ライフサイエンスコーパス: cyclobutane

1 from the sigma antiaromatic CC framework of cyclobutane.

2 orientation of substituents in the transient cyclobutane.

3 a tethered alkyl halide to form the desired cyclobutane.

4 THPs directly without prior isolation of the cyclobutane.

5 he auxiliary guided C-H functionalization of cyclobutanes.

6 ridyl iridium(III) catalyst, to form bridged cyclobutanes.

7 ariety of substituted aryl cyclopropanes and cyclobutanes.

8 enes as regio- and stereoselective routes to cyclobutanes.

9 Cyclobutane-1,2,3,4-tetraone has been both predicted and

10 Cyclobutane-1,2,3,4-tetrone has been both predicted and

11 ave cis,trans,cis-3,4-bis(3,4-dimethylphenyl)cyclobutane-1,2-dicarboxylic acid, 26, in 60% yield.

12 eld and exclusive formation of cis,trans,cis-cyclobutane-1,2-dicarboxylic acids.

13 A previously overlooked building block, cyclobutane-1,3-diacid (CBDA), is introduced to material

14 of normal C-H bond dissociation energies for cyclobutane (100.6 kcal/mol) and very strong vinyl C-H b

15 50 nm irradiation forming both syn- and anti-cyclobutane adducts (17 and 18), which are photoreversib

16 yl group affords the aldehyde-functionalized cyclobutane alpha-truxilaldehyde.

17 he method could distinguish between sites of cyclobutane and 6-4 photoproduct formation.

18 rmal [4 + 2] cycloaddition of donor-acceptor cyclobutanes and aldehydes has been developed.

19 Cyclobutanes and cyclobutenes are important structural m

20 Consequently, [2+2] cycloadditions to access cyclobutanes and cyclobutenes have been established to b

21 ntioselective [2+2] cycloadditions to access cyclobutanes and cyclobutenes.

22 lowed us to achieve small-size rings such as cyclobutanes and cyclopropanes.

23 arkable for their ability to easily assemble cyclobutanes and other strained ring systems that are di

24 mmonly cited bond energies for cyclopropane, cyclobutane, and cyclohexane are 3 to 4 kcal mol-1 too s

25 ic solvent, where ring-opened cyclopropanes, cyclobutanes, and homoallyl products are formed.

26 etidines, tert-butyl carbamates (Boc-group), cyclobutanes, and spirocycles.

27 Enantiomerically enriched cyclobutanes are constructed by a three-component proces

28 The resulting cyclobutane-based products form stereospecifically, quan

29 ein, we report the development of a class of cyclobutane bearing bicyclo[4.2.0]octane mechanophores.

30 a,alpha-tripeptides, consisting of a central cyclobutane beta- or gamma-amino acid being flanked by t

31 des, being superior to peptides containing a cyclobutane beta-amino acid residue.

32 od to predict the backbone folds of designed cyclobutane beta-peptides is based on QM calculations.

33 6 and 32-36 of NPY and PP containing (1R,2S)-cyclobutane (betaCbu) or (1R,2S)-cyclopentane (betaCpe)

34 anism involving a 1,4-biradical derived from cyclobutane bond fragmentation.

35 reoelectronic alignment of the two available cyclobutane bonds with the cyclohexadienone pi-system, w

36 addition reaction to yield the corresponding cyclobutane-bridged dinuclear tetrakis(NHC) complexes.

37 The synthesis of unsymmetrical cyclobutanes by controlled heterodimerization of olefins

38 eta-unsaturated ketones to the corresponding cyclobutanes by using a dual-catalyst system consisting

39 natural products using the first example of cyclobutane C-H arylation.

40 he bond that extends to the less substituted cyclobutane carbon for 13.

41 , tri-, and tetramers) of cis-2-(aminomethyl)cyclobutane carboxylic acid, a gamma-amino acid featurin

42 ng pattern arising from the cyclopropane and cyclobutane CC framework response to a perpendicular mag

43 ramolecular [2 + 2] cycloaddition leading to cyclobutanes competes advantageously.

44 A series of cyclobutane-containing polymers (CBPs), namely poly-alph

45 carbocyclic rings, including cyclopropanes, cyclobutanes, cyclopentanes, cyclohexanes, and cyclohept

46 allowed for the synthesis of enantioenriched cyclobutanes, cyclopentanes, indanes, and six-membered N

47 ical shifts of cyclopropane (delta 0.22) and cyclobutane (delta 1.98) which are shifted upfield and d

48 nomalously low SE of cyclobutene relative to cyclobutane (DeltaSE = 4 kcal/mol) is a consequence of n

49 al route for the synthesis of functionalized cyclobutane derivatives starting from functionalized nor

50 The possibility of retro-PCA of the obtained cyclobutane derivatives to give the starting dyes was sh

51 ds only rctt isomers of bis-crown-containing cyclobutane derivatives.

52 Cyclobutanes derived from the dimerization of cinnamic a

53 affords consistent formation of predictable cyclobutane diastereomers.

54 e syntheses feature a new preparation of cis-cyclobutane dicarboxylates from commercially available c

55 NOE NMR data are consistent with a cis-anti cyclobutane dimer between the 3'-sides of T2 and T7 in a

56 to prepare a template containing the cis-syn-cyclobutane dimer of mCT.

57 Cyclobutane dimer photolyases are proteins that bind to

58 idine to produce the corresponding htt r-ctt cyclobutane dimer, and we present (1)H NMR analysis of t

59 site, T-T (6-4) photoadduct and T-T cis-syn cyclobutane dimer, by transforming strains deleted for R

60 diation at the main absorption band leads to cyclobutane dimers (T<>Ts) and (6-4) adducts via differe

61 between adjacent thymines in DNA leading to cyclobutane dimers (T<>Ts) and (6-4) adducts.

62 ential role for direct DNA damage, including cyclobutane dimers and (6-4) photoproducts, in the etiol

63 olyase uses light energy to split UV-induced cyclobutane dimers in damaged DNA, but its molecular mec

64 thylation on the deamination rate of cis-syn-cyclobutane dimers to prepare a template containing the

65 eases the quantum yield for the formation of cyclobutane dimers while reducing that of (6-4) adducts.

66 n contrast, cytosine within sunlight induced cyclobutane dipyrimidine dimers (CPD's), deaminate withi

67 ons has shed light on many of the details of cyclobutane-formation, in particular, for terpene natura

68 active approach to synthetically challenging cyclobutane frameworks under mild reaction conditions.

69 es, thus providing efficient access to fused cyclobutanes from easily accessed pi-components.

70 cted and highly stereoselective formation of cyclobutanes, functionalizing at the usually inert sites

71 in a tetracyclic norbornyl ketal leads to a cyclobutane-fused derivative as the major or exclusive p

72 ve scission of the vinyl substituent of this cyclobutane gave an aldehyde, which was reacted with an

73 nal interpretation, the CC framework shields cyclobutane hydrogens, and its response to a perpendicul

74 action of these acyclic olefins to construct cyclobutanes in a highly regio- and diastereoselective m

75 s for the rapid synthesis of 1,3-substituted cyclobutanes in high yield under simple and robust react

76 These contain a spiro-cyclobutane instead of spiro-cyclopropane structure.

77 1) the enantioselective preparation of a key cyclobutane intermediate by a tandem Wolff rearrangement

78 The beneficial role of a dominant cyclobutane intermediate in maintaining high stereoselec

79 ne beta-amide ester to form a donor-acceptor cyclobutane intermediate, which subsequently undergoes a

80 ous [2+2] alkene cycloaddition to synthesize cyclobutanes is kinetically accessible by photochemical

81 Biosynthetic production of cyclobutanes leads to many complex natural products.

82 Cyclobutane malonoyl peroxide (7), prepared in a single

83 report a molecular architecture, in which a cyclobutane mechanophore functions as a gate to regulate

84 The [2 + 2] cycloreversion of cyclobutane mechanophores has emerged as a versatile fra

85 mparing the relative reactivities of various cyclobutane mechanophores.

86 Calculations on cyclobutane, methylcyclobutane, and 1,1-dimethylcyclobut

87 rect synthesis of a representative norlignan cyclobutane natural product.

88 alternative approach to access pseudodimeric cyclobutane natural products, such as the dictazole and

89 ortion with an acetaldehyde appendage on the cyclobutane of the northern sector.

90 ch as bicyclo[1.1.1]pentanes, azetidines, or cyclobutanes often outweighs the challenge of synthesizi

91 ds involves the formation of an intermediate cyclobutane phodoadduct composed of (Br)U and U, which u

92 sing by valence isomerization of a precursor cyclobutane photoproduct with cis-syn stereochemistry th

93 The resultant cyclobutane product is functionalized with halogen atoms

94 The functionalized cyclobutane product was formed exclusively in high yield

95 diastereoselectivity in the formation of the cyclobutane products is excellent.

96 Functionalized cyclobutane products were obtained in excellent yields (

97 electivity but also delivered the respective cyclobutane products with significant enantiomeric exces

98 tion resulted in a decrease in the number of cyclobutane pyridimine dimer-positive APC that were foun

99 showed delayed repair of ultraviolet-induced cyclobutane pyrimidine adducts and elevated sensitivity

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

116 However, cyclobutane pyrimidine dimer accumulation was higher in

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

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

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

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

121 The cyclobutane pyrimidine dimer class III photolyases are s

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

148 12 knockout (KO) mice using the formation of cyclobutane pyrimidine dimers (CPD) as an indicator of t

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

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

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

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

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

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

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

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

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

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

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

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

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

162 Cyclobutane pyrimidine dimers (CPDs) are DNA photoproduc

163 Cyclobutane pyrimidine dimers (CPDs) are responsible for

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

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

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

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

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

169 Cyclobutane pyrimidine dimers (CPDs) constitute the most

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

195 Cyclobutane pyrimidine dimers are the major DNA photopro

196 96A displayed a reduced repair efficiency of cyclobutane pyrimidine dimers as compared with cells com

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

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

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

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

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

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

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

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

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

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

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

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

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

210 Cyclobutane pyrimidine dimers induced by direct UVB abso

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

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

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

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

215 When cyclobutane pyrimidine dimers stall DNA replication by D

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

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

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

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

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

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

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

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

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

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

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

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

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

229 Cyclobutane pyrimidine dimers, which have been previousl

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

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

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

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

234 6-4) pyrimidine-pyrimidone photoproducts and cyclobutane pyrimidine dimers.

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

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

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

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

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

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

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

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

243 overexpression qualitatively suppressed the cyclobutane pyrimidine removal defect associated with ME

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

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

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

247 One of the three stereoisomeric cyclobutanes reacts substantially more slowly than the o

248 clohexyl constitutional isomer 5 via a vinyl cyclobutane rearrangement.

249 ential escape routes was undertaken, through cyclobutane ring cleavage to 12-annulenes, sigmatropic 1

250 boxylic acid, a gamma-amino acid featuring a cyclobutane ring constraint, were prepared, and their co

251 etone, and (v) a radical cyclization for the cyclobutane ring formation to provide the tricyclo[5.2.1

252 SAR development around the cyclobutane ring resulted in a 10-fold increase in poten

253 tiated three electron transfer processes and cyclobutane ring splitting by following the entire dynam

254 The cyclobutane ring splitting takes tens of picoseconds, wh

255 l processes, electron-tunneling pathways and cyclobutane ring splitting, were not resolved.

256 h other molecules to form new materials, the cyclobutane ring was able to tolerate acid and base trea

257 (CPD), to two normal bases by splitting the cyclobutane ring.

258 highly functionalized, enantiomerically pure cyclobutane ring.

259 olecules for their unique structure of fused cyclobutane rings as well as their perceived biological

260 According to the X-ray data the cyclobutane rings in both compounds are almost planar (t

261 rbons containing unsaturatively, 1,3-bridged cyclobutane rings, (2) the use of orbital topology for p

262 C(2h) symmetry composed of five edge-sharing cyclobutane rings, or a [5]-ladderane, with acid results

263 action that results in a photodimer with two cyclobutane rings.

264 the anthracene rings precedes rupture of the cyclobutane rings.

265 polymer to generate a pyridyl-functionalized cyclobutane stereoselectively and in quantitative yield.

266 e of unsymmetrical tri- and tetrasubstituted cyclobutane structures can be produced in good yields an

267 is more than 8 kcal mol-1 less strained than cyclobutane, that is, there is at least some thermodynam

268 form unsymmetrical tri- and tetrasubstituted cyclobutanes through a heterodimerization process involv

269 synthesis across a template abasic site or a cyclobutane thymidine dimer.

270 ucleotides, which contained a single cis-syn cyclobutane thymine dimer (CTD) at one of six different

271 odes modified with DNA duplexes containing a cyclobutane thymine dimer (T<>T), here we probe the elec

272 horizontal lineC/C-C stretch vibrations) of cyclobutane thymine dimer and thymine dinucleotide radic

273 The cyclobutane thymine dimer is the major DNA lesion induce

274 Cyclobutane thymine dimer, one of the major lesions in D

275 Dpo2 and Dpo3 bypassed uracil and cis-syn cyclobutane thymine dimer, respectively.

276 , 8-oxoguanine, and either uracil or cis-syn cyclobutane thymine dimer, suggesting their catalyticall

277 m light indicates that the photoproduct is a cyclobutane thymine dimer.

278 ion synthesis (TLS) of site-specific cis-syn cyclobutane thymine dimers (T (wedge)T).

279 Cyclobutane thymine dimers (T-T) comprise the majority o

280 es to extend synthetic primers past template cyclobutane thymine dimers (T[CPD]T) or undamaged T-T un

281 This value is comparable to that of cyclobutane thymine dimers (the major UV-induced lesions

282 The formation of cyclobutane thymine dimers is one of the most important

283 common DNA lesions, such as abasic sites and cyclobutane thymine dimers.

284 e steps during DNA synthesis through cis-syn cyclobutane thymine dimers.

285 rotective role against skin cancer caused by cyclobutane thymine-thymine dimers (TTDs), a frequent fo

286 Cyclobutane-thymine dimers (CTDs), the most common DNA l

287 uch as bicyclo[1.1.1]pentane, azetidine, and cyclobutane to modify their lead compounds.

288 -D13K-C3) to DNA suppressed the formation of cyclobutane-type thymine dimers and promoted the formati

289 s the rapid and stereoselective formation of cyclobutanes under very mild reaction conditions.

290 The resultant cyclobutane undergoes spontaneous retro-Mannich fission

291 rategy for the construction of unsymmetrical cyclobutanes using C-H functionalization logic is demons

292 stly lower strain energy (1.8 kcal/mol) of a cyclobutane versus a cyclopropane.

293 f the incorporation of a ring-expanded fused cyclobutane (vs cyclopropane), its chemical and structur

294 ne providencin containing a tetrasubstituted cyclobutane was synthesized from the bis(acetonide) of d

295 onor-acceptor cyclopropanes or corresponding cyclobutanes were treated with 1,3,5-triazinanes, leadin

296 rivatives, is a unique strategy to construct cyclobutanes, which are building blocks for a variety of

297 n, the nonoptimal geometric alignment of the cyclobutane with the activating cyclohexadienone, and th

298 The thermolysis of polyfused cyclobutanes with a cis,syn,cis- or a cis,anti,cis-relat

299 nocatalysis allowing for the construction of cyclobutanes with four contiguous stereocenters with com

300 ping sequence to give densely functionalized cyclobutanes with high diastereoselectivity.