ライフサイエンスコーパス: cyclobutane pyrimidine dimer

1 two adenines opposite the two thymines of a cyclobutane pyrimidine dimer.

2 aryotic replisome following collision with a cyclobutane pyrimidine dimer.

3 rom these UV-induced linkages is the cis-syn cyclobutane pyrimidine dimer.

4 at it is a bona fide photolyase that repairs cyclobutane pyrimidine dimers.

5 tes the recruitment of XPC and the repair of cyclobutane pyrimidine dimers.

6 on of the most dangerous DNA lesions such as cyclobutane pyrimidine dimers.

7 e three, VcPhr, is a photolyase specific for cyclobutane pyrimidine dimers.

8 inhardtii that is blocked in the excision of cyclobutane pyrimidine dimers.

9 bility to replicate through UV-light-induced cyclobutane pyrimidine dimers.

10 thymine (spore photoproduct [SP]) instead of cyclobutane pyrimidine dimers.

11 fficient translesion synthesis past cis, syn-cyclobutane pyrimidine dimers.

12 ot alter the transcription-coupled repair of cyclobutane pyrimidine dimers.

13 ced by a template carrying two site-specific cyclobutane pyrimidine dimers.

14 ght-induced DNA damage, faithfully bypassing cyclobutane pyrimidine dimers.

15 /-) mice had an increased resolution rate of cyclobutane pyrimidine dimers.

16 on-induced photoproducts in the DNA, such as cyclobutane pyrimidine dimers.

17 v) increased repair of 6-4 photoproducts and cyclobutane pyrimidine dimers.

18 6-4) pyrimidine-pyrimidone photoproducts and cyclobutane pyrimidine dimers.

19 ess, and DNA damage such as 8-oxoguanine and cyclobutane pyrimidine dimers.

20 DinB-1 works in an error-free mode to repair cyclobutane pyrimidine dimers.

21 er 500 or 2500 J/m2 of UV light [0.6 and 0.8 cyclobutane pyrimidine dimer/146 bp (on average), respec

22 by the increased detection of gammaH2AX and cyclobutane pyrimidine dimers 24 hours after UVB radiati

23 a role for Pol zeta has been established for cyclobutane pyrimidine dimers, (6-4) dipyrimidine photop

24 act efficiently repair the bulky DNA lesions cyclobutane pyrimidine dimers,(6-4) photoproducts, and N

25 on-coupled repair at an extent comparable to cyclobutane pyrimidine dimers, a feature not previously

26 However, cyclobutane pyrimidine dimer accumulation was higher in

27 th sequences that form the highest levels of cyclobutane pyrimidine dimers after irradiation with sun

28 cells exhibited reduced repair of UV-induced cyclobutane pyrimidine dimers after PARP inhibition, sug

29 constructs and accelerated the resolution of cyclobutane pyrimidine dimers after UVL exposures in P38

30 and hCRY2 lacked photolyase activity on the cyclobutane pyrimidine dimer and the (6-4) photoproduct.

31 synthesis opposite the UV-induced DNA lesion cyclobutane pyrimidine dimer and was recently found to i

32 cleotide substrates containing site-specific cyclobutane pyrimidine dimers and (6-4) photoproducts fo

33 that mutagenesis resulting from TLS opposite cyclobutane pyrimidine dimers and (6-4) photoproducts fo

34 critical for efficient removal of UV-induced cyclobutane pyrimidine dimers and (iii) p300 is recruite

35 ssays showed that 5 kJ m-2 induced about 1.2 cyclobutane pyrimidine dimers and 0.1 [6-4]photoproducts

36 e two major types of UVB-induced DNA damage, cyclobutane pyrimidine dimers and 6,4-photoproducts, by

37 in global genomic repair of both UV-induced cyclobutane pyrimidine dimers and 6-4 photoproducts but

38 recovery of normal levels of repair of both cyclobutane pyrimidine dimers and 6-4 photoproducts in g

39 d of malignancy-produces DNA lesions such as cyclobutane pyrimidine dimers and 6-4 photoproducts in s

40 apoptosis and markers of DNA damage such as cyclobutane pyrimidine dimers and 8-OHdG.

41 polymerase eta can replicate through cis-syn cyclobutane pyrimidine dimers and 8-oxoguanine lesions w

42 Other photolesions including cyclobutane pyrimidine dimers and pyrimidine (6-4) pyrim

43 to chronic exposure, and excision repair of cyclobutane pyrimidine dimers and pyrimidine(6-4)pyrimid

44 n and/or endothelin-1 enhanced the repair of cyclobutane pyrimidine dimers and reduced the levels of

45 nucleobases, DNA-DNA crosslinks, UV-induced cyclobutane pyrimidine dimers and some chemically induce

46 m group E, enhances global genomic repair of cyclobutane pyrimidine dimers and suppresses UV-induced

47 P7 deficiency severely impairs the repair of cyclobutane pyrimidine dimers and, to a lesser extent, a

48 bypass an abasic site and a thymine-thymine cyclobutane pyrimidine dimer, and predominantly makes ba

49 cient and accurate synthesis of DNA opposite cyclobutane pyrimidine dimers, and inactivation of Polet

50 free replication through ultraviolet-induced cyclobutane pyrimidine dimers, and inactivation of Polet

51 accurate bypass of ultraviolet light-induced cyclobutane pyrimidine dimers, and it also functions in

52 vel of affinity for (6-4) photoproducts than cyclobutane pyrimidine dimers, and some affinity for DNA

53 e A (CsA) and ascomycin inhibited removal of cyclobutane pyrimidine dimers, and that they also inhibi

54 the deamination of cytosines within cis-syn cyclobutane pyrimidine dimers, and these two events comb

55 lective molecular recognition of the cis,syn cyclobutane pyrimidine dimer are reported.

56 From these data, we conclude that cyclobutane pyrimidine dimers are at least 20 to 40 time

57 repair, bulky DNA lesions such as UV-induced cyclobutane pyrimidine dimers are removed from the genom

58 Cyclobutane pyrimidine dimers are the major DNA photopro

59 The lesions induced by UV light, cyclobutane pyrimidine dimers, are known to be repaired

60 96A displayed a reduced repair efficiency of cyclobutane pyrimidine dimers as compared with cells com

61 s chc1 mutant showed similar accumulation of cyclobutane pyrimidine dimers as wild-type plants, in co

62 We had previously analyzed repair rates of cyclobutane pyrimidine dimers at nucleotide resolution a

63 We studied the repair of UV-induced cyclobutane pyrimidine dimers at nucleotide resolution b

64 eta that is able to replicate across cis-syn cyclobutane pyrimidine dimers both accurately and effici

65 ions 7,8-dihydro-8-oxo-2'-deoxyguanosine and cyclobutane pyrimidine dimer but with rates that are 10(

66 cv-PDG is specific not only for the cis-syn cyclobutane pyrimidine dimer, but also for the trans-syn

67 he major UV radiation photoproduct in DNA, a cyclobutane pyrimidine dimer, but no significant direct

68 ate or error-prone, as it is for bypass of a cyclobutane pyrimidine dimer by DNA polymerase eta (XP-V

69 TT reduced the number of nuclei positive for cyclobutane pyrimidine dimers by 40% (P < 0.0002) and fo

70 dynamics or enhance the repair of UV-induced cyclobutane pyrimidine dimers by UV photolyase.

71 at the site of damage and delayed removal of cyclobutane pyrimidine dimers by UV.

72 The repair of UV light-induced cyclobutane pyrimidine dimers can proceed via the base e

73 d into a DNA or RNA strand in proximity to a cyclobutane pyrimidine dimer, can mimic the function of

74 ar radiation is responsible for formation of cyclobutane pyrimidine dimers causing skin cancer.

75 The cyclobutane pyrimidine dimer class III photolyases are s

76 s, but decreased initial rates of removal of cyclobutane pyrimidine dimers, compared with normal cell

77 involves the bypass of a nonadjacent cis-syn cyclobutane pyrimidine dimer containing a single interve

78 wo proteins for their ability to replicate a cyclobutane pyrimidine dimer-containing DNA template and

79 We used high-throughput sequencing of short, cyclobutane pyrimidine dimer-containing ssDNA oligos gen

80 e adduct (AAF-G), a (6-4) photoproduct, or a cyclobutane pyrimidine dimer (CPD) and measured the repa

81 templates containing a specifically located cyclobutane pyrimidine dimer (CPD) and purified RNA poly

82 n induces two major DNA damage products, the cyclobutane pyrimidine dimer (CPD) and, at a lower frequ

83 aviolet) damage sequencing data and analyzed cyclobutane pyrimidine dimer (CPD) formation, DNA repair

84 sites that coincide with sites of UV-induced cyclobutane pyrimidine dimer (CPD) formation.

85 sites that coincide with sites of UV-induced cyclobutane pyrimidine dimer (CPD) formation.

86 sites, which are also sites of preferential cyclobutane pyrimidine dimer (CPD) formation.

87 sites that coincide with sites of UV-induced cyclobutane pyrimidine dimer (CPD) formation.

88 nism of the photolyase-catalyzed repair of a cyclobutane pyrimidine dimer (CPD) lesion using time-res

89 PC orthologue Rad4 bound to DNA containing a cyclobutane pyrimidine dimer (CPD) lesion.

90 ouble stranded oligonucleotides containing a cyclobutane pyrimidine dimer (CPD) lesion.

91 directly replicate through a leading-strand cyclobutane pyrimidine dimer (CPD) lesion.

92 CPD-seq, in E. coli to measure the levels of cyclobutane pyrimidine dimer (CPD) lesions before, durin

93 tors because of their incapability to repair cyclobutane pyrimidine dimer (CPD) lesions in duplex DNA

94 l lines have been studied for years, data on cyclobutane pyrimidine dimer (CPD) repair in these cells

95 complexes arrested at a specifically located cyclobutane pyrimidine dimer (CPD) using enzymatic probe

96 n repair (NER) of the major UV photoproduct (cyclobutane pyrimidine dimer (CPD)) in DNA.

97 l repair of the major UV-induced lesion, the cyclobutane pyrimidine dimer (CPD), but had no effect on

98 removed from the genome much faster than the cyclobutane pyrimidine dimer (CPD), owing to the more ef

99 constructs containing the UV-damaged adduct, cyclobutane pyrimidine dimer (CPD), to transfect human c

100 jor ultraviolet (UV)-induced DNA damage, the cyclobutane pyrimidine dimer (CPD), to two normal bases

101 DNA lesion induced by UV irradiation is the cyclobutane pyrimidine dimer (CPD), which forms at posit

102 ase activity exclusively for single-stranded cyclobutane pyrimidine dimer (CPD)-containing DNA substr

103 g frame (ORF) coding for a putative class II cyclobutane pyrimidine dimer (CPD)-photolyase in the gen

104 ignificant difference in the initial rate of cyclobutane pyrimidine dimer (CPD)-removal from the skin

105 We have developed a cyclobutane pyrimidine dimer (CPD)-specific immunoprecip

106 translesion replication of a thymine-thymine cyclobutane pyrimidine dimer (CPD).

107 We measured cyclobutane pyrimidine dimers (CPD) and 6-4 photoproduct

108 Ultraviolet light induces cyclobutane pyrimidine dimers (CPD) and pyrimidine(6-4)p

109 12 knockout (KO) mice using the formation of cyclobutane pyrimidine dimers (CPD) as an indicator of t

110 cture or in the number of UV-induced cis-syn cyclobutane pyrimidine dimers (CPD) between HTB1 and htb

111 reduced flavin cofactor to repair UV-induced cyclobutane pyrimidine dimers (CPD) formed between two a

112 ecies (ROS) as well as 6-4-photoproducts and cyclobutane pyrimidine dimers (CPD) in the skin, which f

113 I/SNF, negatively affects the elimination of cyclobutane pyrimidine dimers (CPD), but not of pyrimidi

114 t for DNA absorption or for the induction of cyclobutane pyrimidine dimers (CPD).

115 uno-dot blot analysis identified the cis-syn cyclobutane pyrimidine-dimer (CPD) as a distinctive UVB-

116 measured repair of the UV-induced damage of cyclobutane pyrimidine dimers (CPDs) (at 1, 4, 8, 16, 24

117 d the number of epidermal cells positive for cyclobutane pyrimidine dimers (CPDs) 50% immediately pos

118 ent formation of photodimeric lesions, i.e., cyclobutane pyrimidine dimers (CPDs) and (6-4) photoprod

119 f two UV-induced DNA damages in human cells: cyclobutane pyrimidine dimers (CPDs) and (6-4) pyrimidin

120 PLs function predominantly in DNA repair of cyclobutane pyrimidine dimers (CPDs) and 6-4 photolesion

121 (NER) of the major UV-induced photoproducts, cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproduc

122 of Schizosaccharomyces pombe that recognizes cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproduc

123 died the levels of global repair (removal of cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproduc

124 f DNA lesions per cell, mostly of two types: cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproduc

125 ing bulky base adducts, including UV-induced cyclobutane pyrimidine dimers (CPDs) and BaP diol epoxid

126 Solar radiation induces the formation of cyclobutane pyrimidine dimers (CPDs) and other UV photop

127 ne dimers with the predominant lesions being cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4

128 formation of DNA photoproducts, most notably cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4

129 ght also introduce DNA damage in the form of cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4

130 been shown to cleave 5' to UV light-induced cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyri

131 Damage maps of both cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyri

132 nduced DNA damage that occurs in the form of cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyri

133 ation generates two major photoproducts, the cyclobutane pyrimidine dimers (CPDs) and the 6-4 photopr

134 prevalent DNA lesions induced by UVB are the cyclobutane pyrimidine dimers (CPDs) and the pyrimidine

135 Cyclobutane pyrimidine dimers (CPDs) are DNA photoproduc

136 Cyclobutane pyrimidine dimers (CPDs) are formed in DNA f

137 hinese hamster ovary (CHO) cells, UV-induced cyclobutane pyrimidine dimers (CPDs) are preferentially

138 ovary cells while ultraviolet light-induced cyclobutane pyrimidine dimers (CPDs) are preferentially

139 that several types of DNA damage, including cyclobutane pyrimidine dimers (CPDs) are repaired with e

140 Cyclobutane pyrimidine dimers (CPDs) are responsible for

141 Cyclobutane pyrimidine dimers (CPDs) are the major form

142 Cyclobutane pyrimidine dimers (CPDs) are the major produ

143 Cis-syn cyclobutane pyrimidine dimers (CPDs) are the most freque

144 types of UV-induced DNA lesions, the cis-syn cyclobutane pyrimidine dimers (CPDs) are thought to be t

145 ave ultraviolet (UVC) light not only produce cyclobutane pyrimidine dimers (CPDs) as reported but als

146 een adjacent pyrimidines, generating cis-syn cyclobutane pyrimidine dimers (CPDs) as the most common

147 We have analysed the removal of UV-induced cyclobutane pyrimidine dimers (CPDs) at nucleotide resol

148 nown as CPD-seq, to precisely map UV-induced cyclobutane pyrimidine dimers (CPDs) at single-nucleotid

149 d a method to study the repair of UV induced cyclobutane pyrimidine dimers (CPDs) at the level of the

150 pped the repair of ultraviolet light-induced cyclobutane pyrimidine dimers (CPDs) at the nucleotide l

151 (UVB) light results in the formation of anti cyclobutane pyrimidine dimers (CPDs) between loop 1 and

152 utants exhibit enhanced repair of UV-induced cyclobutane pyrimidine dimers (CPDs) compared to wild-ty

153 Cyclobutane pyrimidine dimers (CPDs) constitute the most

154 6B) by strand-specific removal of UV-induced cyclobutane pyrimidine dimers (CPDs) from a 16 Kb fragme

155 DB to hamster cells, and enhanced removal of cyclobutane pyrimidine dimers (CPDs) from genomic DNA an

156 done photoproducts [(6-4) photoproducts] and cyclobutane pyrimidine dimers (CPDs) from the genome of

157 ll as by generation of photoproducts such as cyclobutane pyrimidine dimers (CPDs) has been suggested.

158 amine the repair of ultraviolet (UV)-induced cyclobutane pyrimidine dimers (CPDs) in identical sequen

159 UV-induced cyclobutane pyrimidine dimers (CPDs) in the template DNA

160 report genome-wide repair maps of UV-induced cyclobutane pyrimidine dimers (CPDs) in yeast cells lack

161 A lesions that occur in AT-rich DNA, such as cyclobutane pyrimidine dimers (CPDs) induced by UV radia

162 To assess whether removal of UV-induced cyclobutane pyrimidine dimers (CPDs) occurs with equal e

163 An average of approximately 2 cyclobutane pyrimidine dimers (CPDs) per 214 bp fragment

164 UV-light-induced cyclobutane pyrimidine dimers (CPDs) present a severe bl

165 Analysis of genome-wide repair of UV-induced cyclobutane pyrimidine dimers (CPDs) using CPD-seq indic

166 Photoreactive repair (PR) of cyclobutane pyrimidine dimers (CPDs) was mapped at nucle

167 The repair rate of UV-induced cyclobutane pyrimidine dimers (CPDs) was measured at sin

168 Repair of UV-induced cyclobutane pyrimidine dimers (CPDs) was measured in a y

169 cleotide excision repair (NER) of UV-induced cyclobutane pyrimidine dimers (CPDs) was measured in the

170 s than in the precursor cells, and repair of cyclobutane pyrimidine dimers (CPDs) was not detected in

171 radiation locally, DNA damage in the form of cyclobutane pyrimidine dimers (CPDs) was repaired more e

172 Maximum and comparable cyclobutane pyrimidine dimers (CPDs) were detected immed

173 ll line, formation and removal of UV-induced cyclobutane pyrimidine dimers (CPDs) were measured in th

174 d known as CPD-capture-seq to map UV-induced cyclobutane pyrimidine dimers (CPDs) with high sequencin

175 DNA lesions, such as cyclobutane pyrimidine dimers (CPDs), [6-4] pyrimidine-p

176 ix-distorting and bulky DNA lesions, such as cyclobutane pyrimidine dimers (CPDs), and DNA interstran

177 obal genomic repair especially the repair of cyclobutane pyrimidine dimers (CPDs), and is regulated b

178 ding induces distinct patterns of UV-induced cyclobutane pyrimidine dimers (CPDs), and that these CPD

179 ions in sunlight-induced melanoma arise from cyclobutane pyrimidine dimers (CPDs), DNA photoproducts

180 promotes transcription bypass of UV-induced cyclobutane pyrimidine dimers (CPDs), increases survival

181 DNA glycosylases (pdgs) that initiate BER of cyclobutane pyrimidine dimers (CPDs), the predominant UV

182 However, cyclobutane pyrimidine dimers (CPDs), which do not signi

183 more frequent than ultraviolet (UV)-induced cyclobutane pyrimidine dimers (CPDs).

184 ional signatures associated with UVB-induced cyclobutane pyrimidine dimers (CPDs).

185 (6-4)PPs] is about 10x faster than repair of cyclobutane pyrimidine dimers (CPDs).

186 of other major UV-induced DNA lesion called cyclobutane pyrimidine dimers (CPDs).

187 ces a significant amount of abasic sites and cyclobutane pyrimidine dimers (CPDs).

188 e from translesion synthesis past deaminated cyclobutane pyrimidine dimers (CPDs).

189 sustain significant DNA damage [measured as cyclobutane pyrimidine dimers (CPDs)] during periods of

190 resistance to repair of UVB-induced cis-syn cyclobutane pyrimidine-dimers (CPDs) together with rapid

191 UV-induced photoproducts (cyclobutane pyrimidine dimers, CPDs) in DNA are removed

192 2, thereby facilitating DDB2 localization to cyclobutane pyrimidine dimer crosslinks to govern their

193 ppressive properties of UV-B irradiation, or cyclobutane pyrimidine dimers differ qualitatively from

194 y of pol eta to accurately bypass UV-induced cyclobutane pyrimidine dimers during a process termed tr

195 lesions, such as 8-oxo-2'-deoxyguanosine or cyclobutane pyrimidine dimer, even in the presence of an

196 ne (2M) with the bipyrimidine models affords cyclobutane pyrimidine dimers, even in the presence of b

197 ruited at a reduced efficiency to UV-induced cyclobutane pyrimidine dimer foci.

198 NA synthesis recovery and slower excision of cyclobutane pyrimidine dimers following UVC irradiation;

199 The quantum yield of cyclobutane pyrimidine dimer formation was calculated as

200 Moreover, UV-induced cyclobutane pyrimidine dimer formation was markedly enha

201 ly induces the defence genes at levels where cyclobutane pyrimidine dimer formation, an indicator of

202 nd is associated with high levels of cis-syn cyclobutane pyrimidine dimer formation.

203 The combined data make a strong case that cyclobutane pyrimidine dimers forming preferentially at

204 uciferase expression vector, the excision of cyclobutane pyrimidine dimers from bulk DNA, or unschedu

205 s are deficient in the removal of UV-induced cyclobutane pyrimidine dimers from genomic DNA, but stil

206 oci and concomitantly reduced the removal of cyclobutane pyrimidine dimers from the entire genome.

207 hia coli uvrA, uvrB, and uvrC genes, removes cyclobutane pyrimidine dimers from the genome in a manne

208 different DNA repair genes on the removal of cyclobutane pyrimidine dimers from the individual strand

209 Elimination of cyclobutane pyrimidine dimers from the UV-damaged DNA by

210 of many DNA helix-distorting lesions such as cyclobutane pyrimidine dimers have been shown to be coup

211 We found that DDB can indeed recognize a cyclobutane pyrimidine dimer in DNA with an affinity (K(

212 Translesion replication (TR) past a cyclobutane pyrimidine dimer in Escherichia coli normall

213 had impaired repair of UV radiation-induced cyclobutane pyrimidine dimers in association with reduce

214 ioned as a proto-flavin capable of repairing cyclobutane pyrimidine dimers in DNA or RNA by photoindu

215 ulations can be used to predict the yield of cyclobutane pyrimidine dimers in DNA.

216 in immune responses through the induction of cyclobutane pyrimidine dimers in DNA.

217 -free bypass of ultraviolet ray (UV)-induced cyclobutane pyrimidine dimers in DNA.

218 -free bypass of ultraviolet ray (UV)-induced cyclobutane pyrimidine dimers in DNA.

219 ASA reduced UVB-induced 8-oxoguanine and cyclobutane pyrimidine dimers in Melan-A melanocytes and

220 arkedly reduced the PR and NER of UV-induced cyclobutane pyrimidine dimers in MFA2 but much less so i

221 hat hamster cells fail to efficiently repair cyclobutane pyrimidine dimers in nontranscribed DNA and

222 tolyases with high degree of specificity for cyclobutane pyrimidine dimers in ssDNA.

223 e documented transcription-coupled repair of cyclobutane pyrimidine dimers in the ataxia telangiectas

224 o study removal of ultraviolet light-induced cyclobutane pyrimidine dimers in the MDR1 gene at differ

225 A spectrum of deaminated cis-syn cyclobutane pyrimidine dimers in the supF gene was deter

226 The frequency of cyclobutane pyrimidine dimers in UV-irradiated pRGC.FOS.

227 appa in the extension reaction opposite from cyclobutane pyrimidine dimers in vivo.

228 The repair of UV-induced photoproducts (cyclobutane pyrimidine dimers) in a well-characterized m

229 that it replicates past 5'T-T3' and 5'T-U3' cyclobutane pyrimidine dimers, incorporating G or T nucl

230 The major UV-induced lesion, the cyclobutane pyrimidine dimer, increased in frequency in

231 Cyclobutane pyrimidine dimers induced by direct UVB abso

232 53 promoters is nearly twice as sensitive to cyclobutane pyrimidine dimer induction by UV irradiation

233 photolyase, a photoenzyme, splits UV-induced cyclobutane pyrimidine dimer into two normal bases.

234 the glycosyl bond of the 5' pyrimidine of a cyclobutane pyrimidine dimer is hypothesized to occur th

235 roperties, the capacity of guanine to repair cyclobutane pyrimidine dimer is not clearly established.

236 we demonstrate that a single, site-specific, cyclobutane pyrimidine dimer leading-strand template les

237 opposite strand preference is observed for a cyclobutane pyrimidine dimer lesion.

238 UVB-induced sunburn cells, 8-oxoguanine, and cyclobutane pyrimidine dimer lesions in skin of melanoma

239 ressing cells exhibit compromised removal of cyclobutane pyrimidine dimer lesions, a characteristic o

240 teins that bind to UV-damaged DNA containing cyclobutane pyrimidine dimer lesions.

241 ytosine deamination rates in UV-induced CPD (cyclobutane pyrimidine dimer) lesions to precisely map t

242 ial nucleotide excision repair of UV-induced cyclobutane pyrimidine dimers located in transcribed mam

243 UVB readily induces cyclobutane pyrimidine dimers, mainly thymine dimers (TT

244 ttermates (1) elevated the levels of neither cyclobutane pyrimidine dimer nor pyrimidine (6-4) pyrimi

245 uction of T4 endonuclease V accessibility to cyclobutane pyrimidine dimers on UV-irradiated mononucle

246 ubstrates containing a single, site-specific cyclobutane pyrimidine dimer or a pyrimidine (6-4) pyrim

247 coli replisome can directly bypass a single cyclobutane pyrimidine dimer or abasic site by translesi

248 rs and nucleosome-positioning DNA containing cyclobutane pyrimidine dimers or 6-4 photoproducts photo

249 utilized monoclonal antibodies specific for cyclobutane pyrimidine dimers or 6-4 photoproducts, resp

250 However, recent studies of repair of cyclobutane pyrimidine dimers or benzo[a]pyrene diol epo

251 ells, like XP cells, could not repair either cyclobutane pyrimidine dimers or non-dimer photoproducts

252 UVR, no significant differences in epidermal cyclobutane pyrimidine dimers or sunburn cell (SBC) form

253 Remarkably, more than 10(10) cyclobutane pyrimidine dimers or(6-4) photoproducts are

254 51-mers containing site-specific T-T cis-syn-cyclobutane pyrimidine-dimers or T-T pyrimidine-(6-4')py

255 aracterized intrastrand cross-links, such as cyclobutane pyrimidines dimers or cisplatin-DNA complex

256 violet (UV) photoproducts (primarily cis-syn cyclobutane pyrimidine dimers, or CPDs) in chromatin.

257 ctrum and is capable of faithfully bypassing cyclobutane pyrimidine dimer photolesions.

258 The presence of a cyclobutane pyrimidine dimer photolyase homologue in FPV

259 ligase), a photoreactivation repair pathway (cyclobutane pyrimidine dimer photolyase), a LINE-type re

260 D to substrate, in a manner analogous to the cyclobutane pyrimidine dimer photolyase.

261 observed that MSH2 can facilitate TLS across cyclobutane pyrimidine dimers photoproducts in living ce

262 on and NF-kappaB inhibition markedly reduced cyclobutane pyrimidine dimers-positive cells.

263 % relative humidity resulted in formation of cyclobutane pyrimidine dimers (Py lozengePy) or SP, resp

264 Cis-syn cyclobutane pyrimidine dimers (pyrimidine dimers) are th

265 The frequency of all possible cyclobutane pyrimidine dimers, pyrimidine (6-4) pyrimido

266 ical fluorescein adducts, abasic sites nor a cyclobutane pyrimidine dimer, regardless of whether thes

267 By 72 hours, 54 +/- 5% cyclobutane pyrimidine dimers remained in vehicle-fed ve

268 ntioxidant N-acetyl cysteine also attenuated cyclobutane pyrimidine dimer removal but did not enhance

269 xcision repair is normal, but the pattern of cyclobutane pyrimidine dimer removal suggests that trans

270 ation via Cox-2 enzyme inhibition, increased cyclobutane pyrimidine dimer removal, and reduction of o

271 the Structure of Chromatin) and show greater cyclobutane pyrimidine dimer repair compared with unacet

272 mutated) activation, decreased efficiency in cyclobutane pyrimidine dimer repair, and elevated sensit

273 ns of PARP inhibitor, PJ-34, caused WT-level cyclobutane pyrimidine dimer repair.

274 tasets of XR-seq, Damage-seq, adductSeq, and cyclobutane pyrimidine dimer-seq, we show that neither r

275 C nuclease, but resistant to cleavage by the cyclobutane pyrimidine dimer-specific enzyme T4 endonucl

276 When cyclobutane pyrimidine dimers stall DNA replication by D

277 ed in binding of the flavin cofactor and the cyclobutane pyrimidine dimer substrate, we report our di

278 ta indicate that Pol eta-dependent bypass of cyclobutane pyrimidine dimers suppresses UV light-induce

279 dithymine photoproducts, namely, the cis,syn-cyclobutane pyrimidine dimer (T[c,s]T) and the pyrimidin

280 deoxycytidine is more efficiently generating cyclobutane pyrimidine dimers than 5-formyl-2'-deoxyurid

281 Previously we reported that a cyclobutane pyrimidine dimer that is repaired preferenti

282 excision repair protein that incises DNA at cyclobutane pyrimidine dimers that are formed as a conse

283 UV radiation principally produces cyclobutane pyrimidine dimers that are repaired by nucle

284 romoting DNA synthesis past sunlight-induced cyclobutane pyrimidine dimers that escape nucleotide exc

285 When two rATPs were inserted opposite a cyclobutane pyrimidine dimer, the substrate was less eff

286 nsitizers and have the potential to generate cyclobutane pyrimidine dimers upon irradiation with UV l

287 e context upon RNA polymerase II arrest by a cyclobutane pyrimidine dimer using an in vitro transcrip

288 Replication of a cyclobutane pyrimidine dimer was accurate, whereas repli

289 UVB-induced DNA damage (cyclobutane pyrimidine dimers) was resolved rapidly in G

290 quently as intermediates in the formation of cyclobutane pyrimidine dimers, we find neither computati

291 enome scale analysis of repair of UV-induced cyclobutane pyrimidine dimers, we find that the Mfd prot

292 The distribution and persistence of cyclobutane pyrimidine dimers were investigated in mouse

293 nd global genomic repair (GGR) of UV-induced cyclobutane pyrimidine dimers were investigated in the y

294 M13 ss DNA molecules containing cyclobutane pyrimidine dimers were maintained but not re

295 h after 10 J/m2 irradiation, only 4% of the cyclobutane pyrimidine dimers were removed in the BCL2-o

296 DNA synthesis much more than persistence of cyclobutane pyrimidine dimers (which appear to be effici

297 Cyclobutane pyrimidine dimers, which have been previousl

298 UVB increased the repair rate of UVB-induced cyclobutane pyrimidine dimers, while inhibiting UVB-indu

299 the repair of ultraviolet radiation-induced cyclobutane pyrimidine dimers within exon 8 of p53 gene

300 l eta to efficiently bypass UV light-induced cyclobutane pyrimidine dimers, XPV cells lacking Pol eta