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1 the cytosine or 5-methylcytosine within the pyrimidine dimer.
2 s opposite the two thymines of a cyclobutane pyrimidine dimer.
3 isome following collision with a cyclobutane pyrimidine dimer.
4 -induced linkages is the cis-syn cyclobutane pyrimidine dimer.
5 damage such as 8-oxoguanine and cyclobutane pyrimidine dimers.
6 bles replication through ultraviolet-induced pyrimidine dimers.
7 in an error-free mode to repair cyclobutane pyrimidine dimers.
8 ona fide photolyase that repairs cyclobutane pyrimidine dimers.
9 uitment of XPC and the repair of cyclobutane pyrimidine dimers.
10 as a representative agent acting by inducing pyrimidine dimers.
11 hr, is a photolyase specific for cyclobutane pyrimidine dimers.
12 at is blocked in the excision of cyclobutane pyrimidine dimers.
13 st dangerous DNA lesions such as cyclobutane pyrimidine dimers.
14 plicate through UV-light-induced cyclobutane pyrimidine dimers.
15 the levels of frequent photoproducts such as pyrimidine dimers.
16 atalyzes the photorepair of cyclobutane-type pyrimidine dimers.
17 re photoproduct [SP]) instead of cyclobutane pyrimidine dimers.
18 se (PDG) that initiates repair of UV-induced pyrimidine dimers.
19 nslesion synthesis past cis, syn-cyclobutane pyrimidine dimers.
20 or deficient (CTag) in bypass replication of pyrimidine dimers.
21 that catalyzes the light-dependent repair of pyrimidine dimers.
22 ected mismatch repair and excision repair of pyrimidine dimers.
23 DNA damage, faithfully bypassing cyclobutane pyrimidine dimers.
24 plate carrying two site-specific cyclobutane pyrimidine dimers.
25 and recently identified for Pol II bypass of pyrimidine dimers.
26 an increased resolution rate of cyclobutane pyrimidine dimers.
27 hotoproducts in the DNA, such as cyclobutane pyrimidine dimers.
28 repair of 6-4 photoproducts and cyclobutane pyrimidine dimers.
29 ine-pyrimidone photoproducts and cyclobutane pyrimidine dimers.
31 ol zeta has been established for cyclobutane pyrimidine dimers, (6-4) dipyrimidine photoproducts, and
32 sible for correctly replicating T-containing pyrimidine dimers, a phenomenon known as the 'A-rule'.
34 that form the highest levels of cyclobutane pyrimidine dimers after irradiation with sunlight but no
35 ted reduced repair of UV-induced cyclobutane pyrimidine dimers after PARP inhibition, suggesting that
36 nd accelerated the resolution of cyclobutane pyrimidine dimers after UVL exposures in P388 and XS52.
37 mage, such as the formation of abasic sites, pyrimidine dimers, alkylation adducts, or oxidative lesi
38 posite the UV-induced DNA lesion cyclobutane pyrimidine dimer and was recently found to incorporate r
39 strates containing site-specific cyclobutane pyrimidine dimers and (6-4) photoproducts for the charac
40 esis resulting from TLS opposite cyclobutane pyrimidine dimers and (6-4) photoproducts formed at the
41 efficient removal of UV-induced cyclobutane pyrimidine dimers and (iii) p300 is recruited to DNA dam
42 that 5 kJ m-2 induced about 1.2 cyclobutane pyrimidine dimers and 0.1 [6-4]photoproducts per kbp of
43 types of UVB-induced DNA damage, cyclobutane pyrimidine dimers and 6,4-photoproducts, by facilitating
46 ta can replicate through cis-syn cyclobutane pyrimidine dimers and 8-oxoguanine lesions with the same
48 Other photolesions including cyclobutane pyrimidine dimers and pyrimidine (6-4) pyrimidone photop
49 exposure, and excision repair of cyclobutane pyrimidine dimers and pyrimidine(6-4)pyrimidone dimers w
50 othelin-1 enhanced the repair of cyclobutane pyrimidine dimers and reduced the levels of hydrogen per
51 abled analysis of local sequence bias around pyrimidine dimers and suggested a preference for an aden
52 nhances global genomic repair of cyclobutane pyrimidine dimers and suppresses UV-induced mutagenesis.
53 ollowing UV light-induced DNA damage such as pyrimidine dimers and the 6-(1,2)-dihydro-2-oxo-4-pyrimi
54 y severely impairs the repair of cyclobutane pyrimidine dimers and, to a lesser extent, affects the r
55 basic site and a thymine-thymine cyclobutane pyrimidine dimer, and predominantly makes base pair subs
56 tion through ultraviolet-induced cyclobutane pyrimidine dimers, and inactivation of Poleta (also know
57 curate synthesis of DNA opposite cyclobutane pyrimidine dimers, and inactivation of Poleta in humans
58 ity for (6-4) photoproducts than cyclobutane pyrimidine dimers, and some affinity for DNA treated wit
59 d ascomycin inhibited removal of cyclobutane pyrimidine dimers, and that they also inhibited UVB-indu
60 tion of cytosines within cis-syn cyclobutane pyrimidine dimers, and these two events combined led to
62 rom these data, we conclude that cyclobutane pyrimidine dimers are at least 20 to 40 times more frequ
63 y DNA lesions such as UV-induced cyclobutane pyrimidine dimers are removed from the genome by concert
66 The lesions induced by UV light, cyclobutane pyrimidine dimers, are known to be repaired by TCR where
67 d a reduced repair efficiency of cyclobutane pyrimidine dimers as compared with cells complemented wi
68 ut normal levels of XPC, continued to repair pyrimidine dimers as efficiently as control cells with n
69 t showed similar accumulation of cyclobutane pyrimidine dimers as wild-type plants, in contrast to th
71 ydro-8-oxo-2'-deoxyguanosine and cyclobutane pyrimidine dimer but with rates that are 10(3)-fold lowe
72 pecific not only for the cis-syn cyclobutane pyrimidine dimer, but also for the trans-syn-II isomer.
73 radiation photoproduct in DNA, a cyclobutane pyrimidine dimer, but no significant direct binding of D
74 -prone, as it is for bypass of a cyclobutane pyrimidine dimer by DNA polymerase eta (XP-V or Rad30) o
75 tween the catalytic cofactor FADH(-) and the pyrimidine dimer by the method of interatomic tunneling
76 he number of nuclei positive for cyclobutane pyrimidine dimers by 40% (P < 0.0002) and for 8-hydroxy-
77 a and zeta, which creates C>T transitions at pyrimidine dimers by incorporating two dAMPs opposite of
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
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
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
100 the genome much faster than the cyclobutane pyrimidine dimer (CPD), owing to the more efficient reco
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
104 ) coding for a putative class II cyclobutane pyrimidine dimer (CPD)-photolyase in the genome of FPV.
105 ifference in the initial rate of cyclobutane pyrimidine dimer (CPD)-removal from the skin following U
110 (KO) mice using the formation of cyclobutane pyrimidine dimers (CPD) as an indicator of the extent of
111 the number of UV-induced cis-syn cyclobutane pyrimidine dimers (CPD) between HTB1 and htb1-3 strains.
112 as well as 6-4-photoproducts and cyclobutane pyrimidine dimers (CPD) in the skin, which further cause
113 ively affects the elimination of cyclobutane pyrimidine dimers (CPD), but not of pyrimidine (6, 4)pyr
114 analysis identified the cis-syn cyclobutane pyrimidine-dimer (CPD) as a distinctive UVB-induced lesi
115 pair of the UV-induced damage of cyclobutane pyrimidine dimers (CPDs) (at 1, 4, 8, 16, 24, and 48 h)
116 of epidermal cells positive for cyclobutane pyrimidine dimers (CPDs) 50% immediately post-irradiatio
117 n of photodimeric lesions, i.e., cyclobutane pyrimidine dimers (CPDs) and (6-4) photoproducts [(6-4)P
118 uced DNA damages in human cells: cyclobutane pyrimidine dimers (CPDs) and (6-4) pyrimidine-pyrimidone
119 n predominantly in DNA repair of cyclobutane pyrimidine dimers (CPDs) and 6-4 photolesions caused by
120 charomyces pombe that recognizes cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4 PPs)
121 major UV-induced photoproducts, cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs),
122 s per cell, mostly of two types: cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs).
123 se adducts, including UV-induced cyclobutane pyrimidine dimers (CPDs) and BaP diol epoxide-deoxyguano
124 th the predominant lesions being cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4) pyrimidone
125 DNA photoproducts, most notably cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4) pyrimidone
126 roduce DNA damage in the form of cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4) pyrimidone
127 to cleave 5' to UV light-induced cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyrimidone (6-4)
129 amage that occurs in the form of cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyrimidone (6-4)
130 tes two major photoproducts, the cyclobutane pyrimidine dimers (CPDs) and the 6-4 photoproducts (6-4
131 A lesions induced by UVB are the cyclobutane pyrimidine dimers (CPDs) and the pyrimidine (6-4) pyrimi
133 er ovary (CHO) cells, UV-induced cyclobutane pyrimidine dimers (CPDs) are preferentially repaired in
134 while ultraviolet light-induced cyclobutane pyrimidine dimers (CPDs) are preferentially repaired in
135 l types of DNA damage, including cyclobutane pyrimidine dimers (CPDs) are repaired with equal efficie
138 let (UVC) light not only produce cyclobutane pyrimidine dimers (CPDs) as reported but also cause sign
140 alysed the removal of UV-induced cyclobutane pyrimidine dimers (CPDs) at nucleotide resolution from t
141 seq, to precisely map UV-induced cyclobutane pyrimidine dimers (CPDs) at single-nucleotide resolution
142 air of ultraviolet light-induced cyclobutane pyrimidine dimers (CPDs) at the nucleotide level in exon
143 results in the formation of anti cyclobutane pyrimidine dimers (CPDs) between loop 1 and loop 3 in th
144 it enhanced repair of UV-induced cyclobutane pyrimidine dimers (CPDs) compared to wild-type (wt).
146 d-specific removal of UV-induced cyclobutane pyrimidine dimers (CPDs) from a 16 Kb fragment of the p5
147 r cells, and enhanced removal of cyclobutane pyrimidine dimers (CPDs) from genomic DNA and from the n
149 pair of ultraviolet (UV)-induced cyclobutane pyrimidine dimers (CPDs) in identical sequences under bo
152 ss whether removal of UV-induced cyclobutane pyrimidine dimers (CPDs) occurs with equal efficiency at
154 Photoreactive repair (PR) of cyclobutane pyrimidine dimers (CPDs) was mapped at nucleotide resolu
156 ision repair (NER) of UV-induced cyclobutane pyrimidine dimers (CPDs) was measured in the individual
157 e precursor cells, and repair of cyclobutane pyrimidine dimers (CPDs) was not detected in the hNT neu
158 cally, DNA damage in the form of cyclobutane pyrimidine dimers (CPDs) was repaired more efficiently i
161 g and bulky DNA lesions, such as cyclobutane pyrimidine dimers (CPDs), and DNA interstrand cross-link
162 repair especially the repair of cyclobutane pyrimidine dimers (CPDs), and is regulated by p53 in hum
163 ight-induced melanoma arise from cyclobutane pyrimidine dimers (CPDs), DNA photoproducts that are typ
164 anscription bypass of UV-induced cyclobutane pyrimidine dimers (CPDs), increases survival of UV irrad
165 ases (pdgs) that initiate BER of cyclobutane pyrimidine dimers (CPDs), the predominant UV-induced les
169 to repair of UVB-induced cis-syn cyclobutane pyrimidine-dimers (CPDs) together with rapid removal of
171 acilitating DDB2 localization to cyclobutane pyrimidine dimer crosslinks to govern their repair.
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 Purified polV(R391) can also bypass a T-T pyrimidine dimer efficiently and displays greater accura
175 er, how bulky base damage such as UV-induced pyrimidine dimers elicits a checkpoint response has rema
176 ch as 8-oxo-2'-deoxyguanosine or cyclobutane pyrimidine dimer, even in the presence of an equal amoun
177 the bipyrimidine models affords cyclobutane pyrimidine dimers, even in the presence of bulky substit
179 deamination of cytosine, producing uracil in pyrimidine dimers, followed by monomerization of the dim
180 also used Excision-seq to identify sites of pyrimidine dimer formation induced by UV light exposure,
184 tations may be derived from solar UV-induced pyrimidine dimers forming at sequences that contain 5-me
185 ned data make a strong case that cyclobutane pyrimidine dimers forming preferentially at dipyrimidine
186 pression vector, the excision of cyclobutane pyrimidine dimers from bulk DNA, or unscheduled DNA synt
188 A, uvrB, and uvrC genes, removes cyclobutane pyrimidine dimers from the genome in a manner identical
190 dg, homology modeling of the Chlorella virus pyrimidine dimer glycosylase (cv-pdg) predicted that a c
193 dine residue at position 16 in the mature T4 pyrimidine dimer glycosylase (T4-PDG) protein has been s
194 ntified a critical residue (His16) in the T4-pyrimidine dimer glycosylase (T4-Pdg) that, when mutated
196 ructural information on the bacteriophage T4 pyrimidine dimer glycosylase (T4-pdg), the catalytic mec
197 ly slower than the rate of formation of a T4-pyrimidine dimer glycosylase (T4-pdg)-DNA intermediate.
200 -His-Arg-Gly-Tyr, and the 16 kDa protein, T4 pyrimidine dimer glycosylase/apurinic/apyrimidinic site
201 ific DPCs, the catalytic chemistry of the T4 pyrimidine dimer glycosylase/apurinic/apyrimidinic site
202 helix-distorting lesions such as cyclobutane pyrimidine dimers have been shown to be coupled in cells
203 that DDB can indeed recognize a cyclobutane pyrimidine dimer in DNA with an affinity (K(app)a) 6-fol
204 d repair of UV radiation-induced cyclobutane pyrimidine dimers in association with reduced levels of
205 a light-activated flavoenzyme that binds to pyrimidine dimers in DNA and repairs them in a reaction
207 roto-flavin capable of repairing cyclobutane pyrimidine dimers in DNA or RNA by photoinduced electron
210 ced UVB-induced 8-oxoguanine and cyclobutane pyrimidine dimers in Melan-A melanocytes and HaCaT kerat
211 ced the PR and NER of UV-induced cyclobutane pyrimidine dimers in MFA2 but much less so in RPB2, wher
212 cells fail to efficiently repair cyclobutane pyrimidine dimers in nontranscribed DNA and fail to expr
213 artificial photolyase models that recognize pyrimidine dimers in protic and aprotic organic solvents
215 transcription-coupled repair of cyclobutane pyrimidine dimers in the ataxia telangiectasia-mutated (
216 tified as photolyases that remove UV-induced pyrimidine dimers in the presence of visible light.
217 A spectrum of deaminated cis-syn cyclobutane pyrimidine dimers in the supF gene was determined using
220 licates past 5'T-T3' and 5'T-U3' cyclobutane pyrimidine dimers, incorporating G or T nucleotides oppo
222 poleta) is required for bypass of UV-induced pyrimidine dimers inserting adenine nucleotides opposite
224 l bond of the 5' pyrimidine of a cyclobutane pyrimidine dimer is hypothesized to occur through the de
225 demonstrate that deamination of cytosine in pyrimidine dimers is a significant event that most likel
226 te that a single, site-specific, cyclobutane pyrimidine dimer leading-strand template lesion provides
230 sunburn cells, 8-oxoguanine, and cyclobutane pyrimidine dimer lesions in skin of melanoma-prone TN(61
231 s exhibit compromised removal of cyclobutane pyrimidine dimer lesions, a characteristic of cells that
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
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
248 hotoreactivation repair pathway (cyclobutane pyrimidine dimer photolyase), a LINE-type reverse transc
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
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
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
265 ivation, decreased efficiency in cyclobutane pyrimidine dimer repair, and elevated sensitivity of cel
268 were consistent with the predicted number of pyrimidine dimers/repeat unit, with higher GFP activatio
269 de mapping of UVB-induced DNA photoproducts (pyrimidine dimers) showed that this may be explained by
270 this study, including double-strand breaks, pyrimidine dimers, single-strand breaks, base damage, an
271 ific BRAF tandem mutations, nearby potential pyrimidine dimer sites, the properties of specialized DN
273 Certain prokaryotes and viruses produce pyrimidine dimer-specific DNA glycosylases (pdgs) that i
275 dsDNA-containing chlorella viruses encode a pyrimidine dimer-specific glycosylase (PDG) that initiat
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
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 o rATPs were inserted opposite a cyclobutane pyrimidine dimer, the substrate was less efficiently cle
286 ads to clean and rapid cycloreversion of the pyrimidine dimer through photoinduced electron transfer
287 state of the purine donates an electron to a pyrimidine dimer to initiate bond cleavage; subsequent b
288 on RNA polymerase II arrest by a cyclobutane pyrimidine dimer using an in vitro transcription system
292 distribution and persistence of cyclobutane pyrimidine dimers were investigated in mouse skin after
293 nomic repair (GGR) of UV-induced cyclobutane pyrimidine dimers were investigated in the yeast GAL1-10
294 of K(a) = 1.0 x 10(3) M(-1) with the cis,syn pyrimidine dimer, whereas binding of the trans,syn isome
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