

269 cals that themselves create life-threatening DNA lesions that must be repaired within minutes to mini

270 This damage causes DNA lesions that, if not repaired quickly, are prone to

271 is influenced by the physical nature of the DNA lesion, that is, miscoding versus non-instructional.

272 ding that a mutagenic benzo[a]pyrene-derived DNA lesion, the base-displaced intercalated 10R-(+)-cis-

273 bypass of the 8-oxoguanine and thymine dimer DNA lesions, though with a 10(3) and 10(2)-fold lower ef

274 n protein Crb2 binds to modified histones at DNA lesions to mediate the activation of Chk1 by Rad3ATR

275 t and stabilization of XPC at the UV-induced DNA lesions to promote GG-NER.

276 ination and subsequently recombination-based DNA lesion tolerance.

277 lar neurodegenerative diseases; however, the DNA lesions underpinning disease etiology are unknown.

278 mes and frequently stall when they encounter DNA lesions, unusual DNA structures, RNA polymerases, or

279 slesion DNA synthesis (TLS) allows bypass of DNA lesions using error-prone TLS polymerases.

280 T7 replisome is fundamentally permissive of DNA lesions via pathways that do not require fork adjust

281 ntributing to genome stability via repair of DNA lesions via the base excision repair pathway.

282 While recruitment to the oxidative DNA lesions was abrogated by the anti-oxidant N-acetylcy

283 ecruitment of 53BP1-T1609A/S1618A to mitotic DNA lesions was associated with significant mitotic defe

284 reactive oxygen species (ROS) that can cause DNA lesions, we examined the role of NBS1 in macrophage

285 of the transcriptional properties of several DNA lesions, we have engineered specific fluorescent rep

286 imaging and laser microirradiation to induce DNA lesions, we show that the local chromatin relaxation

287 The results showed that the oxidant-induced DNA lesions were significantly reduced in cells pre-trea

288 ght that TLS was the last recourse to bypass DNA lesions when repair and nonmutagenic DA mechanisms h

289 poration of dCMP opposite these minor-groove DNA lesions, whereas only Pol V was indispensable for th

290 xic or mutagenic effects of various types of DNA lesions, which are sensed by distinct pathways to re

291 is only degraded in the presence of specific DNA lesions, which are the substrates of nucleotide exci

292 uch as Rev1, have the ability to bypass some DNA lesions, which can circumvent the process leading to

293 aC) suggests these modified cytosines act as DNA lesions, which could threaten genome integrity.

294 d by poly(ADP-ribose) polymerases (PARPs) at DNA lesions, which facilitates DNA damage repair.

295 lymerases can copy over replication blocking DNA lesions while temporarily leaving them unrepaired, p

296 The detection of DNA lesions within chromatin represents a critical step

297 DNA lesions within CRE modulate CREB1 binding negatively

298 or clustered mutagenesis is the induction of DNA lesions within unusually long and persistent single-

299 inhibition aggravates replication-originated DNA lesions without inducing S phase arrest in cells lac

300 at the expense of stable binding at sites of DNA lesions, without diminishing cellular UV resistance