ライフサイエンスコーパス: Crick

1 1-A C(alpha) root mean square deviation of a Crick-ideal backbone.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

20 ary helical structures, which reduces to the Crick parameterization as a special case.

21 natural alpha-helical coiled coils using the Crick parameterization.

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

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

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

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

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

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

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

29 ate for the free energy change when a Watson-Crick base pair in stem 2 is changed, (2) the loop entro

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

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

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

33 upon addition of dCTP, which forms a Watson-Crick base pair with template dG and not during mispairi

34 rier ligand and secondarily to form a Watson-Crick base pair.

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

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

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

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

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

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

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

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

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

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

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

46 ificity through an intramolecular G:A Watson-Crick/sugar-edge base interaction, an unusual pairing pr

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

48 alyzes an unexpected second activity: Watson-Crick-dependent 3'-5' nucleotide addition that occurs in

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

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

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

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

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

54 nowledge of helical DNA structure and Watson-Crick base pairing rules, scientists have constructed a

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

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

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

58 ded by Watson-Crick pairs, the AG and Watson-Crick pairs are all head-to-head imino-paired (cis Watso

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

60 e stabilities relative to native base Watson-Crick pairings, and this phenomenon is used here to engi

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

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

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

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

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

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

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

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

72 For loops bounded by Watson-Crick pairs, the AG and Watson-Crick pairs are all head-

73 helical regions composed of canonical Watson-Crick and related base pairs, as well as single-stranded

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

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

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

79 y indistinguishable from a canonical, Watson-Crick base pair in double-stranded DNA.

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

81 opts canonical UG wobble pairing (cis Watson-Crick/Watson-Crick), with AG pairs that are only weakly

82 re all head-to-head imino-paired (cis Watson-Crick/Watson-Crick).

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

84 ghbors, with CA adjacent to a closing Watson-Crick pair, are further stabilized when the pH is lowere

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

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

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

88 ing and instead have 11-12 contiguous Watson-Crick pairs to the center of the miRNA.

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

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

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

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

93 in competition with the corresponding Watson-Crick duplex.

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

95 e we show that intentionally creating Watson-Crick mismatches near the cleavage site relaxes the site

96 l UG wobble pairing (cis Watson-Crick/Watson-Crick), with AG pairs that are only weakly imino-paired.

97 o-head imino-paired (cis Watson-Crick/Watson-Crick).

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

99 quence-specific manner through direct Watson-Crick base pairing.

100 thought to identify targets by direct Watson-Crick pairing with invasive 'protospacer' DNA, but how t

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

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

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

104 dehydrated environment that envelops Watson-Crick nascent base pairs and serve to enhance base selec

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

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

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

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

109 Because of the extensive Watson-Crick complementarity between deoxyribozyme and substrat

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

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

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

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

114 ro assays revealed an active role for Watson-Crick base-pairing at positions 9 and 10 in promoting st

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

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

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

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

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

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

121 mase does not absolutely need to form Watson-Crick hydrogen bonds to efficiently polymerize a NTP.

122 6-Aminopyridin-2-ones form Watson-Crick pairs with complementary purine analogues to add a

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

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

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

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

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

128 me substrate sequences even when full Watson-Crick complementarity is maintained, corresponding to a

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

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

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

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

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

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

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

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

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

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

139 5'-end nucleotide need not engage in Watson-Crick (W/C) H-bonding but must fit the general shape of

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

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

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

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

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

145 ds and cross-pair with RNA and DNA in Watson-Crick fashion.

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

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

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

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

150 cleoside analogs (xDNA) that maintain Watson-Crick base pairing and base stacking ability; however, t

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

152 s of magnitude relative to a matched (Watson-Crick) control.

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

154 n underappreciated role in modulating Watson-Crick base pairing strength and potentially pi-pi stacki

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

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

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

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

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

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

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

162 hermophilus Kt-23 has two further non-Watson-Crick base pairs within the non-canonical helix, three a

163 istort the DNA backbone to detect non-Watson-Crick base pairs without duplex intercalation.

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

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

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

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

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

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

170 eals that domain II has multiple, non-Watson-Crick features that mimic A-form dsRNA.

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

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

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

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

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

178 is possible with an alternative, non-Watson-Crick-paired duplex that selectively binds a complementa

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

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

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

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

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

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

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

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

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

188 The specificity and predictability of Watson-Crick base pairing make DNA a powerful and versatile mat

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

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

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

192 Intermolecular enol tautomers of Watson-Crick base pairs could emerge spontaneously via interbas

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

194 ions, based on the complementarity of Watson-Crick binding.

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 on spectra establish the formation of Watson-Crick G.C alignment for the two base pairs between the l

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

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

200 aining hydrophobic bases incapable of Watson-Crick hydrogen bonding opposite natural template bases.

201 8, and GN2, pointing to an absence of Watson-Crick hydrogen bonding, yet the presence of some type of

202 ting a significant destabilization of Watson-Crick hydrogen bonding.

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

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

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

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

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

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

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

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

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

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

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

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

215 y a DNA template according to precise Watson-Crick base pairing.

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

217 must select nucleotides that preserve Watson-Crick base pairing rules and choose substrates with the

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

219 thus providing a platform to promote Watson-Crick base pairing between C9 of the decaloop and the fi

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

221 The fraudulent, pseudo-Watson-Crick ClU-A base pair is sufficiently stable to avoid gl

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

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

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

225 NA double helix structure that retain Watson-Crick base-pairing have important roles in DNA recogniti

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

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

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

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

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

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

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

233 tiary interactions rather than simple Watson-Crick pairing.

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

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

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

237 kissing dimer is formed via standard Watson-Crick base pairs and then converted into a more stable e

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

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

240 fic tertiary interactions rather than Watson-Crick pairing.

241 NMR data reveal that Watson-Crick base pairing is maintained at both the 5' and 3' n

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

243 ether, these results demonstrate that Watson-Crick template-dependent 3'-5' nucleotide addition is a

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

245 rted into the helix, remaining in the Watson-Crick alignment.

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

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

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

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

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

251 Simulations suggest that the Watson-Crick base-pairing between G8 and C3, the hydrogen bond

252 ty is determined by the nature of the Watson-Crick base-pairing region of the NTP base and the nature

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

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

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

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

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

258 utions to recognition provided by the Watson-Crick face of the nucleobase, lesser contributions from

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

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

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

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

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

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

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

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

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

268 e-positioned guanine amino group, the Watson-Crick partner to C3, acts as a wedge; facilitated by a h

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

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

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

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

273 the tRNA anticodon, stack with their Watson-Crick edges rotated toward the minor groove and exhibit

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

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

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

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

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

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

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

281 base pair; intercalators that bind to Watson-Crick base pairs promote the polymerization of oligonucl

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

283 mirror those observed in traditional Watson-Crick complexes.

284 g a sheared GG pair (G4-G6*, GG trans Watson-Crick/Hoogsteen), both uracils (U7 and U7*) flipped out

285 ymerize NTPs incapable of forming two Watson-Crick hydrogen bonds with the templating base with the e

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

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

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

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

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

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

292 he nanoscale can be achieved by using Watson-Crick base-pairing to direct the assembly and operation

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

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

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

296 s recognized within a deep pocket via Watson-Crick pairing with C15.

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

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

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

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