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 pairs in dsDNA exist in dynamic equili

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

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

12 t nearly 100% heteroplasmy, which disrupts a Watson-Crick base pair in the T-stem-loop.

13 erved that the probability a G/U will form a Watson-Crick (WC) base pair depends on sequence context.

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

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

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

17 ing Hoogsteen base pairing with adenine in a Watson-Crick-like geometry.

18 The opening of a Watson-Crick double helix is required for crucial cellul

19 damaged nucleotides, with the exception of a Watson-Crick-like dGTP insertion opposite T, using BER D

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

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

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

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

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

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

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

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 is, allowing the concurrent formation of all Watson-Crick bases.

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

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

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

34 rticle.See also the editorial by Kallmes and Watson in this issue.

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

36 age contrast in conjunction with Paxinos and Watson's (2007) stereotaxic rat brain atlas.

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

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 ermediates in the transition pathway between Watson-Crick and HG base pairs for both naked B-DNA and

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 Relative to unpaired adenines in a bulge, Watson-Crick A-T base pairs in dsDNA only conferred ~130

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

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

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

48 n in tumorigenesis.See related commentary by Watson and Bitler, p.

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

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

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

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

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

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

55 leic acid analogs designed to bind to RNA by Watson-Crick base pairing.

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

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

58 its high programmability based on canonical Watson-Crick base pairing, with crystal assembly in all

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

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

61 an form many structures beyond the canonical Watson-Crick double helix.

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

63 are an alternative base pairing to canonical Watson-Crick bps and are thought to play important bioch

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

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

66 The Chick-Watson inactivation kinetic model, based on integral CT

67 The extension of the Chick-Watson model, in the ICT domain, described well the redu

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

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

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

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

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

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

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

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

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

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

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

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

80 nodeoxyadenosine (epsilondA), which disrupts Watson-Crick base pairing, occurs via Poliota/Polzeta-,

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

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

83 raying individual base blocks, DSSR can draw Watson-Crick pairs as long blocks and highlight the mino

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

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

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

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

88 It exhibits Watson-Crick connectivity as found in DNA but which is u

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

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

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

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

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

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

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

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

97 NN predictions for Watson-Crick and modified base pairs yielded an overall

98 ly disfavored anti conformation required for Watson-Crick pairing is responsible for the reduced anne

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

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

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

102 6-Aminopyridin-2-ones form Watson-Crick pairs with complementary purine analogues t

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

104 oogsteen bps in crystal structures that form Watson-Crick bps when examined under solution conditions

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

106 oxoA adopted an anti conformation and formed Watson-Crick base pair.

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

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

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

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

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

112 In contrast to the Galton-Watson model, our model can recreate the log-normal segm

113 asses the statistical accuracy of the Galton-Watson model, which is the most commonly employed model

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

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

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

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

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

119 d into the helix and forms a trans Hoogsteen-Watson-Crick base pair with a uridine, thus becoming an

120 is based on the Langmuir-Hinshelwood-Hougen-Watson (L-H-H-W) postulates and considers the adsorption

121 n-based, cross-sectional analysis of the IBM Watson Health MarketScan insurance claim dataset, which

122 cal milieu, is characterized by the iconical Watson-Crick nucleo-base pairing.

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

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

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

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

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

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

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

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

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

132 bone-for example, the bases participating in Watson-Crick pairing in the double helix, or the side ch

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

134 display noncovalent interactions, including Watson-Crick base pairing, Hoogsteen H-bonding, and pai-

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

136 within known structured RNAs are folded into Watson-Crick (WC) base pairs, and sequence changes that

137 igned branched kissing-loop motif, involving Watson-Crick base pairing between the single-stranded re

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

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

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

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

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

143 he end of the substrate-binding pocket mimic Watson-Crick interactions providing guanine base specifi

144 ity through a conformational shift of native Watson-Crick pair to a wobble-like pattern with the form

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

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

147 rs for modified nucleotides with neighboring Watson-Crick base pairs.

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

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

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

151 n for these residues in recognition of a non-Watson-Crick G(-1):A(73) bp, which had not been describe

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

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

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

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

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

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

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

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

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

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

162 ters for qualitative characterization of non-Watson-Crick double-helical structures; new structural p

163 specific differences in the formation of non-Watson-Crick G-quadruplex (GQ) structures.

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

165 acterized by the absence of the peculiar non-Watson-Crick interactions in the loop region.

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

167 fer through RNA duplexes and through the non-Watson-Crick base-paired region of an RNA aptamer.

168 and physicochemical properties of these non-Watson-Crick G4 structures make them important targets f

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

170 erefore, electron transport also through non-Watson-Crick base-paired regions might be required.

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

172 ecursor messenger RNA (pre-mRNA) through non-Watson-Crick pairing with the 5'SS and the branch adenos

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

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

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

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

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

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

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

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

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

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

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

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

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

186 ative to a DNA duplex consisting entirely of Watson-Crick base-pairs.

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

188 automeric forms that enable the formation of Watson-Crick-like (WC-like) mispairs, which have been pr

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

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

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

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

193 loring the discrete two-dimensional space of Watson-Crick base pairing possibilities.

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

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

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

197 aughter cells derives from inheriting 'older Watson' versus 'older Crick' DNA strand from the parenta

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

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

200 ethods used to probe RNA structure report on Watson-Crick pairing, but tertiary structure parameters

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

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

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

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

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

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

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

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

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

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

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

212 8, which in tRNA3(Lys) is modified to remove Watson-Crick pairing.

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

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

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

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

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

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

219 ity, responsible for the formation of robust Watson-Crick H-bonded cyclic tetramers, and nucleation-g

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

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

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

223 cts, van der Waals interactions and specific Watson-Crick polar hydrogen bonds to ensure high enzymat

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

225 led nanoscale architectures through specific Watson-Crick base-pairing, molecular plasticity, and int

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

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

228 In a previous study (Watson et al., 2017), we characterised the drivers selec

229 ion by dimethyl sulfate (DMS) when in an A-T Watson-Crick versus Hoogsteen conformation.

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

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

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

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

234 Our results indicate that Watson-Crick faces of nucleobases are accessible to alky

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

236 As the Watson-Crick faces of nucleobases are protected in dsDNA

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

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

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

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

241 um with Hoogsteen base pairs that expose the Watson-Crick faces of purine nucleobases to solvent.

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

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

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

245 otifs of protein-adenine interactions in the Watson-Crick edge of adenine and shows that all of adeni

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

247 larger than those induced by changes in the Watson-Crick sequence.

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

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

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

251 bonds along the entire Hoogsteen edge of the Watson-Crick base pair.

252 The specificity and predictability of the Watson-Crick base pairing make DNA an excellent building

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

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

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

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

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

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

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

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

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

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

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

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

265 However, damage to the Watson-Crick faces of nucleobases has been reported in d

266 ed that deleterious alkylation damage to the Watson-Crick faces of nucleobases predominantly occurs w

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

268 zed compound that covalently attaches to the Watson-Crick-Franklin face of several nucleobases, addre

269 ortune in my career were to stumble upon the Watson-Gilbert laboratory at Harvard when I entered grad

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

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

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

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

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

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

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

277 ymine, is a left-handed helix formed through Watson-Crick pairing between nucleobases.

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

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

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

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

282 o the lack of modular specificity similar to Watson-Crick base pairing.

283 ch they offer versatility beyond traditional Watson-Crick interactions.

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

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

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

287 058 stacking leading to disrupted A752-U2609 Watson-Crick (WC) interactions as well as hydrogen bondi

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

289 is of a novel bio-MOF featuring unobstructed Watson-Crick faces of adenine (Ade) pointing towards the

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

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

292 aining two nucleic acid elements coupled via Watson-Crick base pairing: (i) an aptamer sequence, whic

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

294 y of l-DNA to interact with native d-RNA via Watson-Crick base pairing.

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

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

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

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

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

300 mation and formed a Hoogsteen base pair with Watson-Crick-like geometry, highlighting the dual-coding

301 ombinations involve cognate recognition with Watson-Crick pairs and 59 involve near-cognate recogniti