ライフサイエンスコーパス: pyrimidine dimer

1 the cytosine or 5-methylcytosine within the pyrimidine dimer.

2 s opposite the two thymines of a cyclobutane pyrimidine dimer.

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

4 ona fide photolyase that repairs cyclobutane pyrimidine dimers.

5 uitment of XPC and the repair of cyclobutane pyrimidine dimers.

6 as a representative agent acting by inducing pyrimidine dimers.

7 hr, is a photolyase specific for cyclobutane pyrimidine dimers.

8 at is blocked in the excision of cyclobutane pyrimidine dimers.

9 plicate through UV-light-induced cyclobutane pyrimidine dimers.

10 the levels of frequent photoproducts such as pyrimidine dimers.

11 DNA damage, faithfully bypassing cyclobutane pyrimidine dimers.

12 atalyzes the photorepair of cyclobutane-type pyrimidine dimers.

13 re photoproduct [SP]) instead of cyclobutane pyrimidine dimers.

14 se (PDG) that initiates repair of UV-induced pyrimidine dimers.

15 nslesion synthesis past cis, syn-cyclobutane pyrimidine dimers.

16 or deficient (CTag) in bypass replication of pyrimidine dimers.

17 that catalyzes the light-dependent repair of pyrimidine dimers.

18 ected mismatch repair and excision repair of pyrimidine dimers.

19 and recently identified for Pol II bypass of pyrimidine dimers.

20 an increased resolution rate of cyclobutane pyrimidine dimers.

21 hotoproducts in the DNA, such as cyclobutane pyrimidine dimers.

22 repair of 6-4 photoproducts and cyclobutane pyrimidine dimers.

23 ine-pyrimidone photoproducts and cyclobutane pyrimidine dimers.

24 bles replication through ultraviolet-induced pyrimidine dimers.

25 in an error-free mode to repair cyclobutane pyrimidine dimers.

26 oth DNA partners contain ultraviolet-induced pyrimidine dimers (0.6 dimer per 100 nt).

27 eased detection of gammaH2AX and cyclobutane pyrimidine dimers 24 hours after UVB radiation.

28 ol zeta has been established for cyclobutane pyrimidine dimers, (6-4) dipyrimidine photoproducts, and

29 However, cyclobutane pyrimidine dimer accumulation was higher in ham1 than in

30 that form the highest levels of cyclobutane pyrimidine dimers after irradiation with sunlight but no

31 ted reduced repair of UV-induced cyclobutane pyrimidine dimers after PARP inhibition, suggesting that

32 nd accelerated the resolution of cyclobutane pyrimidine dimers after UVL exposures in P388 and XS52.

33 mage, such as the formation of abasic sites, pyrimidine dimers, alkylation adducts, or oxidative lesi

34 lysis indicated a reduction in the extent of pyrimidine dimer and 6-4 photoproduct removal in the Dna

35 posite the UV-induced DNA lesion cyclobutane pyrimidine dimer and was recently found to incorporate r

36 strates containing site-specific cyclobutane pyrimidine dimers and (6-4) photoproducts for the charac

37 esis resulting from TLS opposite cyclobutane pyrimidine dimers and (6-4) photoproducts formed at the

38 efficient removal of UV-induced cyclobutane pyrimidine dimers and (iii) p300 is recruited to DNA dam

39 that 5 kJ m-2 induced about 1.2 cyclobutane pyrimidine dimers and 0.1 [6-4]photoproducts per kbp of

40 types of UVB-induced DNA damage, cyclobutane pyrimidine dimers and 6,4-photoproducts, by facilitating

41 enomic repair of both UV-induced cyclobutane pyrimidine dimers and 6-4 photoproducts but exhibited no

42 ncy-produces DNA lesions such as cyclobutane pyrimidine dimers and 6-4 photoproducts in skin.

43 nd markers of DNA damage such as cyclobutane pyrimidine dimers and 8-OHdG.

44 ta can replicate through cis-syn cyclobutane pyrimidine dimers and 8-oxoguanine lesions with the same

45 (Glu-23) would be important for catalysis at pyrimidine dimers and abasic sites.

46 same enzyme system responsible for removing pyrimidine dimers and other bulky DNA adducts.

47 Other photolesions including cyclobutane pyrimidine dimers and pyrimidine (6-4) pyrimidone photop

48 exposure, and excision repair of cyclobutane pyrimidine dimers and pyrimidine(6-4)pyrimidone dimers w

49 othelin-1 enhanced the repair of cyclobutane pyrimidine dimers and reduced the levels of hydrogen per

50 abled analysis of local sequence bias around pyrimidine dimers and suggested a preference for an aden

51 nhances global genomic repair of cyclobutane pyrimidine dimers and suppresses UV-induced mutagenesis.

52 ollowing UV light-induced DNA damage such as pyrimidine dimers and the 6-(1,2)-dihydro-2-oxo-4-pyrimi

53 y severely impairs the repair of cyclobutane pyrimidine dimers and, to a lesser extent, affects the r

54 basic site and a thymine-thymine cyclobutane pyrimidine dimer, and predominantly makes base pair subs

55 tion through ultraviolet-induced cyclobutane pyrimidine dimers, and inactivation of Poleta (also know

56 curate synthesis of DNA opposite cyclobutane pyrimidine dimers, and inactivation of Poleta in humans

57 ity for (6-4) photoproducts than cyclobutane pyrimidine dimers, and some affinity for DNA treated wit

58 d ascomycin inhibited removal of cyclobutane pyrimidine dimers, and that they also inhibited UVB-indu

59 tion of cytosines within cis-syn cyclobutane pyrimidine dimers, and these two events combined led to

60 cular recognition of the cis,syn cyclobutane pyrimidine dimer are reported.

61 rom these data, we conclude that cyclobutane pyrimidine dimers are at least 20 to 40 times more frequ

62 onstrates that DNAs containing both types of pyrimidine dimers are cleaved by the enzyme with similar

63 Cyclobutane pyrimidine dimers are the major DNA photoproducts produc

64 Low yields of photoproducts, namely pyrimidine dimers, are also revealed using the enzyme T4

65 The lesions induced by UV light, cyclobutane pyrimidine dimers, are known to be repaired by TCR where

66 d a reduced repair efficiency of cyclobutane pyrimidine dimers as compared with cells complemented wi

67 ut normal levels of XPC, continued to repair pyrimidine dimers as efficiently as control cells with n

68 t showed similar accumulation of cyclobutane pyrimidine dimers as wild-type plants, in contrast to th

69 ferent gene products for effective repair of pyrimidine dimers, as well as the nonspecific nature of

70 viously analyzed repair rates of cyclobutane pyrimidine dimers at nucleotide resolution along the hum

71 able to replicate across cis-syn cyclobutane pyrimidine dimers both accurately and efficiently.

72 ydro-8-oxo-2'-deoxyguanosine and cyclobutane pyrimidine dimer but with rates that are 10(3)-fold lowe

73 pecific not only for the cis-syn cyclobutane pyrimidine dimer, but also for the trans-syn-II isomer.

74 radiation photoproduct in DNA, a cyclobutane pyrimidine dimer, but no significant direct binding of D

75 -prone, as it is for bypass of a cyclobutane pyrimidine dimer by DNA polymerase eta (XP-V or Rad30) o

76 tween the catalytic cofactor FADH(-) and the pyrimidine dimer by the method of interatomic tunneling

77 he number of nuclei positive for cyclobutane pyrimidine dimers by 40% (P < 0.0002) and for 8-hydroxy-

78 enhance the repair of UV-induced cyclobutane pyrimidine dimers by UV photolyase.

79 The repair of UV light-induced cyclobutane pyrimidine dimers can proceed via the base excision repa

80 or RNA strand in proximity to a cyclobutane pyrimidine dimer, can mimic the function of a flavin in

81 is responsible for formation of cyclobutane pyrimidine dimers causing skin cancer.

82 The cyclobutane pyrimidine dimer class III photolyases are structurally

83 bypass of a nonadjacent cis-syn cyclobutane pyrimidine dimer containing a single intervening nucleot

84 for their ability to replicate a cyclobutane pyrimidine dimer-containing DNA template and find that b

85 -throughput sequencing of short, cyclobutane pyrimidine dimer-containing ssDNA oligos generated durin

86 F-G), a (6-4) photoproduct, or a cyclobutane pyrimidine dimer (CPD) and measured the repair of these

87 ontaining a specifically located cyclobutane pyrimidine dimer (CPD) and purified RNA polymerase II (R

88 o major DNA damage products, the cyclobutane pyrimidine dimer (CPD) and, at a lower frequency, the py

89 oincide with sites of UV-induced cyclobutane pyrimidine dimer (CPD) formation.

90 oincide with sites of UV-induced cyclobutane pyrimidine dimer (CPD) formation.

91 h are also sites of preferential cyclobutane pyrimidine dimer (CPD) formation.

92 oincide with sites of UV-induced cyclobutane pyrimidine dimer (CPD) formation.

93 e Rad4 bound to DNA containing a cyclobutane pyrimidine dimer (CPD) lesion.

94 ed oligonucleotides containing a cyclobutane pyrimidine dimer (CPD) lesion.

95 plicate through a leading-strand cyclobutane pyrimidine dimer (CPD) lesion.

96 of their incapability to repair cyclobutane pyrimidine dimer (CPD) lesions in duplex DNA.

97 been studied for years, data on cyclobutane pyrimidine dimer (CPD) repair in these cells at differen

98 rested at a specifically located cyclobutane pyrimidine dimer (CPD) using enzymatic probes and an in

99 R) of the major UV photoproduct (cyclobutane pyrimidine dimer (CPD)) in DNA.

100 the major UV-induced lesion, the cyclobutane pyrimidine dimer (CPD), but had no effect on the global

101 ontaining the UV-damaged adduct, cyclobutane pyrimidine dimer (CPD), to transfect human cells, and re

102 let (UV)-induced DNA damage, the cyclobutane pyrimidine dimer (CPD), to two normal bases by splitting

103 induced by UV irradiation is the cyclobutane pyrimidine dimer (CPD), which forms at positions of neig

104 exclusively for single-stranded cyclobutane pyrimidine dimer (CPD)-containing DNA substrate.

105 ) coding for a putative class II cyclobutane pyrimidine dimer (CPD)-photolyase in the genome of FPV.

106 ifference in the initial rate of cyclobutane pyrimidine dimer (CPD)-removal from the skin following U

107 We have developed a cyclobutane pyrimidine dimer (CPD)-specific immunoprecipitation meth

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

109 We measured cyclobutane pyrimidine dimers (CPD) and 6-4 photoproducts (6-4PP) by

110 Ultraviolet light induces cyclobutane pyrimidine dimers (CPD) and pyrimidine(6-4)pyrimidone ph

111 (KO) mice using the formation of cyclobutane pyrimidine dimers (CPD) as an indicator of the extent of

112 the number of UV-induced cis-syn cyclobutane pyrimidine dimers (CPD) between HTB1 and htb1-3 strains.

113 as well as 6-4-photoproducts and cyclobutane pyrimidine dimers (CPD) in the skin, which further cause

114 ively affects the elimination of cyclobutane pyrimidine dimers (CPD), but not of pyrimidine (6, 4)pyr

115 sorption or for the induction of cyclobutane pyrimidine dimers (CPD).

116 analysis identified the cis-syn cyclobutane pyrimidine-dimer (CPD) as a distinctive UVB-induced lesi

117 pair of the UV-induced damage of cyclobutane pyrimidine dimers (CPDs) (at 1, 4, 8, 16, 24, and 48 h)

118 of epidermal cells positive for cyclobutane pyrimidine dimers (CPDs) 50% immediately post-irradiatio

119 n of photodimeric lesions, i.e., cyclobutane pyrimidine dimers (CPDs) and (6-4) photoproducts [(6-4)P

120 uced DNA damages in human cells: cyclobutane pyrimidine dimers (CPDs) and (6-4) pyrimidine-pyrimidone

121 n predominantly in DNA repair of cyclobutane pyrimidine dimers (CPDs) and 6-4 photolesions caused by

122 charomyces pombe that recognizes cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4 PPs)

123 major UV-induced photoproducts, cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs),

124 els of global repair (removal of cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts) and tran

125 se adducts, including UV-induced cyclobutane pyrimidine dimers (CPDs) and BaP diol epoxide-deoxyguano

126 roduce DNA damage in the form of cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4) pyrimidone

127 th the predominant lesions being cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4) pyrimidone

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

129 amage that occurs in the form of cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyrimidone (6-4)

130 to cleave 5' to UV light-induced cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyrimidone (6-4)

131 Damage maps of both cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyrimidone (6-4)

132 tes two major photoproducts, the cyclobutane pyrimidine dimers (CPDs) and the 6-4 photoproducts (6-4

133 A lesions induced by UVB are the cyclobutane pyrimidine dimers (CPDs) and the pyrimidine (6-4) pyrimi

134 Cyclobutane pyrimidine dimers (CPDs) are DNA photoproducts linked to

135 er ovary (CHO) cells, UV-induced cyclobutane pyrimidine dimers (CPDs) are preferentially repaired in

136 while ultraviolet light-induced cyclobutane pyrimidine dimers (CPDs) are preferentially repaired in

137 l types of DNA damage, including cyclobutane pyrimidine dimers (CPDs) are repaired with equal efficie

138 Cyclobutane pyrimidine dimers (CPDs) are responsible for a considera

139 Cis-syn cyclobutane pyrimidine dimers (CPDs) are the most frequently formed

140 induced DNA lesions, the cis-syn cyclobutane pyrimidine dimers (CPDs) are thought to be the most muta

141 let (UVC) light not only produce cyclobutane pyrimidine dimers (CPDs) as reported but also cause sign

142 pyrimidines, generating cis-syn cyclobutane pyrimidine dimers (CPDs) as the most common lesion.

143 alysed the removal of UV-induced cyclobutane pyrimidine dimers (CPDs) at nucleotide resolution from t

144 seq, to precisely map UV-induced cyclobutane pyrimidine dimers (CPDs) at single-nucleotide resolution

145 air of ultraviolet light-induced cyclobutane pyrimidine dimers (CPDs) at the nucleotide level in exon

146 results in the formation of anti cyclobutane pyrimidine dimers (CPDs) between loop 1 and loop 3 in th

147 it enhanced repair of UV-induced cyclobutane pyrimidine dimers (CPDs) compared to wild-type (wt).

148 Cyclobutane pyrimidine dimers (CPDs) constitute the most frequent UV

149 d-specific removal of UV-induced cyclobutane pyrimidine dimers (CPDs) from a 16 Kb fragment of the p5

150 r cells, and enhanced removal of cyclobutane pyrimidine dimers (CPDs) from genomic DNA and from the n

151 eration of photoproducts such as cyclobutane pyrimidine dimers (CPDs) has been suggested.

152 pair of ultraviolet (UV)-induced cyclobutane pyrimidine dimers (CPDs) in identical sequences under bo

153 UV-induced cyclobutane pyrimidine dimers (CPDs) in the template DNA strand stal

154 at occur in AT-rich DNA, such as cyclobutane pyrimidine dimers (CPDs) induced by UV radiation.

155 ss whether removal of UV-induced cyclobutane pyrimidine dimers (CPDs) occurs with equal efficiency at

156 UV-light-induced cyclobutane pyrimidine dimers (CPDs) present a severe block to synth

157 Photoreactive repair (PR) of cyclobutane pyrimidine dimers (CPDs) was mapped at nucleotide resolu

158 Repair of UV-induced cyclobutane pyrimidine dimers (CPDs) was measured in a yeast minichr

159 ision repair (NER) of UV-induced cyclobutane pyrimidine dimers (CPDs) was measured in the individual

160 e precursor cells, and repair of cyclobutane pyrimidine dimers (CPDs) was not detected in the hNT neu

161 cally, DNA damage in the form of cyclobutane pyrimidine dimers (CPDs) was repaired more efficiently i

162 Maximum and comparable cyclobutane pyrimidine dimers (CPDs) were detected immediately after

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

164 repair especially the repair of cyclobutane pyrimidine dimers (CPDs), and is regulated by p53 in hum

165 ight-induced melanoma arise from cyclobutane pyrimidine dimers (CPDs), DNA photoproducts that are typ

166 anscription bypass of UV-induced cyclobutane pyrimidine dimers (CPDs), increases survival of UV irrad

167 ases (pdgs) that initiate BER of cyclobutane pyrimidine dimers (CPDs), the predominant UV-induced les

168 icant amount of abasic sites and cyclobutane pyrimidine dimers (CPDs).

169 lesion synthesis past deaminated cyclobutane pyrimidine dimers (CPDs).

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

171 UV-induced photoproducts (cyclobutane pyrimidine dimers, CPDs) in DNA are removed by nucleotid

172 operties of UV-B irradiation, or cyclobutane pyrimidine dimers differ qualitatively from double-stran

173 to accurately bypass UV-induced cyclobutane pyrimidine dimers during a process termed translesion sy

174 izing radiation and normal ability to bypass pyrimidine dimers during DNA replication soon after UVC

175 Purified polV(R391) can also bypass a T-T pyrimidine dimer efficiently and displays greater accura

176 er, how bulky base damage such as UV-induced pyrimidine dimers elicits a checkpoint response has rema

177 ch as 8-oxo-2'-deoxyguanosine or cyclobutane pyrimidine dimer, even in the presence of an equal amoun

178 reduced efficiency to UV-induced cyclobutane pyrimidine dimer foci.

179 also used Excision-seq to identify sites of pyrimidine dimer formation induced by UV light exposure,

180 The quantum yield of cyclobutane pyrimidine dimer formation was calculated as the number

181 Moreover, UV-induced cyclobutane pyrimidine dimer formation was markedly enhanced in ribo

182 ated with high levels of cis-syn cyclobutane pyrimidine dimer formation.

183 tations may be derived from solar UV-induced pyrimidine dimers forming at sequences that contain 5-me

184 ned data make a strong case that cyclobutane pyrimidine dimers forming preferentially at dipyrimidine

185 pression vector, the excision of cyclobutane pyrimidine dimers from bulk DNA, or unscheduled DNA synt

186 omitantly reduced the removal of cyclobutane pyrimidine dimers from the entire genome.

187 Elimination of cyclobutane pyrimidine dimers from the UV-damaged DNA by enzymatic p

188 dg, homology modeling of the Chlorella virus pyrimidine dimer glycosylase (cv-pdg) predicted that a c

189 as been investigated for the Chlorella virus pyrimidine dimer glycosylase (cv-pdg).

190 Bacteriophage T4 pyrimidine dimer glycosylase (T4-Pdg) is a base excision

191 dine residue at position 16 in the mature T4 pyrimidine dimer glycosylase (T4-PDG) protein has been s

192 ntified a critical residue (His16) in the T4-pyrimidine dimer glycosylase (T4-Pdg) that, when mutated

193 from the bacteriophage T4 (T4 bacteriophage pyrimidine dimer glycosylase (T4-pdg)).

194 ructural information on the bacteriophage T4 pyrimidine dimer glycosylase (T4-pdg), the catalytic mec

195 ly slower than the rate of formation of a T4-pyrimidine dimer glycosylase (T4-pdg)-DNA intermediate.

196 These enzymes, pyrimidine dimer glycosylase I and II (Nmu-pdg I and Nmu

197 ical characterization of the chlorella virus pyrimidine dimer glycosylase, cv-PDG.

198 -His-Arg-Gly-Tyr, and the 16 kDa protein, T4 pyrimidine dimer glycosylase/apurinic/apyrimidinic site

199 ific DPCs, the catalytic chemistry of the T4 pyrimidine dimer glycosylase/apurinic/apyrimidinic site

200 helix-distorting lesions such as cyclobutane pyrimidine dimers have been shown to be coupled in cells

201 that DDB can indeed recognize a cyclobutane pyrimidine dimer in DNA with an affinity (K(app)a) 6-fol

202 nslesion replication (TR) past a cyclobutane pyrimidine dimer in Escherichia coli normally requires t

203 d repair of UV radiation-induced cyclobutane pyrimidine dimers in association with reduced levels of

204 a light-activated flavoenzyme that binds to pyrimidine dimers in DNA and repairs them in a reaction

205 Induction of pyrimidine dimers in DNA by solar UV radiation has drast

206 roto-flavin capable of repairing cyclobutane pyrimidine dimers in DNA or RNA by photoinduced electron

207 be used to predict the yield of cyclobutane pyrimidine dimers in DNA.

208 sponses through the induction of cyclobutane pyrimidine dimers in DNA.

209 ced the PR and NER of UV-induced cyclobutane pyrimidine dimers in MFA2 but much less so in RPB2, wher

210 cells fail to efficiently repair cyclobutane pyrimidine dimers in nontranscribed DNA and fail to expr

211 artificial photolyase models that recognize pyrimidine dimers in protic and aprotic organic solvents

212 h high degree of specificity for cyclobutane pyrimidine dimers in ssDNA.

213 transcription-coupled repair of cyclobutane pyrimidine dimers in the ataxia telangiectasia-mutated (

214 tified as photolyases that remove UV-induced pyrimidine dimers in the presence of visible light.

215 A spectrum of deaminated cis-syn cyclobutane pyrimidine dimers in the supF gene was determined using

216 can nontarget DNA and processively incise at pyrimidine dimers in UV-irradiated DNA.

217 The frequency of cyclobutane pyrimidine dimers in UV-irradiated pRGC.FOS.CAT was dete

218 promote efficient and accurate bypass of T-T pyrimidine dimers in vivo.

219 extension reaction opposite from cyclobutane pyrimidine dimers in vivo.

220 licates past 5'T-T3' and 5'T-U3' cyclobutane pyrimidine dimers, incorporating G or T nucleotides oppo

221 Cyclobutane pyrimidine dimers induced by direct UVB absorption were

222 poleta) is required for bypass of UV-induced pyrimidine dimers inserting adenine nucleotides opposite

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

224 cherichia coli photolyase suggested that the pyrimidine dimer is flipped out of the DNA helix and int

225 l bond of the 5' pyrimidine of a cyclobutane pyrimidine dimer is hypothesized to occur through the de

226 demonstrate that deamination of cytosine in pyrimidine dimers is a significant event that most likel

227 te that a single, site-specific, cyclobutane pyrimidine dimer leading-strand template lesion provides

228 m an excited pi --> pi* singlet state to the pyrimidine dimer lesion of DNA.

229 and preference is observed for a cyclobutane pyrimidine dimer lesion.

230 DNA photolyase repairs pyrimidine dimer lesions in DNA through light-induced el

231 s exhibit compromised removal of cyclobutane pyrimidine dimer lesions, a characteristic of cells that

232 ind to UV-damaged DNA containing cyclobutane pyrimidine dimer lesions.

233 , is the only identified nonphotoactivatable pyrimidine dimer lyase.

234 UVB readily induces cyclobutane pyrimidine dimers, mainly thymine dimers (TTs), and pyri

235 ) elevated the levels of neither cyclobutane pyrimidine dimer nor pyrimidine (6-4) pyrimidone dimer,

236 re, these mutations point to a major role of pyrimidine dimers not only in UVB but also in UVA mutage

237 th an FAD chromophore that repair UV-induced pyrimidine dimers on the DNA in a light-dependent manner

238 endonuclease V accessibility to cyclobutane pyrimidine dimers on UV-irradiated mononucleosomes but n

239 ome can directly bypass a single cyclobutane pyrimidine dimer or abasic site by translesion synthesis

240 ses are specific for either cyclobutane-type pyrimidine dimers or (6-4) photoproducts.

241 osome-positioning DNA containing cyclobutane pyrimidine dimers or 6-4 photoproducts photolesions.

242 ificant differences in epidermal cyclobutane pyrimidine dimers or sunburn cell (SBC) formation were o

243 aining site-specific T-T cis-syn-cyclobutane pyrimidine-dimers or T-T pyrimidine-(6-4')pyrimidinone p

244 intrastrand cross-links, such as cyclobutane pyrimidines dimers or cisplatin-DNA complex adduct, is a

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

246 capable of faithfully bypassing cyclobutane pyrimidine dimer photolesions.

247 The presence of a cyclobutane pyrimidine dimer photolyase homologue in FPV suggests th

248 hotoreactivation repair pathway (cyclobutane pyrimidine dimer photolyase), a LINE-type reverse transc

249 te, in a manner analogous to the cyclobutane pyrimidine dimer photolyase.

250 induces predominantly cyclobutane and (6-4) pyrimidine dimer photoproducts in DNA.

251 e bypass probability of non-cyclobutane-type pyrimidine dimer photoproducts should not be dismissed.

252 t MSH2 can facilitate TLS across cyclobutane pyrimidine dimers photoproducts in living cells, present

253 UV radiation produces clusters of cyclobutyl pyrimidine dimers, photoproducts that occur individually

254 ppaB inhibition markedly reduced cyclobutane pyrimidine dimers-positive cells.

255 radation depends on the amount of unrepaired pyrimidine dimers present; this degradation rate is init

256 umidity resulted in formation of cyclobutane pyrimidine dimers (Py lozengePy) or SP, respectively.

257 The frequency of all possible cyclobutane pyrimidine dimers, pyrimidine (6-4) pyrimidone photoprod

258 cein adducts, abasic sites nor a cyclobutane pyrimidine dimer, regardless of whether these modificati

259 By 72 hours, 54 +/- 5% cyclobutane pyrimidine dimers remained in vehicle-fed versus 31 +/-

260 ir is normal, but the pattern of cyclobutane pyrimidine dimer removal suggests that transcription-cou

261 x-2 enzyme inhibition, increased cyclobutane pyrimidine dimer removal, and reduction of oxidative DNA

262 *) form is also transiently generated during pyrimidine dimer repair by photoinduced electron transfe

263 e of Chromatin) and show greater cyclobutane pyrimidine dimer repair compared with unacetylated nucle

264 Pyrimidine dimer repair was accelerated in UV-irradiated

265 ivation, decreased efficiency in cyclobutane pyrimidine dimer repair, and elevated sensitivity of cel

266 nhibitor, PJ-34, caused WT-level cyclobutane pyrimidine dimer repair.

267 were consistent with the predicted number of pyrimidine dimers/repeat unit, with higher GFP activatio

268 this study, including double-strand breaks, pyrimidine dimers, single-strand breaks, base damage, an

269 ific BRAF tandem mutations, nearby potential pyrimidine dimer sites, the properties of specialized DN

270 Certain prokaryotes and viruses produce pyrimidine dimer-specific DNA glycosylases (pdgs) that i

271 Moreover, two different pyrimidine dimer-specific endonucleases cut approximatel

272 but resistant to cleavage by the cyclobutane pyrimidine dimer-specific enzyme T4 endonuclease V.

273 dsDNA-containing chlorella viruses encode a pyrimidine dimer-specific glycosylase (PDG) that initiat

274 clease V from bacteriophage T4, is a cis-syn pyrimidine dimer-specific glycosylase.

275 entification of this new enzyme with broader pyrimidine dimer specificity raises the intriguing possi

276 When cyclobutane pyrimidine dimers stall DNA replication by DNA polymeras

277 g of the flavin cofactor and the cyclobutane pyrimidine dimer substrate, we report our direct deconvo

278 that Pol eta-dependent bypass of cyclobutane pyrimidine dimers suppresses UV light-induced skin cance

279 otoproducts, namely, the cis,syn-cyclobutane pyrimidine dimer (T[c,s]T) and the pyrimidine(6-4)pyrimi

280 ceptibility to UV because of fewer potential pyrimidine dimer targets.

281 pair protein that incises DNA at cyclobutane pyrimidine dimers that are formed as a consequence of ex

282 V radiation principally produces cyclobutane pyrimidine dimers that are repaired by nucleotide excisi

283 synthesis past sunlight-induced cyclobutane pyrimidine dimers that escape nucleotide excision repair

284 DNA damage products, largely in the form of pyrimidine dimers, that are both toxic and mutagenic.

285 ads to clean and rapid cycloreversion of the pyrimidine dimer through photoinduced electron transfer

286 state of the purine donates an electron to a pyrimidine dimer to initiate bond cleavage; subsequent b

287 on RNA polymerase II arrest by a cyclobutane pyrimidine dimer using an in vitro transcription system

288 DNA photolyases repair pyrimidine dimers via a reaction in which light energy d

289 Replication of a cyclobutane pyrimidine dimer was accurate, whereas replication of an

290 UVB-induced DNA damage (cyclobutane pyrimidine dimers) was resolved rapidly in GTPs-treated

291 distribution and persistence of cyclobutane pyrimidine dimers were investigated in mouse skin after

292 nomic repair (GGR) of UV-induced cyclobutane pyrimidine dimers were investigated in the yeast GAL1-10

293 raction is capable of excision of UV-induced pyrimidine dimers when reconstituted with a cytoplasmic

294 of K(a) = 1.0 x 10(3) M(-1) with the cis,syn pyrimidine dimer, whereas binding of the trans,syn isome

295 Cyclobutane pyrimidine dimers, which have been previously shown to b

296 d the repair rate of UVB-induced cyclobutane pyrimidine dimers, while inhibiting UVB-induced increase

297 tudies show that it forms a 1:1 complex with pyrimidine dimers with binding constants of approximatel

298 des a DNA photolyase that repairs UV-induced pyrimidine dimers with energy provided by visible light.

299 of ultraviolet radiation-induced cyclobutane pyrimidine dimers within exon 8 of p53 gene in normal an

300 iciently bypass UV light-induced cyclobutane pyrimidine dimers, XPV cells lacking Pol eta have dimini