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 ective effects (reduced induction of initial DNA lesions).

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

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

5 polymerase with an incoming rNTP opposite a DNA lesion.

6 ymerase correctly and incorrectly bypasses a DNA lesion.

7 which then recruits nucleases to remove the DNA lesion.

8 examined the histone removal process at the DNA lesion.

9 he most frequent type of naturally occurring DNA lesion.

10 suppressed the immediate histone eviction at DNA lesions.

11 d mediates the repair of multiple classes of DNA lesions.

12 s the misreplication of structurally diverse DNA lesions.

13 the stabilization and exclusion of Rad9 from DNA lesions.

14 rand cross-links are exceptionally bioactive DNA lesions.

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

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

17 evolved to incorporate nucleotides opposite DNA lesions.

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

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

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

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

22 A phosphorylation modes during the repair of DNA lesions.

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

24 ub, cells exhibit accumulation of unrepaired DNA lesions.

25 the regulation of susceptibility to acquire DNA lesions.

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

27 uffer from genomic instability and increased DNA lesions.

28 ation was associated with histone removal at DNA lesions.

29 geting of non-Ig loci can generate oncogenic DNA lesions.

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

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

32 DNA damage response to replication-blocking DNA lesions.

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

34 mulation at challenged replication forks and DNA lesions.

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

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

37 chanisms to bypass nuclear and mitochondrial DNA lesions.

38 he biological significance of this family of DNA lesions.

39 it hinders access and processing of certain DNA lesions.

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

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

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

43 for maintaining replication bypass of these DNA lesions.

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

45 nt mechanism of fork protection at different DNA lesions.

46 -established role in the repair of oxidative DNA lesions.

47 a major DNA repair pathway for a variety of DNA lesions.

48 ation is one of the most ubiquitous forms of DNA lesions.

49 gradation by reinitiating DNA synthesis past DNA lesions.

50 t regulates early histone barrier removal at DNA lesions.

51 protein, to chromatin following induction of DNA lesions.

52 ) carries out extension from a wide range of DNA lesions.

53 r triggered by stalling of RNA polymerase at DNA lesions.

54 incision of phosphodiester bonds adjacent to DNA lesions.

55 ng stalling of RNA polymerase II (RNAPII) at DNA lesions.

56 hat can be attributed to specific sources of DNA lesions.

57 ected interplay between distinct ROS-induced DNA lesions.

58 Abasic sites are one of the most common DNA lesions.

59 helicases in the repair of these detrimental DNA lesions.

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

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

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

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

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

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

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

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

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

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

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

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

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

73 is controlled by PP4 during the repair of a DNA lesion and demonstrate that the attenuation of its k

74 acromolecular complexes that assemble at the DNA lesion and mediate repair.

75 uble-strand breaks (DSBs) are the most toxic DNA lesion and their repair is orchestrated by the ATM k

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

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

78 Nuclear GAPDH is recruited to DNA lesions and associates with DNA polymerase beta (Pol

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

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

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

82 ctivation-induced cytidine deaminase-induced DNA lesions and error-prone repair that underlie SHM are

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

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

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

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

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

88 ies on DNA damage sensor kinases that detect DNA lesions and phosphorylate an extensive network of su

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

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

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

92 NA template that include naturally occurring DNA lesions and secondary structures that are difficult

93 ered N- and C-termini, loses specificity for DNA lesions and shows less pausing on damaged DNA.

94 regulatory step of NHEJ complex assembly at DNA lesions and suggest additional possibilities for can

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

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

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

98 PCR analysis revealed an increase in (mt)DNA lesions and the frequency of mitochondrial common de

99 mediate the initial nucleolytic resection of DNA lesions and the recruitment and regulation of the re

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

101 ten use multiple pathways to repair the same DNA lesion, and the choice of pathway has substantial im

102 bition of EGFR phosphorylation, induction of DNA lesions, and blockade of their repair) into a single

103 es 53BP1 and RIF1 co-recruitment to sites of DNA lesions, and inhibits 53BP1-dependent fusion of dysf

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

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

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

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

108 DNA lesions are initially detected by NER factors XPC an

109 Underreplicated DNA lesions are known to be transmitted through mitosis

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

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

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

113 Here we reveal that most mutagenic DNA lesions are not resolved into a mutated DNA base pai

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

115 he direction of replication, suggesting that DNA lesions are resolved asymmetrically.

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

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

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

119 s of SHM revealed that a certain fraction of DNA lesions at C:G bp was indeed repaired in an error-fr

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

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

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

123 dihydro-8-oxoguanine, 8-oxoG) is a dangerous DNA lesion because it can mispair with adenine (A) durin

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

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

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

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

128 thymine-thymine (T-T) dimers and other bulky DNA lesions, but pol eta also has other cellular roles.

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

130 tion of error-free transcriptional bypass of DNA lesions by Rad26 facilitates TC-NER.

131 rally diverse helix-destabilizing/distorting DNA lesions by selectively 'opening' these sites while r

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

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

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

135 DNA lesions can severely compromise transcription and bl

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

137 s may be involved in the removal of the same DNA lesion caused by endogenous or exogenous agents.

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

139 s often encounter obstacles, including bulky DNA lesions caused by reactive metabolites and chemother

140 eotide excision repair (NER) removes various DNA lesions caused by UV light and chemical carcinogens.

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

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

143 uorescence reporter in concert with specific DNA lesion-containing substrates, the UBER probe can be

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

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

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

147 pontaneous DNA damage, including age-related DNA lesions, DNA breaks induced by several agents (bleom

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

149 continuously recruited to and exchanging at DNA lesions due to attenuated XRCC1-LIG3 recruitment and

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

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

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

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

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

155 DNA lesions encountered by replicative polymerases threa

156 DNA damage tolerance permits bypass of DNA lesions encountered during S-phase and may be carrie

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

158 s) act as docking sites to anchor particular DNA lesions facilitating DNA repair by elusive mechanism

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

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

161 2'-deoxyguanosine (O(6)-MeG) is a ubiquitous DNA lesion, formed not only by xenobiotic carcinogens bu

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

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

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

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

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

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

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

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

170 egrity, as premature recruitment of 53BP1 to DNA lesions impairs mitotic fidelity.

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

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

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

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

175 osis of GC B cells, likely due to unresolved DNA lesions in cells attempting to undergo class-switch

176 base loss, are the most abundant endogenous DNA lesions in cells.

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

178 ype is associated with a higher frequency of DNA lesions in fbl17 and increased cell death in the roo

179 in late mitosis to allow its recruitment to DNA lesions in G1.

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

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

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

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

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

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

186 ints in combination with repair of cisplatin-DNA lesions in vivo using RNAi nanocarriers, and motivat

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

188 xcision repair (NER) removes a wide range of DNA lesions, including UV-induced photoproducts and bulk

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

190 DNA lesions induce recruitment and accumulation of vario

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

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

193 Increased 53BP1 occupancy at DNA lesions induced by enoxacin ultimately suppresses ho

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

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

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

197 These guanine-derived oxidative DNA lesions interfere with both replication and transcri

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

199 The role of Rad53 in response to a DNA lesion is central for the accurate orchestration of

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

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

202 loops, which contributes to the emergence of DNA lesions, leading to the firing of backup origins tha

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

204 Unrepaired DNA lesions may compromise genomic integrity by inhibiti

205 DNA lesions may reduce the electron density at the nucle

206 f-field exposure; (iii) the yield of initial DNA lesions measured with half-field exposure is smaller

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

210 ced senescence was triggered by the specific DNA lesion O(6)-methylguanine (O(6)MeG) and characterize

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

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

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

216 e enzymes that can bypass potentially deadly DNA lesions on the template strand during DNA replicatio

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 DNA lesions or other barriers frequently compromise repl

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

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

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

224 iologic dose of which generates thousands of DNA lesions per cell, mostly of two types: cyclobutane p

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

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

227 the abasic site being one of the most common DNA lesions produced continuously by multiple pathways,

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

229 Thus, HMCES is an ancient DNA lesion recognition protein that preserves genome int

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

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

232 on recognition by ATL and directly visualize DNA lesion search by highly motile ATL and ATL-UvrA comp

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

234 Instead, DNA lesions segregate, unrepaired, into daughter cells f

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

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

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

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

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

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

241 DNA lesions stall the replisome and proper resolution of

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

243 ncluding the formation of the most dangerous DNA lesions such as cyclobutane pyrimidine dimers.

244 The proper repair of deleterious DNA lesions such as double strand breaks prevents genomi

245 s translesion synthesis at sites of covalent DNA lesions such as UV radiation-induced photoproducts.

246 In nucleotide excision repair, bulky DNA lesions such as UV-induced cyclobutane pyrimidine di

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

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

249 dation of guanine generates several types of DNA lesions, such as 8-oxoguanine (8OG), 5-guanidinohyda

250 hemically induced helix-distorting and bulky DNA lesions, such as cyclobutane pyrimidine dimers (CPDs

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

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

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

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

255 g the most mutagenic and prevalent alkylated DNA lesions that are associated with cancer initiation a

256 terstrand crosslinks (ICLs) are highly toxic DNA lesions that are repaired via a complex process requ

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

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 Abasic (AP) sites are one of the most common DNA lesions that block replicative polymerases.

261 on repair pathway, abasic sites are frequent DNA lesions that can lead to mutations and strand breaks

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

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

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

268 nous chemicals can react with DNA to produce DNA lesions that may block DNA replication.

269 n essential cellular mechanism for bypassing DNA lesions that obstruct DNA replication progression.

270 A-protein crosslinks (DPCs) are highly toxic DNA lesions that threaten genomic integrity.

271 cycle progression and replication-associated DNA lesions that were reversible upon overexpression of

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

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

274 When replication forks encounter template DNA lesions, the lesion is simply skipped in some cases.

275 y fulfill overlapping roles in the repair of DNA lesions, the mechanisms coordinating different pathw

276 , when RNF8 is rapidly recruited to sites of DNA lesions, the p97-ATX3 machinery stimulates the extra

277 ed the sumoylation of the first responder to DNA lesions, the ssDNA-binding protein complex replicati

278 DNA, however, in the presence of UV-induced DNA lesions these complexes stall.

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

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

281 A, so it can tether Smc5-Smc6 at replicative DNA lesions to promote survival.

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

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

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

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

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

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

288 n, replicative DNA polymerases may encounter DNA lesions, which can stall replication forks.

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

290 ytosolic DNA fragments because of unresolved DNA lesions, which in turn activated the DNA-sensing cGA

291 contributes to the ability of DPO4 to bypass DNA lesions, which is a known biological role of Y-famil

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

293 suggests that cross-links formed by reacting DNA lesions with proteins may play a significant role in

294 lex in the prevention of replication-related DNA lesions, with particular relevance to adaptive immun

295 DNA lesions within CRE modulate CREB1 binding negatively

296 ZNF281 is recruited to DNA lesions within seconds after DNA damage through a me

297 DNA lesions within the rDNA arrays are repaired in an RA

298 uncovered molecular interactions of several DNA lesions within the transcription elongation complex.

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

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