ライフサイエンスコーパス: CPD

1 CPD formation is also inhibited by DNA-bound transcripti

2 CPD hotspots occur almost equally in genic and intergeni

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

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

5 CPDs can be directly repaired by DNA photolyase (PL) upo

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

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

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

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

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

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

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

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

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

15 and nicotine metabolites for smokers of <20 CPD.

16 10(-12)) and rs6474412-T (effect size = 0.29 CPD, P = 1.4 x 10(-8)), respectively.

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

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

19 CPDs and UVB dose is almost linear, with 4.4 CPDs produced per Mbp per J/m(2) of UVB radiation.

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

21 which on average produced approximately 0.5 CPD per single plasmid.

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

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

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

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

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

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

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

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

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

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

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

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

34 that, subsequent to cleavage, the activated CPD may shift to an inactive conformation.

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

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

37 Although CPD formation followed the same pattern of increase with

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

39 ential side chains in the ligase, kinase and CPD modules of the plant enzyme.

40 ian Inheritance in Man) database into PD and CPD data sets and performed two independent analyses: (i

41 mutations are pathogenic, comparing PDs and CPDs.

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

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

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

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

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

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

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

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

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

51 on in diluent- and T-oligo-treated skin, but CPDs were strikingly reduced in T-oligo- vs. diluent-tre

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

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

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

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

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

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

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

59 ) is shown to be recycled, while the cleaved CPD becomes incapable of further binding of InsP(6).

60 Upon quenching, intact 1 and the ring-closed CPD 2 were obtained in a 3:2 or 3:1 ratio, depending on

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

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 r the prompt repair of UV-induced DNA damage CPD.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

79 termed 'compensated pathogenic deviations' (CPDs).

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

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

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

83 f preferential cyclobutane pyrimidine dimer (CPD) formation.

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

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

86 A containing a cyclobutane pyrimidine dimer (CPD) lesion.

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

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

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

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

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

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

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

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

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

96 limination of cyclobutane pyrimidine dimers (CPD), but not of pyrimidine (6, 4)pyrimidone photoproduc

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

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

99 positive for cyclobutane pyrimidine dimers (CPDs) 50% immediately post-irradiation.

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

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

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

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

104 lesions being cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6-4) pyrimidone adducts (6-4PPs).

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

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

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

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

109 Cyclobutane pyrimidine dimers (CPDs) are responsible for a considerable fraction of sun

110 only produce cyclobutane pyrimidine dimers (CPDs) as reported but also cause significant DNA degrada

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

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

113 of UV-induced cyclobutane pyrimidine dimers (CPDs) compared to wild-type (wt).

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

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

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

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

118 nd comparable cyclobutane pyrimidine dimers (CPDs) were detected immediately after UV irradiation in

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

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

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

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

123 sic sites and cyclobutane pyrimidine dimers (CPDs).

124 st deaminated cyclobutane pyrimidine dimers (CPDs).

125 duced cis-syn cyclobutane pyrimidine-dimers (CPDs) together with rapid removal of UVA-induced oxidize

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

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

128 xin by an embedded cysteine protease domain (CPD) is essential for this toxin to induce actin depolym

129 e have defined the cysteine protease domain (CPD) responsible for autoprocessing within toxin A (TcdA

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

131 sed by an internal cysteine protease domain (CPD).

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

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

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

135 While it is known that methylation enhances CPD formation in sunlight, little is known about the eff

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

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

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

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

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

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

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

143 in the promoter of the BR biosynthesis gene CPD.

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

145 A homologous CPD is also present in the large clostridial toxin TcdB

146 sing, conserved residues among 24 identified CPDs were mutagenized.

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

148 r otherwise clinically beneficial effects in CPD patients.

149 ated with enhanced cognition and function in CPD patients.

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

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

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

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

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

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

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

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

158 tures decreased XPA expression and inhibited CPD repair.

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

160 These changes most likely make CPD binding less energetically favorable and, hence, ins

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

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

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

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

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

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

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

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

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

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

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

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

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

174 Biochemical and kinetic analyses of CPD mutants indicate that InsP6 binding induces an allos

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

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

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

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

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

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

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

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

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

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

185 ccurred at a time when the early outcomes of CPD patients have improved.

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

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

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

189 he predicted metric is the best predictor of CPD.

190 sus diluent-pretreated explants, the rate of CPD removal was also more rapid, approximately 80 vs 45%

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

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

193 Identification of structural features of CPDs and detection of specific compensatory events will

194 NA damage, as determined by the formation of CPDs and the number of sunburn cells, was resolved more

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

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

197 ch are the established signature mutation of CPDs.

198 oses, the relationship between the number of CPDs and UVB dose is almost linear, with 4.4 CPDs produc

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

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

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

202 model, where it rapidly initiated removal of CPDs.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

220 Processed CPD did not bind InsP(6) indicating that, subsequent to

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

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

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

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

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

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

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

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

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

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

231 sely paralleled the decline in self-reported CPD between 1988-1994 and 1999-2002.

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

233 resent the 2.1 angstrom structure of the RTX CPD in complex with InsP6.

234 The RTX CPD is efficiently activated by the eukaryote-specific s

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

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

237 43 studies, we extracted the heavy smokers (CPD >20) and light smokers (CPD </=10) with age-at-onset

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

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

240 cifically adapted to synthesize past cis-syn CPDs.

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

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

243 ployed four different templates containing T[CPD]Ts, and two containing pyrimidine (6-4')-pyrimidinon

244 past template cyclobutane thymine dimers (T[CPD]T) or undamaged T-T under physiological conditions (

245 Evolutionary conservation of efficient T[CPD]T bypass by HsPoleta and AtPoleta may reflect a high

246 e depressed ( N - 1) insertion upstream of T[CPD]T (but not T-T) may reduce the extent of gratuitous

247 three successive insertions [opposite the T[CPD]T and (N + 1) nucleotides] that define bypass nearly

248 ion opposite the ( N - 1) nucleotide 3' to T[CPD]T by HsPoleta and especially AtPoleta, but not ScPol

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

250 These data suggest that CPD may represent a proxy for exposure to nicotine and p

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

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

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

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

255 Results suggest that CPDs are responsible for most of the UV-associated toxic

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

257 The CPD is activated upon binding inositol hexakisphosphate

258 The CPD is shown to bind InsP(6) (K(d), 0.6 microm), and Ins

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

260 l in which basic residues located across the CPD structure form an InsP(6) binding pocket and that th

261 nsP(6) stimulates processing by altering the CPD to an activated conformation.

262 airing and stacking interactions between the CPD and the duplex DNA substrate.

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

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

265 t the local region around the 5'-side of the CPD lesion was more disrupted and destacked than the 3'-

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 found to insert dGMP opposite the mC of the CPD with about a 120:1 selectivity relative to dAMP.

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

270 his work, the autoprocessing activity of the CPD within MARTX(Vc) is similarly found to be inducible

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

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

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

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

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

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

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

278 he autoprocessing of TcdB dependent upon the CPD.

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

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

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

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

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

284 ompensatory mutations spatially close to the CPDs and, (ii) using our SAAPdb database, we examined li

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

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

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

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

289 rand are recognized by Rad4, whereas the two CPD-linked nucleotides become disordered.

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

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

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

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

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

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

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

297 nd dynamic chromatin changes associated with CPD hotspots.

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

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