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

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

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

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

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

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

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

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

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

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

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

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

14 6-4) pyrimidine-pyrimidone photoproducts and cyclobutane pyrimidine dimers.

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

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

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

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

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

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

21 However, cyclobutane pyrimidine dimer accumulation was higher in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 Cyclobutane pyrimidine dimers are the major DNA photopro

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

52 96A displayed a reduced repair efficiency of cyclobutane pyrimidine dimers as compared with cells com

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

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

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

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

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

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

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

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

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

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

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

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

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

66 The cyclobutane pyrimidine dimer class III photolyases are s

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

96 12 knockout (KO) mice using the formation of cyclobutane pyrimidine dimers (CPD) as an indicator of t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

119 Cyclobutane pyrimidine dimers (CPDs) are DNA photoproduc

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

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

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

123 Cyclobutane pyrimidine dimers (CPDs) are responsible for

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

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

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

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

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

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

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

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

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

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

134 Cyclobutane pyrimidine dimers (CPDs) constitute the most

135 6B) by strand-specific removal of UV-induced cyclobutane pyrimidine dimers (CPDs) from a 16 Kb fragme

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

195 Cyclobutane pyrimidine dimers induced by direct UVB abso

196 53 promoters is nearly twice as sensitive to cyclobutane pyrimidine dimer induction by UV irradiation

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

214 51-mers containing site-specific T-T cis-syn-cyclobutane pyrimidine-dimers or T-T pyrimidine-(6-4')py

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

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

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

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

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

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

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

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

223 % relative humidity resulted in formation of cyclobutane pyrimidine dimers (Py lozengePy) or SP, resp

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

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

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

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

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

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

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

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

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

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

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

235 When cyclobutane pyrimidine dimers stall DNA replication by D

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

251 Cyclobutane pyrimidine dimers, which have been previousl

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

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

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