ライフサイエンスコーパス: Crick

1 In 1953, Watson and Crick not only described the double-helix structure of D

2 lesions that covalently link the Watson and Crick strands of the double helix, are repaired by a com

3 processor is used to separate the Watson and Crick strands of the double-stranded chromosomal DNA in

4 MCM pore loops touch both the Watson and Crick strands, constraining duplex DNA in a bent configu

5 describing the DNA double helix, Watson and Crick suggested that "spontaneous mutation may be due to

6 from ideal, rigid helices allowed Watson and Crick to unravel the DNA structure, thereby elucidating

7 Since Watson and Crick's historical papers on the structure and function

8 n pairing interactions outside of Watson and Crick's rules.

9 double helix symmetry revealed by Watson and Crick, classical X-ray diffraction patterns of DNA conta

10 structure of DNA was published by Watson and Crick, Sanger's group announced the first amino acid seq

11 her-daughter bias with respect to Watson and Crick-containing strands of DNA.

12 ic range were originally proposed in 1965 by Crick and Wyman in a manuscript circulated among the pro

13 ractions were predicted over 50 years ago by Crick, and limited experimental data obtained in solutio

14 Since a seminal paper by Crick and Koch (1998) claimed that a science of consciou

15 In September 1957, Francis Crick gave a lecture in which he outlined key ideas abou

16 nal posthumously released article of Francis Crick, written with Christof Koch, the claustrum was sug

17 from inheriting 'older Watson' versus 'older Crick' DNA strand from the parental cell, strands that a

18 renewed interest in the last 15 years since Crick and Koch's article.

19 e clear consensus has emerged which supports Crick and Koch's primary interest in the claustrum: the

20 ch, by covalently binding the Watson and the Crick strands of DNA, impede replication and transcripti

21 es produced by varying the parameters in the Crick coiled coil-generating equations.

22 eer, as well as his lab's future move to the Crick Institute.

23 We used the Crick generating equations(5) to produce millions of fou

24 The DNA 13-mer, BET66, self-assembles via Crick-Watson and noncanonical base pairs to form crystal

25 Watson-Crick base pairing of the modified guanine with the part

26 Watson-Crick base pairs in dsDNA exist in dynamic equilibrium w

27 Watson-Crick base-pairing slows the rate of vibrational cooling

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

29 ions, a free 5'-flap (if present), a Watson-Crick base pair at the terminus of the reacting duplex,

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

31 y 100% heteroplasmy, which disrupts a Watson-Crick base pair in the T-stem-loop.

32 that whereas hydrogen bonds between a Watson-Crick base pair of template DNA and incoming NTP are cri

33 ue to its anti-conformation forming a Watson-Crick base pair with correct deoxycytidine 5'-triphospha

34 Moreover, dCTP forms a Watson-Crick base pair with dG, two nucleotides upstream from t

35 The opening of a Watson-Crick double helix is required for crucial cellular proc

36 A Watson-Crick pair leads to an inability to fold in metal ions a

37 e base of the incoming dNTP to form a Watson-Crick pair with the template base but also distinguish t

38 asis of its poor geometric match to a Watson-Crick pair.

39 ic functional groups in stabilizing a Watson-Crick pair.

40 zyl) that can alternatively pair in a Watson-Crick sense opposite cytosine (C) or as a Hoogsteen pair

41 tate, polbeta appears to allow only a Watson-Crick-like conformation for purine*pyrimidine base pairs

42 cale conformational change to adopt a Watson-Crick-like dG*dTTP base pair and a closed protein confor

43 nucleotides, with the exception of a Watson-Crick-like dGTP insertion opposite T, using BER DNA liga

44 rms three hydrogen bonds and adopts a Watson-Crick-like geometry rather than a wobble geometry, sugge

45 errors occur when mismatches adopt a Watson-Crick-like geometry through tautomerization and/or ioniz

46 gsteen base pairing with adenine in a Watson-Crick-like geometry.

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

48 ution, which selectively knocks out a Watson-Crick-type (G)N2H2...O2(T) hydrogen bond, significantly

49 The abundant Watson-Crick face methylations in biological RNAs such as N(1)

50 ad antiparallel G4 with an additional Watson-Crick CG base pair.

51 and type and orientation of adjacent Watson-Crick pairs.

52 nd classify modifications that affect Watson-Crick base pairing at three different levels of the Arab

53 owing the concurrent formation of all Watson-Crick bases.

54 tes mutagenic replication by allowing Watson-Crick-mode for O6MeG.T but not for O6MeG.C in the enzyme

55 ring DNA synthesis, base stacking and Watson-Crick (WC) hydrogen bonding increase the stability of na

56 nce of both stacking interactions and Watson-Crick base pairing.

57 coiled DNA via combined Hoogsteen and Watson-Crick binding.

58 es show Hoogsteen BrG.G base pair and Watson-Crick BrG.C base pair.

59 except when the mutations occurred at Watson-Crick paired sites.

60 tes in the transition pathway between Watson-Crick and HG base pairs for both naked B-DNA and A-RNA d

61 anionic species form hydrogen-bonded Watson-Crick-like base pairs.

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

63 n nonadjacent regions and employ both Watson-Crick and non-Watson-Crick base-pairing, screening of ca

64 tive to unpaired adenines in a bulge, Watson-Crick A-T base pairs in dsDNA only conferred ~130-fold p

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

66 Sequence specificity is provided by Watson-Crick base pairing between the DNA substrate and two oli

67 Self-assembly of these oligomers by Watson-Crick base pairing of the recognition sequences creates

68 s to the selection of correct dNTP by Watson-Crick base pairing, but it cannot explain how low-fideli

69 r with an extended triangle strand by Watson-Crick base pairing.

70 optical detection can be achieved by Watson-Crick base pairing.

71 exes to their target nucleic acids by Watson-Crick base pairing.

72 id analogs designed to bind to RNA by Watson-Crick base pairing.

73 oparticle-QD assemblies programmed by Watson-Crick base-pairing.

74 tide is bound in either the canonical Watson-Crick base pair or a nonplanar base pair.

75 reveals that Fm7dG forms a canonical Watson-Crick base pair with dCTP, but metal ion coordination is

76 gh programmability based on canonical Watson-Crick base pairing, with crystal assembly in all three d

77 We propose that canonical Watson-Crick base triplets serve as the fundamental unit of pai

78 alternative base pairing to canonical Watson-Crick bps and are thought to play important biochemical

79 many structures beyond the canonical Watson-Crick double helix.

80 of the codon occurs in the canonical Watson-Crick geometry.

81 t stacks onto the pseudo-knot-closing Watson-Crick base pair.

82 le-check" provided by the concomitant Watson-Crick and Hoogsteen base pairings involved in target rec

83 pocket with planar stacking contacts, Watson-Crick polar hydrogen bonds and van der Waals interaction

84 y are incapable of forming contiguous Watson-Crick base pairs with each other-has enforced a "homochi

85 eliminates the need for conventional Watson-Crick base pairing.

86 ase to insert a mismatch with correct Watson-Crick geometry.

87 ease without the formation of correct Watson-Crick hydrogen bonds.

88 tion is strictly dependent on correct Watson-Crick pairing.

89 in competition with the corresponding Watson-Crick duplex.

90 nd A and engages in the corresponding Watson-Crick-like base pairs, forming stable duplexes.

91 conformational change of the designed Watson-Crick duplex region resulted in crystal packing differen

92 h p53, the current structures display Watson-Crick base pairs associated with direct or water-mediate

93 adenosine (epsilondA), which disrupts Watson-Crick base pairing, occurs via Poliota/Polzeta-, Rev1-,

94 ethyl-G, which results in a distorted Watson-Crick geometry at pH >9.

95 They disturb Watson-Crick base-pairing and base-stacking interactions, and c

96 individual base blocks, DSSR can draw Watson-Crick pairs as long blocks and highlight the minor-groov

97 These mispairs can evade Watson-Crick fidelity checkpoints and form with probabilities (

98 NA) bound to site I in RecA exchanges Watson-Crick pairing with a sequence-matched ssDNA that was par

99 It exhibits Watson-Crick connectivity as found in DNA but which is unusual

100 oparticle arrays and lattices exploit Watson-Crick base pairing of single-stranded DNA sequences as a

101 e design of these structures exploits Watson-Crick hybridization and strand exchange to stitch linear

102 o causes the enzyme to favor faithful Watson-Crick base pairing over mutagenic configurations.

103 vides a means to distinguish faithful Watson-Crick base-paired DNA from damaged DNA.

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

105 NN predictions for Watson-Crick and modified base pairs yielded an overall RMSD of

106 obase pairs follow standard rules for Watson-Crick base pairing but have rearranged hydrogen bonding

107 eA suggests that despite its need for Watson-Crick hydrogen bonding, Poleta can stabilize the adduct

108 avored anti conformation required for Watson-Crick pairing is responsible for the reduced annealing r

109 tta recovers the 10 NN parameters for Watson-Crick stacked base pairs and 32 single-nucleotide dangli

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

111 the two phosphate backbones, forcing Watson-Crick base-pairs within the duplex to flip outward.

112 oth guanines of the Pt-GG lesion form Watson-Crick base pairing with the primer terminus dC and the i

113 n, bases in the dsDNA attempt to form Watson-Crick bonds with the corresponding bases in the initiati

114 n bps in crystal structures that form Watson-Crick bps when examined under solution conditions.

115 6-Aminopyridin-2-ones form Watson-Crick pairs with complementary purine analogues to add a

116 -lived and low-abundance species form Watson-Crick-like base pairs, their conformation could not be d

117 opted an anti conformation and formed Watson-Crick base pair.

118 in the anti conformation and forming Watson-Crick pairs with dCTP or dC.

119 rG adopts anti conformation and forms Watson-Crick base pairing with the incoming dCTP analog.

120 s a fluorescent nucleotide that forms Watson-Crick base pairs with dG.

121 equence-specific excursions away from Watson-Crick base-pairing at CA and TA steps inside canonical d

122 hpoint are unpaired, despite the full Watson-Crick complementarity of the molecule.

123 biradicals return to the original GC Watson-Crick pairs, but up to 10% of the initially excited mole

124 n of individual guanine-cytosine (GC) Watson-Crick base pairs by ultrafast time-resolved UV/visible a

125 The mismatch has Watson-Crick geometry consistent with a tautomeric or ionized b

126 he loop residues of two hairpins have Watson-Crick complementarity.

127 can originate from a mismatch having Watson-Crick geometry, and they suggest a common catalytic mech

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

129 the helix and forms a trans Hoogsteen-Watson-Crick base pair with a uridine, thus becoming an integra

130 ieu, is characterized by the iconical Watson-Crick nucleo-base pairing.

131 argets (triplex association) and (ii) Watson-Crick complement-mediated displacement of the TFO and re

132 The 1-MeA lesion impairs Watson-Crick base pairing and blocks normal DNA replication.

133 ue to its inability to participate in Watson-Crick (W-C) base pairing.

134 5'-end nucleotide need not engage in Watson-Crick (W/C) H-bonding but must fit the general shape of

135 side analogue that can participate in Watson-Crick base pairing.

136 NA stability and increase affinity in Watson-Crick base pairing.

137 tron-driven proton transfer (EDPT) in Watson-Crick base pairs.

138 h a thymine-thymine (T-T) mismatch in Watson-Crick base-pairs and the ligative disassembly of MB.Hg(2

139 at there is a significant decrease in Watson-Crick duplex stability of the heterogeneous backbone chi

140 r example, the bases participating in Watson-Crick pairing in the double helix, or the side chains co

141 d alignment software can also include Watson-Crick base pairs, but none adequately addresses the need

142 y noncovalent interactions, including Watson-Crick base pairing, Hoogsteen H-bonding, and pai-pai sta

143 rogrammable intra- and intermolecular Watson-Crick base-pairing interactions.

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

145 ranched kissing-loop motif, involving Watson-Crick base pairing between the single-stranded regions o

146 ymerase incorporates ZTP opposite its Watson-Crick complement, imidazo[1,2-a]-1,3,5-triazin-4(8H)one

147 ween the complementary strand and its Watson-Crick pairing partners promotes the rapid unbinding of n

148 -phenothiazine, tCfTP) that maintains Watson-Crick base pairing with guanine.

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

150 of the substrate-binding pocket mimic Watson-Crick interactions providing guanine base specificity, w

151 ough a conformational shift of native Watson-Crick pair to a wobble-like pattern with the formation o

152 airs that are larger than the natural Watson-Crick architecture.

153 that the Z:P pair mimics the natural Watson-Crick geometry in RNA in the first example of a crystal

154 modified nucleotides with neighboring Watson-Crick base pairs.

155 odel of loop 6 that specifies all non-Watson-Crick base pair interactions, derived by isostericity-ba

156 nger RNAs (mRNAs) and can involve non-Watson-Crick base pairing in the miRNA seed region.

157 ' ss is mainly recognized through non-Watson-Crick base pairing with the 5' ss and branch point.

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

159 isostericity of Watson-Crick and non-Watson-Crick base pairs, along with the collapsing (horizontall

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

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

162 and employ both Watson-Crick and non-Watson-Crick base-pairing, screening of candidate binder ensemb

163 most such loops are structured by non-Watson-Crick basepairs and base stacking.

164 Isostericity relations between non-Watson-Crick basepairs are used in scoring sequence variants.

165 de building blocks catalyzed by a non-Watson-Crick DNA secondary structure (see picture).

166 on-Crick base pairing to catalyze non-Watson-Crick dNTP incorporation.

167 r qualitative characterization of non-Watson-Crick double-helical structures; new structural paramete

168 hese residues in recognition of a non-Watson-Crick G(-1):A(73) bp, which had not been described previ

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

170 ysicochemical properties of these non-Watson-Crick G4 structures make them important targets for drug

171 g mode, and a novel mechanism for non-Watson-Crick incorporation by a low-fidelity DNA polymerase.

172 Non-Watson-Crick interactions between the branch helix and 5'-splic

173 ed by the absence of the peculiar non-Watson-Crick interactions in the loop region.

174 ecoding mechanisms: Watson-Crick, non-Watson-Crick or both types of interactions.

175 inucleotide is recognized through non-Watson-Crick pairing with the 5' splice site and the branch-poi

176 messenger RNA (pre-mRNA) through non-Watson-Crick pairing with the 5'SS and the branch adenosine, in

177 ry (Pol X:DNA:MgdGTP with dG:dGTP non-Watson-Crick pairing) forms, along with functional analyses, to

178 ocally influence the formation of non-Watson-Crick structures from otherwise complementary sequences.

179 Mismatched (non-Watson-Crick) base pairs represent the most common type of DNA

180 ry structures displaying noncanonical Watson-Crick base pairing, have recently emerged as key control

181 y, could be replaced with noncovalent Watson-Crick hydrogen bonds without significantly affecting its

182 misfolded microstates with nonnative Watson-Crick (WC) and non-WC contacts.

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

184 rnary complex but deviate from normal Watson-Crick base-pairs.

185 o different means to assemble DNA-NPs-Watson-Crick base-pairing interactions and depletion interactio

186 hat HCV IRES activity requires a 3-nt Watson-Crick base-pairing interaction between the apical loop o

187 ntly discovered transient flipping of Watson-Crick (WC) pairs into Hoogsteen (HG) pairs (HG breathing

188 an alignment based on isostericity of Watson-Crick and non-Watson-Crick base pairs, along with the co

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

190 hin the active site in the absence of Watson-Crick base pairing with template and mapped movements of

191 nanoscale through the specificity of Watson-Crick base pairing, allowing both complex self-assembled

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

193 The predictable chemistry of Watson-Crick base-pairing imparts a unique structural programma

194 o a DNA duplex consisting entirely of Watson-Crick base-pairs.

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

196 onents and different architectures of Watson-Crick complementary single-stranded DNA ("sticky end") l

197 re still significantly exceed that of Watson-Crick G.C base pairs, such that DNA i-motif conformation

198 8, and GN2, pointing to an absence of Watson-Crick hydrogen bonding, yet the presence of some type of

199 However, in the absence of Watson-Crick pairings, DNA can be structurally more diverse.

200 provide insight into the stability of Watson-Crick pairs and the role of specific functional groups i

201 ic forms that enable the formation of Watson-Crick-like (WC-like) mispairs, which have been proposed

202 anwhile, nucleic acid probes based on Watson-Crick base-pairing rules are also being widely applied i

203 d that which can be achieved based on Watson-Crick base-pairing.

204 used to probe RNA structure report on Watson-Crick pairing, but tertiary structure parameters such as

205 sed to classic probes solely based on Watson-Crick recognition.

206 a Z:P pair with a standard "edge on" Watson-Crick geometry, but joined by rearranged hydrogen bond d

207 ne and 6-amino-5-nitropyridin-2-one), Watson-Crick complements from an artificially expanded genetic

208 low-fidelity DNA polymerases overcome Watson-Crick base pairing to catalyze non-Watson-Crick dNTP inc

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

210 brium with short-lived, low-populated Watson-Crick-like mispairs that are stabilized by rare enolic o

211 tif DNA, consistent with the possible Watson-Crick interaction of 2 and G14.

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

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

214 losed protein conformation and pseudo-Watson-Crick base pair.

215 e pair, the first structure of pseudo-Watson-Crick O6MeG.T formed in the active site of a DNA polymer

216 ses with high 3'-5' regioselectivity, Watson-Crick base pairing between the RNA monomers and the temp

217 h in tRNA3(Lys) is modified to remove Watson-Crick pairing.

218 vage site (e.g. T^G), while retaining Watson-Crick sequence generality beyond those nucleotides along

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

220 This observation of reverse Watson-Crick base pairing is further supported by thermal melti

221 Reverse Watson-Crick G:C basepairs (G:C W:W Trans) occur frequently in

222 aA base is intrahelical, in a reverse Watson-Crick orientation, and forms a weak base pair with a thy

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

224 sponsible for the formation of robust Watson-Crick H-bonded cyclic tetramers, and nucleation-growth c

225 e vs. contiguous pairs) and sequence (Watson-Crick vs. G:U pairs) preferences for human and mouse miR

226 tiary interactions rather than simple Watson-Crick pairing.

227 y the need to forward-design specific Watson-Crick base pairing manually for any given target structu

228 oscale architectures through specific Watson-Crick base-pairing, molecular plasticity, and intermolec

229 n der Waals interactions and specific Watson-Crick polar hydrogen bonds to ensure high enzymatic spec

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

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

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

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

234 istent with stabilization by tertiary Watson-Crick base pairing found in the folded Diels-Alderase st

235 fic tertiary interactions rather than Watson-Crick pairing.

236 nly DNA components, establishing that Watson-Crick base-pairing interactions alone suffice for comple

237 Our results indicate that Watson-Crick faces of nucleobases are accessible to alkylating

238 D structures, which describe only the Watson-Crick (WC) base pairs.

239 able properties, the linearity of the Watson-Crick B-form duplex imposes limitations on 3D crystal de

240 pg uses an aromatic wedge to open the Watson-Crick base pair and everts the lesion into its active si

241 ed nucleotide monomers maintained the Watson-Crick base pair fidelity.

242 long the entire Hoogsteen edge of the Watson-Crick base pair.

243 specificity and predictability of the Watson-Crick base pairing make DNA an excellent building materi

244 amma-HMHP-dA is expected to block the Watson-Crick base pairing of the adducted adenine with thymine,

245 ikely due to the competition from the Watson-Crick base pairing.

246 by Kool and colleagues challenged the Watson-Crick dogma that hydrogen bonds between complementary ba

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

248 f protein-adenine interactions in the Watson-Crick edge of adenine and shows that all of adenine's ed

249 oordinating a Mg(2+) ion bound at the Watson-Crick edge of residue C7, or the N3 position of residue

250 pted the syn conformation placing the Watson-Crick edge of the modified dG into the major groove.

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

252 difications, e.g., methylation of the Watson-Crick face of unpaired adenine and cytosine residues by

253 tically preferred syn geometry on the Watson-Crick face to the higher-energy anti conformation, posit

254 As the Watson-Crick faces of nucleobases are protected in dsDNA, it is

255 However, damage to the Watson-Crick faces of nucleobases has been reported in dsDNA in

256 deleterious alkylation damage to the Watson-Crick faces of nucleobases predominantly occurs when DNA

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

258 ill significantly exceed those of the Watson-Crick G*C and neutral C*C base pairs, suggesting that C(

259 U(34).G(3) wobble base pair is in the Watson-Crick geometry, requiring unusual hydrogen bonding to G

260 Thus, the Watson-Crick hydrogen bonding groups of a pyrimidine clearly pl

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

262 ed with almost no perturbation of the Watson-Crick hydrogen-bond network and induces bend and unwindi

263 ir tension due to the transfer of the Watson-Crick pairing of the complementary strand bases from the

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

265 MBD4 specifically recognizes the Watson-Crick polar edge of thymine or 5hmU via the O2, N3 and O

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

267 pound that covalently attaches to the Watson-Crick-Franklin face of several nucleobases, addresses th

268 rs based on their ability to form the Watson-Crick-like conformation.

269 tional nucleobases could expose their Watson-Crick and/or Hoogsteen faces for recognition in the majo

270 pecifier nucleotides stack with their Watson-Crick edges displaced toward the minor groove.

271 tor groups, all while retaining their Watson-Crick geometries.

272 t quantum chemical estimates of their Watson-Crick interaction energy, pi-pi stacking energies, as we

273 how that the L-nucleotide forms three Watson-Crick hydrogen bonds with the templating nucleotide dG a

274 nces would uniquely associate through Watson-Crick assembly to form closed-cycle or linear arrays of

275 e can spontaneously associate through Watson-Crick canonical H-bonding and pi-pi stacking to form sta

276 is a left-handed helix formed through Watson-Crick pairing between nucleobases.

277 tation of the purine base relative to Watson-Crick (WC) base pairing within DNA duplexes, creating al

278 de an alternative pairing geometry to Watson-Crick (WC) bps and can play unique functional roles in d

279 ack of modular specificity similar to Watson-Crick base pairing.

280 *C proton-bound dimers as compared to Watson-Crick G*C base pairs are the major forces responsible fo

281 mirror those observed in traditional Watson-Crick complexes.

282 offer versatility beyond traditional Watson-Crick interactions.

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

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

285 cking leading to disrupted A752-U2609 Watson-Crick (WC) interactions as well as hydrogen bonding betw

286 at are fully determined by underlying Watson-Crick base pairing.

287 novel bio-MOF featuring unobstructed Watson-Crick faces of adenine (Ade) pointing towards the MOF ca

288 s of the codon, which show an unusual Watson-Crick/Hoogsteen geometry.

289 e gene in cell-free translation using Watson-Crick base pairing between the mRNA and a complementary

290 ll adapted to accommodate the 5'T via Watson-Crick base pairing, in accord with a proposed role for P

291 DNA to interact with native d-RNA via Watson-Crick base pairing.

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

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

294 of disease-associated transcripts via Watson-Crick hybridization.

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

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

297 lassical intercalation motif in which Watson-Crick base pairing is intact at the lesion site and (2)

298 ions involve cognate recognition with Watson-Crick pairs and 59 involve near-cognate recognition pair

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

300 orm a natural base-base mismatch with Watson-Crick-like geometry.