ライフサイエンスコーパス: Watson

1 Watson and Puelles now newly propose that the mammalian

2 Watson-Crick base pairing of the modified guanine with t

3 Watson-Crick base pairing was conserved at the S-cdG.dC

4 Watson-Crick base-pairing slows the rate of vibrational

5 In 1953, Watson and Crick not only described the double-helix str

6 A Watson-Crick pair leads to an inability to fold in metal

7 large-scale conformational change to adopt a Watson-Crick-like dG*dTTP base pair and a closed protein

8 taneous errors occur when mismatches adopt a Watson-Crick-like geometry through tautomerization and/o

9 pair forms three hydrogen bonds and adopts a Watson-Crick-like geometry rather than a wobble geometry

10 base pair configuration that approximates a Watson-Crick base pair at higher pH.

11 e find that whereas hydrogen bonds between a Watson-Crick base pair of template DNA and incoming NTP

12 features: (i) the loop region is closed by a Watson-Crick base pair between Psi1911 and A1919, which

13 lect the base of the incoming dNTP to form a Watson-Crick pair with the template base but also distin

14 vivo due to its anti-conformation forming a Watson-Crick base pair with correct deoxycytidine 5'-tri

15 Moreover, dCTP forms a Watson-Crick base pair with dG, two nucleotides upstream

16 ng specificity through an intramolecular G:A Watson-Crick/sugar-edge base interaction, an unusual pai

17 yl, benzyl) that can alternatively pair in a Watson-Crick sense opposite cytosine (C) or as a Hoogste

18 ation state, polbeta appears to allow only a Watson-Crick-like conformation for purine*pyrimidine bas

19 substitution, which selectively knocks out a Watson-Crick-type (G)N2H2...O2(T) hydrogen bond, signifi

20 t metal ions, a free 5'-flap (if present), a Watson-Crick base pair at the terminus of the reacting d

21 The structures revealed a Watson-Crick-like pairing between O(6)-MeG and 2"-deoxyt

22 specific functional groups in stabilizing a Watson-Crick pair.

23 n the basis of its poor geometric match to a Watson-Crick pair.

24 e estimate for the free energy change when a Watson-Crick base pair in stem 2 is changed, (2) the loo

25 The abundant Watson-Crick face methylations in biological RNAs such a

26 hg1 catalyzes an unexpected second activity: Watson-Crick-dependent 3'-5' nucleotide addition that oc

27 G-tetrad antiparallel G4 with an additional Watson-Crick CG base pair.

28 duplex, and type and orientation of adjacent Watson-Crick pairs.

29 ntify and classify modifications that affect Watson-Crick base pairing at three different levels of t

30 iffraction from ideal, rigid helices allowed Watson and Crick to unravel the DNA structure, thereby e

31 d promotes mutagenic replication by allowing Watson-Crick-mode for O6MeG.T but not for O6MeG.C in the

32 ps bounded by Watson-Crick pairs, the AG and Watson-Crick pairs are all head-to-head imino-paired (ci

33 o supercoiled DNA via combined Hoogsteen and Watson-Crick binding.

34 occurrence of both stacking interactions and Watson-Crick base pairing.

35 tructures show Hoogsteen BrG.G base pair and Watson-Crick BrG.C base pair.

36 During DNA synthesis, base stacking and Watson-Crick (WC) hydrogen bonding increase the stabilit

37 f the knowledge of helical DNA structure and Watson-Crick base pairing rules, scientists have constru

38 Cognitive systems, such as Watson for Genomics (WG), integrate massive amounts of n

39 bias, except when the mutations occurred at Watson-Crick paired sites.

40 h unique stabilities relative to native base Watson-Crick pairings, and this phenomenon is used here

41 ric and anionic species form hydrogen-bonded Watson-Crick-like base pairs.

42 between nonadjacent regions and employ both Watson-Crick and non-Watson-Crick base-pairing, screenin

43 In the 12 solved structures, both Watson-Crick (anti-8-oxoG:anti-dCTP) and Hoogsteen (syn-

44 , where optical detection can be achieved by Watson-Crick base pairing.

45 n complexes to their target nucleic acids by Watson-Crick base pairing.

46 For loops bounded by Watson-Crick pairs, the AG and Watson-Crick pairs are al

47 school of thought, originally championed by Watson [5] and Skinner [6].

48 tributes to the selection of correct dNTP by Watson-Crick base pairing, but it cannot explain how low

49 As bind via Hoogsteen-arm first, followed by Watson-Crick arm invasion, initiated at the tail.

50 Self-assembly of these oligomers by Watson-Crick base pairing of the recognition sequences c

51 old nanoparticle-QD assemblies programmed by Watson-Crick base-pairing.

52 Sequence specificity is provided by Watson-Crick base pairing between the DNA substrate and

53 uble helix structure of DNA was published by Watson and Crick, Sanger's group announced the first ami

54 ion to the double helix symmetry revealed by Watson and Crick, classical X-ray diffraction patterns o

55 to pair with an extended triangle strand by Watson-Crick base pairing.

56 nalysis reveals that Fm7dG forms a canonical Watson-Crick base pair with dCTP, but metal ion coordina

57 d into helical regions composed of canonical Watson-Crick and related base pairs, as well as single-s

58 We propose that canonical Watson-Crick base triplets serve as the fundamental unit

59 nucleotide is bound in either the canonical Watson-Crick base pair or a nonplanar base pair.

60 mplete purine ring that allows the canonical Watson-Crick base pairing to be maintained.

61 osition of the codon occurs in the canonical Watson-Crick geometry.

62 irtually indistinguishable from a canonical, Watson-Crick base pair in double-stranded DNA.

63 ch experiments was well described by a Chick-Watson model with first-order dependences on disinfectan

64 trating the applicability of classical Chick-Watson kinetics for all fullerenes employed in this stud

65 lly Referential Food Grunts of Chimpanzees", Watson et al.[1] claimed that they "provide the first ev

66 -3'...5'-GAC-3' flanked on both sides by cis Watson-Crick G/C and G/U wobble base pairs.

67 pairs are all head-to-head imino-paired (cis Watson-Crick/Watson-Crick).

68 loop adopts canonical UG wobble pairing (cis Watson-Crick/Watson-Crick), with AG pairs that are only

69 est neighbors, with CA adjacent to a closing Watson-Crick pair, are further stabilized when the pH is

70 ide that stacks onto the pseudo-knot-closing Watson-Crick base pair.

71 r "double-check" provided by the concomitant Watson-Crick and Hoogsteen base pairings involved in tar

72 e-site pocket with planar stacking contacts, Watson-Crick polar hydrogen bonds and van der Waals inte

73 ry pairing and instead have 11-12 contiguous Watson-Crick pairs to the center of the miRNA.

74 hirality are incapable of forming contiguous Watson-Crick base pairs with each other-has enforced a "

75 , which eliminates the need for conventional Watson-Crick base pairing.

76 ce increase without the formation of correct Watson-Crick hydrogen bonds.

77 recognition is strictly dependent on correct Watson-Crick pairing.

78 polymerase to insert a mismatch with correct Watson-Crick geometry.

79 ill be in competition with the corresponding Watson-Crick duplex.

80 oth T and A and engages in the corresponding Watson-Crick-like base pairs, forming stable duplexes.

81 ugh here we show that intentionally creating Watson-Crick mismatches near the cleavage site relaxes t

82 DNA 13-mer, BET66, self-assembles via Crick-Watson and noncanonical base pairs to form crystals.

83 anonical UG wobble pairing (cis Watson-Crick/Watson-Crick), with AG pairs that are only weakly imino-

84 head-to-head imino-paired (cis Watson-Crick/Watson-Crick).

85 gly, a conformational change of the designed Watson-Crick duplex region resulted in crystal packing d

86 rs are thought to identify targets by direct Watson-Crick pairing with invasive 'protospacer' DNA, bu

87 ghly sequence-specific manner through direct Watson-Crick base pairing.

88 ons with p53, the current structures display Watson-Crick base pairs associated with direct or water-

89 in N1-methyl-G, which results in a distorted Watson-Crick geometry at pH >9.

90 They disturb Watson-Crick base-pairing and base-stacking interactions

91 lection on spectroscopic data, called Durbin-Watson partial least-squares regression (dwPLS), is prop

92 ariables whose intervals have a lower Durbin-Watson statistic (dw) than a certain optimal cutoff.

93 in the dehydrated environment that envelops Watson-Crick nascent base pairs and serve to enhance bas

94 These mispairs can evade Watson-Crick fidelity checkpoints and form with probabil

95 NA (ssDNA) bound to site I in RecA exchanges Watson-Crick pairing with a sequence-matched ssDNA that

96 of nanoparticle arrays and lattices exploit Watson-Crick base pairing of single-stranded DNA sequenc

97 ts.1 The design of these structures exploits Watson-Crick hybridization and strand exchange to stitch

98 Because of the extensive Watson-Crick complementarity between deoxyribozyme and s

99 his provides a means to distinguish faithful Watson-Crick base-paired DNA from damaged DNA.

100 but also causes the enzyme to favor faithful Watson-Crick base pairing over mutagenic configurations.

101 guanine (dG-N2) provides direct evidence for Watson-Crick (G)N2H2...O2(T) hydrogen bonding in the tra

102 idelity (relative rate of base-extension for Watson-Crick versus mismatched base pairs), replications

103 ugh 1-MeA suggests that despite its need for Watson-Crick hydrogen bonding, Poleta can stabilize the

104 ES-Rosetta recovers the 10 NN parameters for Watson-Crick stacked base pairs and 32 single-nucleotide

105 In vitro assays revealed an active role for Watson-Crick base-pairing at positions 9 and 10 in promo

106 nucleobase pairs follow standard rules for Watson-Crick base pairing but have rearranged hydrogen b

107 sion of the two phosphate backbones, forcing Watson-Crick base-pairs within the duplex to flip outwar

108 tion, both guanines of the Pt-GG lesion form Watson-Crick base pairing with the primer terminus dC an

109 6-Aminopyridin-2-ones form Watson-Crick pairs with complementary purine analogues t

110 y short-lived and low-abundance species form Watson-Crick-like base pairs, their conformation could n

111 rogation, bases in the dsDNA attempt to form Watson-Crick bonds with the corresponding bases in the i

112 Fapy-dG in the anti conformation and forming Watson-Crick pairs with dCTP or dC.

113 ture, BrG adopts anti conformation and forms Watson-Crick base pairing with the incoming dCTP analog.

114 (tC) is a fluorescent nucleotide that forms Watson-Crick base pairs with dG.

115 sient sequence-specific excursions away from Watson-Crick base-pairing at CA and TA steps inside cano

116 e branchpoint are unpaired, despite the full Watson-Crick complementarity of the molecule.

117 for some substrate sequences even when full Watson-Crick complementarity is maintained, correspondin

118 We show that a basic Galton-Watson epidemic model combined with the selection bias o

119 y a stochastic birth-death process of Galton-Watson type.

120 f these biradicals return to the original GC Watson-Crick pairs, but up to 10% of the initially excit

121 citation of individual guanine-cytosine (GC) Watson-Crick base pairs by ultrafast time-resolved UV/vi

122 The mismatch has Watson-Crick geometry consistent with a tautomeric or io

123 when the loop residues of two hairpins have Watson-Crick complementarity.

124 itution can originate from a mismatch having Watson-Crick geometry, and they suggest a common catalyt

125 In describing the DNA double helix, Watson and Crick suggested that "spontaneous mutation ma

126 In the canonical DNA double helix, Watson-Crick (WC) base pairs (bps) exist in dynamic equi

127 dsDNA targets (triplex association) and (ii) Watson-Crick complement-mediated displacement of the TFO

128 The 1-MeA lesion impairs Watson-Crick base pairing and blocks normal DNA replicat

129 hance RNA stability and increase affinity in Watson-Crick base pairing.

130 show that there is a significant decrease in Watson-Crick duplex stability of the heterogeneous backb

131 A strands and cross-pair with RNA and DNA in Watson-Crick fashion.

132 es electron-driven proton transfer (EDPT) in Watson-Crick base pairs.

133 strand 5'-end nucleotide need not engage in Watson-Crick (W/C) H-bonding but must fit the general sh

134 ons with a thymine-thymine (T-T) mismatch in Watson-Crick base-pairs and the ligative disassembly of

135 rases due to its inability to participate in Watson-Crick (W-C) base pairing.

136 nucleoside analogue that can participate in Watson-Crick base pairing.

137 cialized alignment software can also include Watson-Crick base pairs, but none adequately addresses t

138 n and programmable intra- and intermolecular Watson-Crick base-pairing interactions.

139 ion between the complementary strand and its Watson-Crick pairing partners promotes the rapid unbindi

140 RNA polymerase incorporates ZTP opposite its Watson-Crick complement, imidazo[1,2-a]-1,3,5-triazin-4(

141 Using these methods, we compress James Watson's genome to 2.5 megabytes (MB), improving on rece

142 of molecular biology, Sol Spiegelman, James Watson, and Seymour Benzer.

143 deoxynucleoside analogs (xDNA) that maintain Watson-Crick base pairing and base stacking ability; how

144 a-2-oxo-phenothiazine, tCfTP) that maintains Watson-Crick base pairing with guanine.

145 2 orders of magnitude relative to a matched (Watson-Crick) control.

146 he availability of tRNA decoding mechanisms: Watson-Crick, non-Watson-Crick or both types of interact

147 plays an underappreciated role in modulating Watson-Crick base pairing strength and potentially pi-pi

148 cleotide increases as compared to the native Watson-Crick hydrogen-bonded T.A base pair.

149 base pairs that are larger than the natural Watson-Crick architecture.

150 ta show that the Z:P pair mimics the natural Watson-Crick geometry in RNA in the first example of a c

151 model should therefore be divided in the new Watson/Puelles model into a smaller ventral pallium and

152 Non-Watson-Crick interactions between the branch helix and 5

153 and azide building blocks catalyzed by a non-Watson-Crick DNA secondary structure (see picture).

154 tural model of loop 6 that specifies all non-Watson-Crick base pair interactions, derived by isosteri

155 ization is possible with an alternative, non-Watson-Crick-paired duplex that selectively binds a comp

156 ased on isostericity of Watson-Crick and non-Watson-Crick base pairs, along with the collapsing (hori

157 regions and employ both Watson-Crick and non-Watson-Crick base-pairing, screening of candidate binder

158 Isostericity relations between non-Watson-Crick basepairs are used in scoring sequence vari

159 w that most such loops are structured by non-Watson-Crick basepairs and base stacking.

160 me Watson-Crick base pairing to catalyze non-Watson-Crick dNTP incorporation.

161 tRNA decoding mechanisms: Watson-Crick, non-Watson-Crick or both types of interactions.

162 AlkD distort the DNA backbone to detect non-Watson-Crick base pairs without duplex intercalation.

163 d ternary (Pol X:DNA:MgdGTP with dG:dGTP non-Watson-Crick pairing) forms, along with functional analy

164 binding mode, and a novel mechanism for non-Watson-Crick incorporation by a low-fidelity DNA polymer

165 f messenger RNAs (mRNAs) and can involve non-Watson-Crick base pairing in the miRNA seed region.

166 Mismatched (non-Watson-Crick) base pairs represent the most common type

167 son reveals that domain II has multiple, non-Watson-Crick features that mimic A-form dsRNA.

168 s may locally influence the formation of non-Watson-Crick structures from otherwise complementary seq

169 MMR must be able to recognize non-Watson-Crick base pairs and excise the misincorporated n

170 t the 3' ss is mainly recognized through non-Watson-Crick base pairing with the 5' ss and branch poin

171 te AG dinucleotide is recognized through non-Watson-Crick pairing with the 5' splice site and the bra

172 secondary structures displaying noncanonical Watson-Crick base pairing, have recently emerged as key

173 ubfamily, could be replaced with noncovalent Watson-Crick hydrogen bonds without significantly affect

174 des all misfolded microstates with nonnative Watson-Crick (WC) and non-WC contacts.

175 rather than the major groove as in a normal Watson-Crick base pair.

176 pol ternary complex but deviate from normal Watson-Crick base-pairs.

177 used two different means to assemble DNA-NPs-Watson-Crick base-pairing interactions and depletion int

178 show that HCV IRES activity requires a 3-nt Watson-Crick base-pairing interaction between the apical

179 tes within the active site in the absence of Watson-Crick base pairing with template and mapped movem

180 AC8, GC8, and GN2, pointing to an absence of Watson-Crick hydrogen bonding, yet the presence of some

181 However, in the absence of Watson-Crick pairings, DNA can be structurally more dive

182 mi components and different architectures of Watson-Crick complementary single-stranded DNA ("sticky

183 sis of DNA stretching shows that breaking of Watson-Crick bonds is not necessary for the existence of

184 The predictable chemistry of Watson-Crick base-pairing imparts a unique structural pr

185 nteractions, based on the complementarity of Watson-Crick binding.

186 indicating a significant destabilization of Watson-Crick hydrogen bonding.

187 of recently discovered transient flipping of Watson-Crick (WC) pairs into Hoogsteen (HG) pairs (HG br

188 le proton spectra establish the formation of Watson-Crick G.C alignment for the two base pairs betwee

189 Ps containing hydrophobic bases incapable of Watson-Crick hydrogen bonding opposite natural template

190 ion of an alignment based on isostericity of Watson-Crick and non-Watson-Crick base pairs, along with

191 In addition, the loss of Watson-Crick hydrogen bonding between the nucleotide and

192 rticipate in pairing interactions outside of Watson and Crick's rules.

193 The specificity and predictability of Watson-Crick base pairing make DNA a powerful and versat

194 er-represented in the methylation profile of Watson Grade 1 samples (mild hippocampal sclerosis).

195 The programmability of Watson-Crick base pairing, combined with a decrease in t

196 at the nanoscale through the specificity of Watson-Crick base pairing, allowing both complex self-as

197 y, can provide insight into the stability of Watson-Crick pairs and the role of specific functional g

198 Intermolecular enol tautomers of Watson-Crick base pairs could emerge spontaneously via i

199 ined here still significantly exceed that of Watson-Crick G.C base pairs, such that DNA i-motif confo

200 Meanwhile, nucleic acid probes based on Watson-Crick base-pairing rules are also being widely ap

201 y beyond that which can be achieved based on Watson-Crick base-pairing.

202 as opposed to classic probes solely based on Watson-Crick recognition.

203 to form a Z:P pair with a standard "edge on" Watson-Crick geometry, but joined by rearranged hydrogen

204 zin-4-one and 6-amino-5-nitropyridin-2-one), Watson-Crick complements from an artificially expanded g

205 fect of triphosphate/Mg(2+) interaction over Watson-Crick hydrogen bonding was found and discussed.

206 in how low-fidelity DNA polymerases overcome Watson-Crick base pairing to catalyze non-Watson-Crick d

207 loping unnatural base pair to adopt a planar Watson-Crick-like structure.

208 equilibrium with short-lived, low-populated Watson-Crick-like mispairs that are stabilized by rare e

209 he i-motif DNA, consistent with the possible Watson-Crick interaction of 2 and G14.

210 dly copy a DNA template according to precise Watson-Crick base pairing.

211 Although m(6)A does not preclude Watson-Crick base pairing, the N(6)-methyl group alters

212 erases must select nucleotides that preserve Watson-Crick base pairing rules and choose substrates wi

213 A polymerase I (Klenow fragment) to preserve Watson-Crick base-pairing rules.

214 ith a closed protein conformation and pseudo-Watson-Crick base pair.

215 The fraudulent, pseudo-Watson-Crick ClU-A base pair is sufficiently stable to a

216 nar base pair, the first structure of pseudo-Watson-Crick O6MeG.T formed in the active site of a DNA

217 all cases with high 3'-5' regioselectivity, Watson-Crick base pairing between the RNA monomers and t

218 8, which in tRNA3(Lys) is modified to remove Watson-Crick pairing.

219 nical DNA double helix structure that retain Watson-Crick base-pairing have important roles in DNA re

220 he cleavage site (e.g. T^G), while retaining Watson-Crick sequence generality beyond those nucleotide

221 rboxyphenyl)methane ester (Cyt-S4), revealed Watson-Crick type nucleobase pairing of 6TG.

222 Reverse Watson-Crick G:C basepairs (G:C W:W Trans) occur frequen

223 he alphaA base is intrahelical, in a reverse Watson-Crick orientation, and forms a weak base pair wit

224 This observation of reverse Watson-Crick base pairing is further supported by therma

225 ilized by pseudoknot and long-range reversed Watson-Crick and Hoogsteen A*U pair formation.

226 e. bulge vs. contiguous pairs) and sequence (Watson-Crick vs. G:U pairs) preferences for human and mo

227 ugh tertiary interactions rather than simple Watson-Crick pairing.

228 Since Watson and Crick's historical papers on the structure an

229 mited by the need to forward-design specific Watson-Crick base pairing manually for any given target

230 due to the ability of 8-oxoG to form stable Watson-Crick base pairs with deoxycytidine (8-oxoG:dC) a

231 ismatch arrangements, but also in a standard Watson-Crick base pair, adopted the same C3'-endo ribose

232 astable kissing dimer is formed via standard Watson-Crick base pairs and then converted into a more s

233 ored to the 5'-end of the sequence by an A.T Watson-Crick base pair and a potential G.A noncanonical

234 t, consistent with stabilization by tertiary Watson-Crick base pairing found in the folded Diels-Alde

235 y specific tertiary interactions rather than Watson-Crick pairing.

236 ken together, these results demonstrate that Watson-Crick template-dependent 3'-5' nucleotide additio

237 ining only DNA components, establishing that Watson-Crick base-pairing interactions alone suffice for

238 NMR data reveal that Watson-Crick base pairing is maintained at both the 5' a

239 VNTRseek was used to analyze the Watson and Khoisan genomes (454 technology) and two 1000

240 ecule coordinating a Mg(2+) ion bound at the Watson-Crick edge of residue C7, or the N3 position of r

241 crosslinks, which, by covalently binding the Watson and the Crick strands of DNA, impede replication

242 ,N(6)-gamma-HMHP-dA is expected to block the Watson-Crick base pairing of the adducted adenine with t

243 MCM pore loops touch both the Watson and Crick strands, constraining duplex DNA in a b

244 contributions to recognition provided by the Watson-Crick face of the nucleobase, lesser contribution

245 ostere by Kool and colleagues challenged the Watson-Crick dogma that hydrogen bonds between complemen

246 ase pairs based on their ability to form the Watson-Crick-like conformation.

247 sDNA, likely due to the competition from the Watson-Crick base pairing.

248 r groove-positioned guanine amino group, the Watson-Crick partner to C3, acts as a wedge; facilitated

249 In the Watson genome, we identified 752 VNTRs with pattern size

250 re inserted into the helix, remaining in the Watson-Crick alignment.

251 (5)s(2)U(34).G(3) wobble base pair is in the Watson-Crick geometry, requiring unusual hydrogen bondin

252 ighly toxic lesions that covalently link the Watson and Crick strands of the double helix, are repair

253 modified nucleotide monomers maintained the Watson-Crick base pair fidelity.

254 rogrammable properties, the linearity of the Watson-Crick B-form duplex imposes limitations on 3D cry

255 ructures in which at least one strand of the Watson-Crick duplex is composed entirely of XNA.

256 ical modifications, e.g., methylation of the Watson-Crick face of unpaired adenine and cytosine resid

257 mers still significantly exceed those of the Watson-Crick G*C and neutral C*C base pairs, suggesting

258 ommodated with almost no perturbation of the Watson-Crick hydrogen-bond network and induces bend and

259 base pair tension due to the transfer of the Watson-Crick pairing of the complementary strand bases f

260 energetically preferred syn geometry on the Watson-Crick face to the higher-energy anti conformation

261 ed on 2D structures, which describe only the Watson-Crick (WC) base pairs.

262 Fpg uses an aromatic wedge to open the Watson-Crick base pair and everts the lesion into its ac

263 -IQ adopted the syn conformation placing the Watson-Crick edge of the modified dG into the major groo

264 Probing the Watson-Crick edges of the bases shows that bases 2-4 are

265 MBD4 specifically recognizes the Watson-Crick polar edge of thymine or 5hmU via the O2, N

266 Removing the Watson-Crick hydrogen bonding groups of N-3 and N(4)/O(4

267 crofluidic processor is used to separate the Watson and Crick strands of the double-stranded chromoso

268 Simulations suggest that the Watson-Crick base-pairing between G8 and C3, the hydroge

269 Thus, the Watson-Crick hydrogen bonding groups of a pyrimidine cle

270 In addition to the Watson-Crick pairing, the structures contain interesting

271 he additional nucleobases could expose their Watson-Crick and/or Hoogsteen faces for recognition in t

272 w recent quantum chemical estimates of their Watson-Crick interaction energy, pi-pi stacking energies

273 d acceptor groups, all while retaining their Watson-Crick geometries.

274 trand Specifier nucleotides stack with their Watson-Crick edges displaced toward the minor groove.

275 ir with the tRNA anticodon, stack with their Watson-Crick edges rotated toward the minor groove and e

276 r and show that the L-nucleotide forms three Watson-Crick hydrogen bonds with the templating nucleoti

277 n sequences would uniquely associate through Watson-Crick assembly to form closed-cycle or linear arr

278 cleoside can spontaneously associate through Watson-Crick canonical H-bonding and pi-pi stacking to f

279 of the base pair; intercalators that bind to Watson-Crick base pairs promote the polymerization of ol

280 in C(+)*C proton-bound dimers as compared to Watson-Crick G*C base pairs are the major forces respons

281 ) provide an alternative pairing geometry to Watson-Crick (WC) bps and can play unique functional rol

282 rees rotation of the purine base relative to Watson-Crick (WC) base pairing within DNA duplexes, crea

283 e is no mother-daughter bias with respect to Watson and Crick-containing strands of DNA.

284 ns that mirror those observed in traditional Watson-Crick complexes.

285 forming a sheared GG pair (G4-G6*, GG trans Watson-Crick/Hoogsteen), both uracils (U7 and U7*) flipp

286 tly polymerize NTPs incapable of forming two Watson-Crick hydrogen bonds with the templating base wit

287 lectron-hole transport between the other two Watson-Crick-paired stems, across the three-way junction

288 e unique geometry of canonical G.C and A.T/U Watson-Crick base pairs to discriminate against DNA and

289 058 stacking leading to disrupted A752-U2609 Watson-Crick (WC) interactions as well as hydrogen bondi

290 ures that are fully determined by underlying Watson-Crick base pairing.

291 ositions of the codon, which show an unusual Watson-Crick/Hoogsteen geometry.

292 on at the nanoscale can be achieved by using Watson-Crick base-pairing to direct the assembly and ope

293 ciferase gene in cell-free translation using Watson-Crick base pairing between the mRNA and a complem

294 d of the DNAzyme binds the substrate DNA via Watson-Crick bonding and the 3'-end binds through format

295 ably well adapted to accommodate the 5'T via Watson-Crick base pairing, in accord with a proposed rol

296 ession of disease-associated transcripts via Watson-Crick hybridization.

297 looped-out alignment facilitated by weakened Watson-Crick and reversed non-canonical flanking pairs.

298 polymer systems such as nucleic acids, where Watson-Crick H-bonds are fully paired in double-helical

299 ) the classical intercalation motif in which Watson-Crick base pairing is intact at the lesion site a

300 wn to form a natural base-base mismatch with Watson-Crick-like geometry.