ライフサイエンスコーパス: CPD

1 CPD belongs to the 2H phosphotransferase superfamily by

2 CPD can then isomerize back to DHP upon irradiation with

3 CPD formation is also inhibited by DNA-bound transcripti

4 CPD hotspots occur almost equally in genic and intergeni

5 CPD of the ORFs for the G and F surface glycoproteins pr

6 CPD removal from telomeres occurs 1.5-fold faster than t

7 CPD was used previously to redesign several proteins, em

8 of variance, accounting for approximately 1 CPD, and it includes the alpha5 and the alpha3 nicotinic

9 ce of moderate/high-intensity smoking (>/=10 CPD) was 40.5% (95% CI, 38.3%-42.7%) in 1965.

10 te levels in light-to-moderate smokers (1-19 CPD).

11 /=20 CPD); moderate-intensity smokers (10-19 CPD); low-intensity smokers (0-9 CPD).

12 redicted nicotine metabolite levels above 20 CPD (up to 40 CPD).

13 tinine per cigarette did not change above 20 CPD and was 36% lower in heavy smokers (>/=20 CPD) than

14 ncrease of 596% (p < .0001), and smoking >20 CPD (>1 pack) was significantly associated with an IPM3

15 PD and was 36% lower in heavy smokers (>/=20 CPD) than in lighter smokers (<20 CPD) (15.6 ng/mL vs. 2

16 per day (CPD), high-intensity smokers (>/=20 CPD); moderate-intensity smokers (10-19 CPD); low-intens

17 ers (>/=20 CPD) than in lighter smokers (<20 CPD) (15.6 ng/mL vs. 24.5 ng/mL, respectively; P < 0.01)

18 and nicotine metabolites for smokers of <20 CPD.

19 10(-12)) and rs6474412-T (effect size = 0.29 CPD, P = 1.4 x 10(-8)), respectively.

20 resented by rs4105144[C] (effect size = 0.39 CPD, P = 2.2 x 10(-12)) and rs6474412-T (effect size = 0

21 tial with constant, and biexponential) and 4 CPD models (stretched-exponential, modified stretched-ex

22 ine metabolite levels above 20 CPD (up to 40 CPD).

23 resented by rs1051730[A] (effect size = 0.80 CPD, P = 2.4 x 10(-69)), and SNPs at 19q13 and 8p11, rep

24 kers (10-19 CPD); low-intensity smokers (0-9 CPD).

25 tion of an oligodeoxynucleotide containing a CPD of a T(m)CG site, one of the major sites of C methyl

26 However, a CPD RSV containing 1,378 synonymous mutations solely in

27 evidence that synthesis past C or (m)C in a CPD also occurs in an error-free manner is for an (m)C i

28 established that synthesis past T or U in a CPD by pol eta occurs in a highly error-free manner, the

29 ing on solvent polarity, a C or an (m)C in a CPD can adopt three tautomeric forms, one of which could

30 osition on the rate of (m)C deamination in a CPD has not been previously studied.

31 ythroid cells are dynamically regulated in a CPD-dependent manner and that disruption of Fbw7-depende

32 e at progressively increasing temperature, a CPD RSV containing 2,692 synonymous mutations in 9 of 11

33 hat photoexcitation of adenine adjacent to a CPD has no influence on this lesion.

34 from renal tissue and cloned in frame with a CPD (YARKARRQARR) at the amino-terminal end and hexahist

35 e, repaired CPDs slowly, and had accumulated CPDs prior to the experiment.

36 UV exposure revealed hyperhotspots acquiring CPDs up to 170-fold more frequently than the genomic ave

37 e stable FADH(*) radical (300-700 nm) allows CPD photolyase to highly efficiently form FADH(-), makin

38 t individual nucleosomes significantly alter CPD formation, protecting nucleosomal DNA with an inward

39 Although CPD formation followed the same pattern of increase with

40 GE-A3 antibodies recognized both MAGE-A3 and CPD-MAGE-A3 proteins, while CPD antibodies recognized on

41 Conversion between DHP and CPD is thought to proceed via a biradical intermediate;

42 ended conformation in which separate KIN and CPD domains are connected by an unstructured linker.

43 Furthermore, anti CPD formation in K(+) solution was slower for the sequen

44 study, Na(+) was still found to inhibit anti CPD formation in sequences designed to stabilize the for

45 sing T4 endonuclease V, photolyase, and anti-CPD antibodies strongly suggest that CPDs are produced b

46 high-throughput sequencing method, known as CPD-seq, to precisely map UV-induced cyclobutane pyrimid

47 nsitive sites, which are commonly counted as CPDs, are true CPDs; the other 40% are abasic sites.

48 unted for 43%-63% of the association between CPD and nicotine metabolites for smokers of <20 CPD.

49 genome-wide significant associations between CPD and single nucleotide polymorphisms are the result o

50 has revealed the presence of genes for both CPD and (6-4)PP photolyases, as well as genes for nucleo

51 nerated time-resolved UV damage maps of both CPDs and (6-4)PPs by HS-Damage-seq and compared them to

52 ium in humans, are often better described by CPD models like GE and PD, than by discrete rates (ME an

53 nd human pol eta synthesize past the 3'-(m)C CPD in a >99% error-free manner, consistent with the hig

54 by a factor of 4.7, whereas that of a T(m)C CPD positioned away from the surface increases by a fact

55 We now report that deamination of a T(m)C CPD whose sugar phosphate backbone is positioned against

56 In wild-type cells, CPD repair was highly associated with transcription, spe

57 Replacing the G in a T=(m)CG CPD with A greatly decreased the deamination rate.

58 Deamination rates for T(m)CG CPDs have been found to vary 12-fold with rotational pos

59 deamination rates for 10 consecutive T=(m)CG CPDs over a full helical turn at the dyad axis of a nucl

60 e dependence and with smoking efficiency (CO/CPD).

61 smokers, smokers who maintained a consistent CPD had 2.93 times (95% confidence interval (CI): 2.82,

62 of CPDs and include the cytosine-containing CPDs that initiate UV-signature C-->T mutations.

63 ound that the deamination of T(m)C and (m)CT CPDs is about 25-fold faster when flanked by G's than by

64 t isomerizes to light-brown cyclophanediene (CPD) upon irradiation with visible light.

65 were identified, such as carboxypeptidase D (CPD).

66 Dark CPDs arise when UV-induced reactive oxygen and nitrogen

67 ccurs at A(2-15)TTCTY, which developed "dark CPDs" long after UV exposure, repaired CPDs slowly, and

68 These "dark CPDs" constitute the majority of CPDs and include the cy

69 The Cellular Phenotype Database (CPD) is a repository for data derived from high-throughp

70 n an association between cigarettes per day (CPD) and a nonsynonymous single-nucleotide polymorphism

71 emonstrating that cigarettes smoked per day (CPD) and nicotine dependence have distinct genetic corre

72 ficant associations with cigarettes per day (CPD) and risk for lung cancer and chronic obstructive pu

73 for the number of cigarettes smoked per day (CPD) in smokers (n = 31,266) and smoking initiation (n =

74 the number of cigarettes they smoke per day (CPD) over their lifetime.

75 about 1 pack per day (20 cigarettes per day (CPD)) (P < 0.01).

76 king intensity (cotinine/cigarettes per day (CPD)) shared chromosome 19 and chromosome 4 loci with th

77 Number of cigarettes smoked per day (CPD), high-intensity smokers (>/=20 CPD); moderate-inten

78 redicted FTND and cigarettes smoked per day (CPD), suggesting that genes most significantly associate

79 including the concept of cigarettes per day (CPD).

80 Smoking 1-10 cigarettes per day (CPD, 0.5 pack) was significantly associated with an IPM3

81 ine candidates by codon-pair deoptimization (CPD).

82 Codon pair deoptimized (CPD) versions of RSV were attenuated and temperature-sen

83 ent caused a chronic presynaptic depression (CPD) in glutamate release that was most pronounced in co

84 approaches to computational protein design (CPD) aim to capture the determinants of structure from p

85 Computational protein design (CPD) can address the inverse folding problem, exploring

86 termed 'compensated pathogenic deviations' (CPDs).

87 arfilzomib, pomalidomide, and dexamethasone (CPD) in an open-label, multicenter, phase 1, dose-escala

88 dren undergoing chronic peritoneal dialysis (CPD) around the globe.

89 urement of the contact potential difference (CPD) per pixel.

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

91 of UV-induced cyclobutane pyrimidine dimer (CPD) formation.

92 f preferential cyclobutane pyrimidine dimer (CPD) formation.

93 of UV-induced cyclobutane pyrimidine dimer (CPD) formation.

94 leading-strand cyclobutane pyrimidine dimer (CPD) lesion.

95 s containing a cyclobutane pyrimidine dimer (CPD) lesion.

96 lity to repair cyclobutane pyrimidine dimer (CPD) lesions in duplex DNA.

97 aster than the cyclobutane pyrimidine dimer (CPD), owing to the more efficient recognition of 6-4PP b

98 amaged adduct, cyclobutane pyrimidine dimer (CPD), to transfect human cells, and retrieved the oligon

99 NA damage, the cyclobutane pyrimidine dimer (CPD), to two normal bases by splitting the cyclobutane r

100 ve developed a cyclobutane pyrimidine dimer (CPD)-specific immunoprecipitation method and mapped ultr

101 ght induced cyclobutane dipyrimidine dimers (CPD's), deaminate within hours to days.

102 light induces cyclobutane pyrimidine dimers (CPD) and pyrimidine(6-4)pyrimidone photoproducts, which

103 oproducts and cyclobutane pyrimidine dimers (CPD) in the skin, which further cause damage to the skin

104 ses produces thymine cyclopyrimidine dimers (CPDs), the primary ultraviolet DNA photoproduct.

105 ced damage of cyclobutane pyrimidine dimers (CPDs) (at 1, 4, 8, 16, 24, and 48 h) and (6-4)pyrimidine

106 esions, i.e., cyclobutane pyrimidine dimers (CPDs) and (6-4) photoproducts [(6-4)PPs], based on direc

107 human cells: cyclobutane pyrimidine dimers (CPDs) and (6-4) pyrimidine-pyrimidone photoproducts [(6-

108 DNA repair of cyclobutane pyrimidine dimers (CPDs) and 6-4 photolesions caused by ultraviolet radiati

109 of two types: cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs).

110 ng UV-induced cyclobutane pyrimidine dimers (CPDs) and BaP diol epoxide-deoxyguanosine (BPDE-dG), whi

111 n the form of cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4) pyrimidone photoproducts [(6-

112 maps of both cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyrimidone (6-4) photoproducts [(6-

113 n the form of cyclobutane pyrimidine dimers (CPDs) and pyrimidine-pyrimidone (6-4) photoproducts.

114 Cyclobutane pyrimidine dimers (CPDs) are DNA photoproducts linked to skin cancer, whose

115 ap UV-induced cyclobutane pyrimidine dimers (CPDs) at single-nucleotide resolution throughout the yea

116 ation of anti cyclobutane pyrimidine dimers (CPDs) between loop 1 and loop 3 in the presence of potas

117 Cyclobutane pyrimidine dimers (CPDs) constitute the most frequent UV-induced DNA photop

118 (UV)-induced cyclobutane pyrimidine dimers (CPDs) in identical sequences under both circumstances.

119 UV-induced cyclobutane pyrimidine dimers (CPDs) in the template DNA strand stall transcription elo

120 n the form of cyclobutane pyrimidine dimers (CPDs) was repaired more efficiently in the skin and bone

121 ions, such as cyclobutane pyrimidine dimers (CPDs), [6-4] pyrimidine-pyrimidinones, dewar pyrimidinon

122 ions, such as cyclobutane pyrimidine dimers (CPDs), and DNA interstrand cross-links.

123 ma arise from cyclobutane pyrimidine dimers (CPDs), DNA photoproducts that are typically created pico

124 of UV-induced cyclobutane pyrimidine dimers (CPDs), increases survival of UV irradiated yeast cells b

125 itiate BER of cyclobutane pyrimidine dimers (CPDs), the predominant UV-induced lesions.

126 (UV)-induced cyclobutane pyrimidine dimers (CPDs).

127 sic sites and cyclobutane pyrimidine dimers (CPDs).

128 st deaminated cyclobutane pyrimidine dimers (CPDs).

129 Patients with chronic psychotic disorders (CPD) exhibit deficient sensorimotor gating (measured by

130 d that continuous probability distributions (CPD) of decay rates can describe the data more parsimoni

131 ter by continuous probability distributions (CPD) of rates, using only 1-2 parameters.

132 zed by an embedded cysteine protease domain (CPD).

133 Various cell-penetrating domains (CPDs) are known to ferry covalently linked heterologous

134 tive pre-drying and microwave finish-drying (CPD-MVFD) affected physical (bulk density, porosity, col

135 -drying and vacuum-microwave finish drying [(CPD (60 degrees C)-VMFD (480-120 W)], and freeze-drying

136 n-specific photolyases that eliminate either CPDs or 6-4PPs and determined their respective contribut

137 For example, CPDs comprising 40 units are generated in 1 s at pH 7.4

138 The ratio of weights of evidence for CPD versus discrete-rate models was high for blood (12.2

139 longer times was frequently more robust for CPD formalisms.

140 Here we present the excision repair maps for CPDs and BPDE-dG adducts generated by tXR-Seq for the hu

141 positions, and all were much faster than for CPDs at non-TCG sites.

142 on average, more intrinsically prone to form CPD lesions.

143 Four CPD RSV genomes were designed in which the indicated ORF

144 sults implicated that schizophrenia and FTND/CPD/COT shared some genetic liability.

145 schizophrenia were not associated with FTND/CPD, consistent with the self-medication hypothesis.

146 ctive site motifs conserved among the fungal CPD clade of 2H enzymes are identified.

147 in the promoter of the BR biosynthesis gene CPD.

148 dine at the carboxy-terminal end to generate CPD-MAGE-A3 in a pQE-70 expression vector.

149 However, CPD resists such Rad4-induced structural distortions.

150 posure, every cell would have a hyperhotspot CPD in each of the ~20 targeted cell pathways, letting h

151 Yet the associations of such changes in CPD with health risks are unclear.

152 We examined the association of changes in CPD with subsequent death in the period 2004-2011 among

153 a larger benefit than even large declines in CPD.

154 repair revealed that initial differences in CPD damage formation often persist, even at later repair

155 r otherwise clinically beneficial effects in CPD patients.

156 ated with enhanced cognition and function in CPD patients.

157 e the effects of memantine on PPI and MMN in CPD subjects.

158 antine (20 mg) significantly enhanced PPI in CPD subjects, and enhanced MMN across subject groups.

159 Reductions in CPD over the lifetime meaningfully decreased death risk;

160 ields and deamination rates of C and (m)C in CPDs and find that the frequency of UVB-induced CPDs cor

161 The C and 5-methyl-C in CPDs are not stable and deaminate to U and T, respective

162 The C or 5-methyl-C in CPDs are not stable and deaminate to U and T, respective

163 ation at a TTmCG site, but instead increases CPD formation at the adjacent TT site.

164 s and find that the frequency of UVB-induced CPDs correlates with the oxidation potential of the flan

165 at has the energy of a UV photon but induces CPDs by energy transfer to DNA in a radiation-independen

166 tures decreased XPA expression and inhibited CPD repair.

167 a 1.9 angstrom crystal structure of Trl1 KIN-CPD from the pathogenic fungus Candida albicans, which a

168 bolizing genotypes are associated with lower CPD, but the predicted metric is the best predictor of C

169 At this stage of erythroid cell maturation, CPD phosphorylation of cyclin E regulates both cell-cycl

170 erent SHLs, and that the position of maximum CPD formation at all locations is shifted to the 5-side

171 domain of MeCP2 (MBD) greatly enhances C=mC CPD formation at a TCmCG site in duplex DNA and binds wi

172 In comparison, MBD does not enhance T=mC CPD formation at a TTmCG site, but instead increases CPD

173 completely suppress deamination of the T=mCG CPD, suggesting that MeCP2 may have the capability to bo

174 Melanocyte CPD hyperhotspots aligned precisely with recurrent UV si

175 We found that in melanocytes, CPDs are generated for >3 hours after exposure to UVA, a

176 isubstituted-anti-[2.2]metacyclophanedienes (CPD) with alkenyl and alkynyl internal (8,16) groups is

177 Nucleosomes modulate CPD formation, favoring outside facing sites and disfavo

178 n significantly and synergistically modulate CPD formation and deamination that contribute to C to T

179 w that the nucleosome dramatically modulates CPD formation in a T11-tract that covers one full turn o

180 a nucleosome, and that bending is modulating CPD formation.

181 G-Mode KPFM can be used to capture nanoscale CPD and capacitance information with a temporal resoluti

182 In contrast, neither CPD, total daily number of puffs, nor TDPV predicted nic

183 Mechanistically, 6-4PPs, but not CPDs, impeded DNA replication across the genome as revea

184 Analysis of CPD repair revealed that initial differences in CPD dama

185 ons in 10 elementary steps in all classes of CPD photolyases.

186 The combination of CPD is well-tolerated and highly active in patients with

187 Most notably, there was a divergence of CPD and (6-4)PP formation at an irradiation wavelength o

188 s MAGE-A3 and determination of the effect of CPD-MAGE-A3 pulsing on DC phenotypic expression of cell-

189 re of this InsP(6)-bound unprocessed form of CPD was determined and revealed the scissile bond Leu(34

190 Although the frequency of CPD formation and repair is modestly modulated by its ro

191 Methylation of C increases the frequency of CPD formation at PyCG sites which correlate with C-->T m

192 that nucleosomes associated with hotspots of CPD formation are readily rearranged, potentially making

193 In the present study, the kinetics of CPD polymer growth and degradation were monitored in a s

194 lable genetic studies containing measures of CPD and the genotype of rs16969968 or its proxy.

195 A similar pattern of CPD formation in protein-free DNA loops suggests that DN

196 Measurement of DC membrane penetration of CPD-MAGE-A3 vs MAGE-A3 and determination of the effect o

197 omplete spatio-temporal molecular picture of CPD repair by photolyase and elucidate the underlying mo

198 he predicted metric is the best predictor of CPD.

199 Reactivation of CPD allowed cleavage of the MARTX toxin at other sites,

200 erweight, and overweight/obesity at start of CPD was 8.9% and 19.7%, respectively.

201 Rpb1, which impairs transcription bypass of CPDs, enhances TCR.

202 rradiation, there were substantial levels of CPDs in samples irradiated with UVB wavelengths borderli

203 These "dark CPDs" constitute the majority of CPDs and include the cytosine-containing CPDs that initi

204 the mutagenic and carcinogenic potential of CPDs emanating from their replicative bypass.

205 cteristics and novel sequence preferences of CPDs and (6-4)PPs.

206 vivo, we determined the deamination rates of CPDs at TCG sites in a stably positioned nucleosome with

207 wed significant inhibition of the removal of CPDs in UV-irradiated cells and the capacity to sensitiz

208 model, where it rapidly initiated removal of CPDs.

209 Repair of CPDs, which we previously showed is intimately coupled t

210 ce (before UVB exposure) inhibited repair of CPDs, with a concomitant decrease in XPA expression.

211 were age dependent and most evident in older CPD patients, whereas those on MMN were most evident in

212 ecting thousands of genes, but its effect on CPD formation and deamination is unknown.

213 e course of PD BMI SDS tended to increase on CPD in underweight and normal weight children, whereas i

214 cause and effect of nucleosome structure on CPD formation and deamination, we have developed a circu

215 observations, deamination was slower for one CPD located at an intermediate rotational position compa

216 oteins, while CPD antibodies recognized only CPD-MAGE-A3.

217 cis-syn TT dimer in human cells and opposite CPDs formed at TT, TC, and CC sites in mouse cells that

218 ted from TLS occurring specifically opposite CPDs formed at TT, TC, and CC dipyrimidine sites.

219 ly error-free role of Poleta in TLS opposite CPDs in mammalian cells.

220 provide alternate pathways for TLS opposite CPDs wherein Pols kappa and zeta promote mutagenic TLS o

221 appa and zeta promote mutagenic TLS opposite CPDs; and (iii) the absence of mutagenic TLS events oppo

222 ning the initial binding of Rad4 to 6-4PP or CPD.

223 ce, it is greatly enhanced for the outermost CPDs.

224 is regulation requires a Cdc4 phosphodegron (CPD) in LIN-45 that is conserved in BRAF.

225 evolutionarily conserved CDC4 phosphodegron (CPD) signal, a target site of glycogen synthase kinase 3

226 e introduced at its two Cdc4 phosphodegrons (CPDs) to ablate Fbw7-dependent ubiquitination and degrad

227 osed of C-terminal cyclic phosphodiesterase (CPD) and central GTP-dependent polynucleotide kinase (KI

228 ; and a C-terminal cyclic phosphodiesterase (CPD) domain.

229 In this article we present CPD, its data structure and user interface, propose a mi

230 Processed CPD also cleaved other proteins in trans, including the

231 transfer the energy of UVA to DNA to produce CPDs.

232 controversy about the origin of UVA-produced CPDs in DNA.

233 el combination for plum powders production - CPD-MVFD at 70 degrees C/1.2 W g(-1) allowed the best pr

234 Purified CPD-MAGE-A3 exhibited more efficient DC membrane penetra

235 determined for the thermal closing reaction, CPD to DHP, and half-lives at 20 degrees C were found to

236 ht of <310 nm wavelength to photo-reactivate CPD thymine dimers within a substrate DNA.

237 Surprisingly, the recombinant CPD viruses were temperature-sensitive for replication i

238 tory to demonstrate that Arabidopsis removes CPDs and (6-4)PPs by a dual-incision mechanism that is e

239 However, cry-DASH can repair CPDs in single-stranded DNA, but their role in DNA repai

240 "dark CPDs" long after UV exposure, repaired CPDs slowly, and had accumulated CPDs prior to the exper

241 leotides for quantification of the repaired, CPD-free DNA by real-time quantitative PCR.

242 An amphetamine challenge reversed CPD via a dopamine D1-receptor-dependent paradoxical pre

243 toward removing remaining barriers to robust CPD.

244 egradable cell-penetrating poly(disulfide)s (CPDs).

245 We suggest that using a set of several CPD and discrete-rate models, and comparing them by info

246 Simple CPD models often outperform more complex discrete-rate m

247 Upon processing at this site, CPD was converted to a form with 500-fold reduced affini

248 43 studies, we extracted the heavy smokers (CPD >20) and light smokers (CPD </=10) with age-at-onset

249 e heavy smokers (CPD >20) and light smokers (CPD </=10) with age-at-onset information, reducing the s

250 Although T=T CPDs are stable, CPDs containing C or 5-methylcytosine ((m)C) are not and

251 n and adolescents from 35 countries starting CPD who were followed in the International Pediatric PD

252 cifically adapted to synthesize past cis-syn CPDs.

253 for an (m)C in the 5'-position of an (m)C=T CPD.

254 Although T=T CPDs are stable, CPDs containing C or 5-methylcytosine (

255 PPs, although eightfold fewer in number than CPDs, are the trigger for UV-induced DNA damage response

256 a new type of attenuated RSV and showed that CPD can rapidly generate vaccine candidates against nons

257 e, to our knowledge for the first time, that CPD repair is significantly less efficient at translatio

258 lysis results confirm previous findings that CPDs are, on average, 'milder' in their likely structura

259 Thus, it was shown that CPDs of TCG sites deaminate the fastest in vivo and that

260 nd anti-CPD antibodies strongly suggest that CPDs are produced by UVA directly.

261 velengths ~300 nm, our findings suggest that CPDs are the principal lesion responsible for most DNA d

262 The CPD viruses exhibited a range of restriction in mice and

263 rize the minimal degron that encompasses the CPD and is sufficient for SEL-10-mediated, MPK-1-depende

264 antitermination factor M2-1, outside of the CPD area, substantially reversed defective transcription

265 ally reversed defective transcription of the CPD L gene and substantially restored virus fitness in v

266 All of the CPD mutants grew less efficiently in vitro than recombin

267 Considering that formation of the CPD positioned away from the surface is also enhanced by

268 n synthesis (TLS) that enables bypass of the CPD with or without repair.

269 A radical cation), is not able to repair the CPD lesion.

270 the same TG-motifs faithfully reproduces the CPD pattern in the nucleosome, indicating that it is a g

271 but rather binding of InsP(6) stabilized the CPD structure, facilitating formation of the enzyme-subs

272 lso showed that the residues surrounding the CPD residue in the folded protein are more often mutated

273 UV absorption spectroscopy to show that the CPD splits in two sequential steps within 90 ps and the

274 d A radical anion donates an electron to the CPD, inducing ring splitting and repair.

275 d binds with equal or better affinity to the CPD-containing duplex compared with the undamaged duplex

276 deamination of the methylC ((m)C) within the CPD.

277 The CPDs are produced with a cubic to supercubic power depen

278 and deamination is greatly inhibited for the CPDs closest to the histone surface, it is greatly enhan

279 epair machinery does not promptly remove the CPDs, stalled Pol II creates a roadblock for DNA replica

280 We show that the CPDs are confined in all three spatial dimensions, makin

281 lower among participants who decreased their CPD (HR = 2.38, 95% CI: 2.25, 2.52) or quit smoking (for

282 t, decreased, maintained, or increased their CPD between ages 25-29 and 50-59 years.

283 y risk, and participants who increased their CPD had still higher risk (hazard ratio (HR) = 3.37, 95%

284 tonically active interneurons contributes to CPD, PPP, locomotor sensitization, and cognitive ability

285 ) TLS makes a very prominent contribution to CPD bypass on both the DNA strands during replication; (

286 The visible light opening reaction, DHP to CPD, showed relative rates of 1 (X = CN) to 240 (X = CH

287 ng, such that a reliable general solution to CPD has yet to be found.

288 which are commonly counted as CPDs, are true CPDs; the other 40% are abasic sites.

289 survival upon accumulation of the unrepaired CPD lesions in genomic DNA.

290 coli photolyase mutant and repairs in vitro CPD lesions in single-stranded and double-stranded DNA w

291 onsistently positioned at Alu elements where CPD hotspots form, but by 2 h post-irradiation, these sa

292 both MAGE-A3 and CPD-MAGE-A3 proteins, while CPD antibodies recognized only CPD-MAGE-A3.

293 hat cloning and purification of MAGE-A3 with CPD enhances its cytosolic bioavailability in DCs withou

294 nts in three genomic regions associated with CPD (P < 5 x 10(-8)), including previously identified SN

295 cted metric is significantly associated with CPD among African Americans and European American depend

296 nd dynamic chromatin changes associated with CPD hotspots.

297 s nevertheless independently associated with CPD, and with breath carbon monoxide (CO), a phenotype a

298 hared a chromosome 15 locus near CHRNA5 with CPD and Pack-Years (i.e., cumulative exposure).

299 ographical measures, increased linearly with CPD up to a level of about 1 pack per day.

300 e DC phenotype, indicating that pulsing with CPD-MAGE-A3 did not alter specific cell-surface antigens