ライフサイエンスコーパス: B-DNA

1 B-DNA becomes unstable under superhelical stress and is

2 exhibit sequence-induced curvature, adopt a B-DNA conformation as a function of increasing temperatu

3 stretched globally, but locally it adopts a B-DNA-like conformation that restricts the homology sear

4 for the study of this CG-rich sequence as a B-DNA duplex, mimicking the form that would be present i

5 er molecules within the hydration shell of a B-DNA dodecamer, which are of interest for many of its b

6 -44 mus) molecular dynamics simulations of a B-DNA duplex structure that addresses this hypothesis us

7 amics and ab initio quantum simulations on a B-DNA tetradecamer reveal activated reaction pathways th

8 ystal structures of CATGGGCCCATG and other A/B-DNA intermediates support a 'slide first, roll later'

9 ctra, all of the hairpins investigated adopt B-DNA structures, except for a hairpin with a short poly

10 to those previously derived for Family A and B DNA polymerases, parameters for analog incorporation r

11 ontinuum along the transition between A- and B-DNA.

12 A-DNA and B-DNA represent different conformations of the DNA molec

13 cal properties of low-linking number DNA and B-DNA respectively, suggest that removal of guanine meth

14 The interplay between H- and B-DNA and the fact that the process of transcription aff

15 s result in condensation of superhelical and B-DNA, displacement of intercalated ethidium bromide and

16 nate conformation to standard B-DNA known as B'-DNA.

17 orm double helix, Dsx(A) was crystallized as B-DNA and thus provides a model for the prebound conform

18 (CCGCTAGCGG), which has been crystallized as B-DNA, is seen to adopt only the double-helical form at

19 between different DNA conformations such as B-DNA, Z-DNA and S-DNA.

20 of molecular dynamics simulations of Ascona B-DNA consortium, we extracted hydrogen bonding, stackin

21 involving nine research groups, the "Ascona B-DNA Consortium" (ABC).

22 or deletions, reflecting differences between B DNA in BL21(DE3) and integrated restriction fragments

23 A, suggesting there is a correlation between B-DNA stacking and coaxial stacking in DNA junctions.

24 the creation of distorted junctions between B-DNA and Z-DNA.

25 ndergoes a conformational transition between B-DNA, single-stranded DNA, and atypical secondary DNA s

26 sugar puckering are indicative of canonical B DNA throughout the stem.

27 hin an H-palindrome, the H-DNA and canonical B-DNA are in a dynamic equilibrium that shifts toward H-

28 sient Hoogsteen (HG) base pairs in canonical B-DNA based on NMR carbon relaxation dispersion.

29 ing a static vector model based on canonical B-DNA are in good agreement with the experimental spectr

30 ert into adjacent major grooves on canonical B-DNA, implying that conformational changes within the F

31 ed state fully relaxes back to the canonical B-DNA form depends on the cation; however, for all catio

32 turally more rigid compared to the canonical B-DNA without crossover.

33 178-bp satellite sequence containing a CENP-B DNA binding domain (CENP-B box) shown herein to select

34 Clade B DNA and recombinant modified vaccinia Ankara (MVA) vac

35 lution structures of G-T mismatch-containing B-DNA, suggesting a dependence of G-T mismatch-induced s

36 Class B-type CpG DNA (CpG-B DNA) induced activation of PKD1 via a pathway that is

37 t expression of cytokines in response to CpG-B DNA.

38 Upon CpG-B DNA stimulation, PKD1 interacted with the TLR9/MyD88/I

39 Within crystals, B-DNA forms either right-handed crossovers by groove-bac

40 nding of the spatial differences that define B-DNA binding.

41 d to better represent the sequence-dependent B-DNA intrinsic mechanics, in particular with respect to

42 de mixed-sequence double-helical B-form DNA (B-DNA).

43 epresenting three structural classes of DNA (B-DNA, A-DNA, and four-stranded Holliday junctions).

44 lar surface upon Nkx2.5(C56S) binding duplex B-DNA.

45 binds to the AT-tract-containing DNA duplex (B* DNA, d[5'-G(3)A(5)T(5)C(3)-3']) with 1 order of magni

46 hst 33258 conjugates developed for exploring B-DNA groove recognition.

47 Family B DNA polymerases from archaea such as Pyrococcus furios

48 Archaeal family B DNA polymerases bind tightly to template-strand uracil

49 asis of ddNTP selectivity in archaeal family B DNA polymerases by randomly mutagenizing the gene enco

50 Archaeal family B DNA polymerases contain a specialised pocket that bind

51 The interaction of archaeal family B DNA polymerases with deaminated bases has been examine

52 on and inhibition of DNA synthesis by family B DNA polymerases.

53 Instead, Family B DNA polymerase (polB) was observed to rapidly fill the

54 ion factor C (the PCNA clamp loader), family B DNA polymerase, and flap endonuclease.

55 e [but not the exonuclease] domain of family B DNA polymerases, and this ORF has been tentatively ide

56 his paper, we describe mutants of the family B DNA polymerase from Pyrococcus furiosus (Pfu-Pol), wit

57 illustrates the modular nature of the Family B DNA polymerase structure.

58 The family B DNA polymerases replicate the genomes of archaea, one

59 we demonstrate that the thermostable family B DNA polymerase from Pyrococcus furiosus (Pfu Pol) cont

60 d in motif A of any of the four yeast family B DNA polymerases, DNA polymerase alpha, delta, epsilon

61 error prone variants of the archaeal family-B DNA polymerase from Pyrococcus furiosus have been inve

62 Archaeal family-B DNA polymerases bind tightly to deaminated bases and s

63 Archaeal family-B DNA polymerases bind tightly to uracil and hypoxanthin

64 Archaeal family-B DNA polymerases stall replication on encountering the

65 A mutant of the high fidelity family-B DNA polymerase from the archaeon Thermococcus gorgonar

66 /hypoxanthine is addressed, using the family-B DNA polymerase from Pyrococcus furiosus.

67 ochemistry, in contrast to the more flexible B-DNA duplexes.

68 For B-DNA in aqueous solution, the low-energy tail of the CT

69 rization of the structural couplings in free B-DNA in solution has been elusive, because of subtle ef

70 otions of phosphate groups and bases in free B-DNA in solution.

71 Contacts from B-DNA to UDG are mimicked by residues of the p56 helix,

72 a transition of the noncontacted region from B-DNA to B'-DNA.

73 A molecule undergoes a phase transition from B-DNA into an overstretched state at high forces.

74 er conditions that favor the transition from B-DNA to non-B-DNA conformations.

75 chers for decades is how the transition from B-DNA, the prevalent right-handed form of DNA, to Z-DNA

76 he dynamics involved in the transitions from B-DNA and A-RNA to Pauling (P) forms and to denatured st

77 ocking of the Ru-complex onto a rich guanine B-DNA decamer, where a Ru-N7(guanine) interaction is det

78 t no topological changes on the right-handed B-DNA to which they are bound.

79 in the molecular mechanism of double-helical B DNA formation.

80 be applied to various nucleic acid helices: B-DNA, A-DNA, RNA, DNA-PNA, or others.

81 cted by copy number variations and hepatitis B DNA insertions, and it can be found mutated in preneop

82 tion of BALB/c mice indicated that hepatitis B DNA vaccine/Man-CS-Phe polyplexes not only induced mul

83 om a range of -95 degrees to -120 degrees in B DNA, and -77 degrees in the WT M.HhaI complex.

84 d by Raman spectroscopy to assess changes in B-DNA secondary structure induced by superhelical stress

85 quivalent to the mean rise per base found in B-DNA.

86 cs simulations in solution for the lesion in B-DNA duplexes, with four partner bases opposite the NI.

87 e (TG) and 5-methylcytosine guanine (mCG) in B-DNA, we predict that the cross-link lesion, which was

88 oups show distinctive stacking properties in B-DNA, suggesting there is a correlation between B-DNA s

89 -CGCGCGCGCGCG-3')2 dodecamers in solution in B-DNA, A-RNA, Z-DNA and Z-RNA forms.

90 h desolvated ion bridges in the GpC steps in B-DNA and A-RNA; direct binding to backbone oxygens; bin

91 Our results show that in B-DNA, cytosine amino groups are totally inaccessible fo

92 inter- and intrastrand reactions, while, in B-DNA, a more shallow distance dependence is evident wit

93 nition of homology between chemically intact B-DNA molecules should be possible in vivo.

94 ctural analog of H-DNA that cannot flip into B-DNA, and studied the effects of this structure on tran

95 ave sufficient binding free energy to invade B-DNA.

96 The advantages of investigating B-DNA in the hydrated state, as opposed to A-DNA in the

97 or of NF kappa B (IKK) activity and NF kappa B DNA binding potential but not by blocking TNF-induced

98 tor, MG-132, blocked BBS-stimulated NF kappa B DNA binding, and IL-8 and VEGF expression and secretio

99 L-1/TNF-stimulated nuclear factor (NF)-kappa B DNA binding activity and inhibitor of kappa B (I kappa

100 demonstrated that IL-1 beta induced NF-kappa B DNA binding activity in HT-29 cells, and the activated

101 Soon after infection, AP-1 and NF-kappa B DNA binding activity was increased.

102 posure of HASMC to CXCL16 increased NF-kappa B DNA binding activity, induced kappa B-driven luciferas

103 f I kappa B alpha and inhibition of NF-kappa B DNA binding activity.

104 in both cell types without altering NF-kappa B DNA binding activity.

105 eam of NF-kappa B and regulates the NF-kappa B DNA binding activity.

106 and Akt phosphorylation, as well as NF-kappa B DNA binding and NF-kappa B transcriptional activity in

107 with lithium induced both enhanced NF-kappa B DNA binding and NF-kappa B-dependent transcriptional a

108 tion and time dependently activated NF-kappa B DNA binding and suppressed cell contraction to acetylc

109 capacity of the inhibitors to block NF-kappa B DNA binding in 293 cells.

110 , inhibitors of PI 3-kinase blocked NF-kappa B DNA binding in Ikk beta-/- but not Ikk alpha-/- or wil

111 of PI 3-kinase blocked TNF-induced NF-kappa B DNA binding in the 293 line of embryonic kidney cells,

112 tated receptor was unable to induce NF-kappa B DNA binding or transactivation, as demonstrated by ele

113 The NF-kappa B DNA binding was approximately 6-fold greater in cells

114 have observed that a specific type of kappa B DNA sequence motif supports both NF-kappaB p65 homodim

115 her preferentially and assume the well-known B-DNA structure when they do so; the helically repeating

116 produces no substantial change in the local B-DNA conformation.

117 utside the minor groove of the duplex 10-mer B-DNA sequence d(CTACTACTGG).d(CCAGTAGTAG), using densit

118 rse-grained representation designed to mimic B-DNA, to predict the properties of DNA Holliday junctio

119 ng of this transcription activator to a more B-DNA-like conformation.

120 e-fields to predict the structure of two new B-DNA dodecamers, determined herein by means of 1H nucle

121 Non-B DNA structural elements (hairpins and slipped structur

122 Non-B DNA structures (slipped structures with loops, crucifo

123 single-stranded character and, hence, a non-B DNA conformation both in vivo and in vitro.

124 8 is a fragile site, because it adopts a non-B DNA conformation that can be cleaved by the RAG comple

125 The bcl-2 Mbr assumes a non-B DNA conformation, thus explaining its distinctive frag

126 as single-stranded character and hence a non-B DNA conformation.

127 y of the MOR gene promoter by adopting a non-B DNA conformation.

128 ropensity of origins to unwind and adopt non-B DNA structure, rather than the ability to form G4, is

129 uence inserts that do, and do not, adopt non-B DNA structures in vitro.

130 y dynamic and to have potential to adopt non-B DNA structures.

131 d with Friedreich's ataxia (FRDA) adopts non-B DNA structures, (triplexes and sticky DNA).

132 A or CSB leads to polymerase stalling at non-B DNA in a neuroblastoma cell line, in particular at G-q

133 Although both non-B DNA and WRN-KD served to increase the mutation frequen

134 analyzed, breakpoints were explicable by non-B DNA structure formation.

135 We determined non-B DNA-induced mutation frequencies and spectra in human

136 d show high incidence at repetitive DNA, non-B DNA structures, DNA-protein barriers, and highly trans

137 hensive study of the occurrence of B DNA-non-B DNA transition-susceptible sites (non-B DNA motifs) wi

138 ion process invoke an important role for non-B DNA conformations which may be adopted by these repeat

139 the TRs are G rich and predicted to form non-B DNA structures (including G-quadruplex) in vivo.

140 from the human PKD1 gene, known to form non-B DNA structures, induced long deletions and other insta

141 ic kidney disease (PKD1) intron 21 forms non-B DNA secondary structures in vitro.

142 human and mouse genomic features (e.g., non-B DNA structure, recombination rates, and histone modifi

143 Hence, non-B DNA conformations are critical for these mutagenesis m

144 While individual non-B DNA structures have been shown to impact gene expressi

145 f the expansion process the formation of non-B DNA conformations by the repeat sequence has previousl

146 We compared the distributions of non-B DNA motifs in the regulatory regions of operons with t

147 criptional silencing by the formation of non-B DNA structures (triplexes or sticky DNA), the formatio

148 However, the role of non-B DNA structures in many lower organisms, in particular

149 proteins are active in the resolution of non-B DNA structures including interstrand crosslinks, G qua

150 which allows reconciling mutagenicity of non-B DNA structures with their location in functionally imp

151 ming mechanical unfolding experiments of non-B DNA structures.

152 integrating annotations and analysis of non-B DNA-forming sequence motifs.

153 ng sequences that may form more than one non-B DNA structure.

154 uplex-single-strand transitions of other non-B DNA structures, resulting in double-strand breaks in v

155 ese elements, we identified in potential non-B DNA regions a signature of negative selection.

156 wide variation propensities of potential non-B DNA regions and their relation to gene expression.

157 erved that genes downstream of potential non-B DNA regions showed higher expression variation between

158 of eQTL-associated variants in potential non-B DNA regions, opposite to what might be expected from t

159 old into secondary structures [potential non-B DNA structures (PONDS); e.g. triplexes, quadruplexes,

160 The breakpoints occurred at predicted non-B DNA structures.

161 onb.abcc.ncifcrf.gov, catalogs predicted non-B DNA-forming sequence motifs, including Z-DNA, G-quadru

162 rid KIR genes, facilitated by protrusive non-B DNA structures at transposon recombination sites.

163 n stress and could efficiently replicate non-B DNA sequences within CFSs.

164 showed that the distribution of several non-B DNA motifs within intergenic regions separating diverg

165 -non-B DNA transition-susceptible sites (non-B DNA motifs) within the context of the operon structure

166 We found an enrichment of some non-B DNA motifs in regulatory regions, and we show that thi

167 Finally, a preference for some non-B DNA motifs was observed near transcription factor-bind

168 Higher levels of -sigma stabilize non-B DNA conformations (i.e. triplexes, sticky DNA, flexibl

169 gh alternative DNA secondary structures (non-B DNA) can induce genomic rearrangements, their associat

170 of adopting alternative DNA structures (non-B DNA, e.g. H-DNA and G4-DNA), which have been identifie

171 pecific regulatory regions suggests that non-B DNA structures may have roles in the transcriptional r

172 cluding circular dichroism to detect the non-B DNA at the bcl-2 Mbr.

173 he repeating sequences per se, or of the non-B DNA conformations formed by these sequences, in the mu

174 The non-B DNA structure and the chromosomal translocation can be

175 d breaks in vitro, and this requires the non-B DNA structure at the bcl-2 Mbr.

176 Although we could document the non-B DNA structure formation at the bcl-2 Mbr, the structur

177 minichromosomal assay, we show that the non-B DNA structure formation is critical for the breakage a

178 analogue incorporation to show that the non-B DNA structure formation requires Hoogsteen pairing.

179 Bisulfite reactivity shows that the non-B DNA structure is favored by, but not dependent upon, s

180 d that the single-stranded region in the non-B DNA structure observed is stable for days and is asymm

181 ions which promoted the formation of the non-B DNA structures enhanced the genetic instabilities, bot

182 The non-B DNA structures formed by short tandem repeats on the n

183 s and thresholds for motifs, expands the non-B DNA-forming motifs coverage by including short tandem

184 efore, it has been speculated that these non-B DNA motifs can play regulatory roles in gene transcrip

185 Unexpectedly, this non-B DNA conformation elicited the formation of a TRS-lengt

186 This non-B DNA structure is a target of the RAG complex in vivo,

187 suggest a link between PARP-1 binding to non-B DNA structures in genome and its function in the dynam

188 PARP-1 interactions with non-B DNA structures are functional and lead to its catalyti

189 the capacity to adopt alternative (i.e. non-B) DNA structures in the human genome have been implicat

190 adopt multiple inter and intramolecular non-B-DNA conformations that may play an important role in b

191 mismatch and highest affinity for larger non-B-DNA structures.

192 scopy, we characterized the formation of non-B-DNA structures in the Friedreich ataxia-associated (GA

193 Hence, a stable non-B-DNA structure in the human genome appears to be the ba

194 ts that the transition from the B-DNA to non-B-DNA conformation may play an important role in bcl-2 t

195 that favor the transition from B-DNA to non-B-DNA conformations.

196 al parameters close to the values for normal B-DNA of similar length and sequence.

197 structure is more tightly wound than normal B-DNA.

198 With dG* in the normal B-DNA anti conformation, BP seriously disturbs the polym

199 Relative to normal B-DNA, the duplex containing the present tetrahydroepoxi

200 aters were restrained in the major groove of B DNA shows a rapid, spontaneous change from B to A at r

201 rst comprehensive study of the occurrence of B DNA-non-B DNA transition-susceptible sites (non-B DNA

202 emonstrate for the first time the ability of B-DNA to serve as a helical ruler for the study of elect

203 The anisotropy of B-DNA groove bending was quantified for eight DNA sequen

204 n the base pair region are characteristic of B-DNA duplex structures, whereas CD spectra at longer wa

205 mains in the native C2'-endo/C3'-exo form of B-DNA, the deoxyribose of the 5'-nucleoside always adopt

206 ng of small molecules to the minor groove of B-DNA is examined.

207 radius complementary to the major groove of B-DNA.

208 s 26 A, consistent with the close packing of B-DNA.

209 ent among the HUBst-induced perturbations of B-DNA are a conversion of approximately one-third of the

210 s an inadequate model of the photophysics of B-DNA.

211 nding to the length of the helical repeat of B-DNA.

212 ards a coherent, realistic representation of B-DNA in solution, despite residual shortcomings.

213 by the ABC group of laboratories on a set of B-DNA oligomers containing the 136 distinct tetranucleot

214 e metal ions affect the folding stability of B-DNA helices.

215 enzimidazoles showed varied stabilization of B-DNA duplex (1.2-23.4 degrees C), and cytotoxicity stud

216 idinum moiety into the base pair stacking of B-DNA.

217 e we describe an accurate X-ray structure of B-DNA, painstakingly fit to a multistate model that cont

218 first high-resolution experimental study of B-DNA structure at high pressure, using NMR data acquire

219 o that of A-DNA (20 degrees) than to that of B-DNA (6 degrees).

220 between intercalation sites remains that of B-DNA.

221 Transitions of B-DNA to alternative DNA structures (ADS) can be trigger

222 FRET-measurements over more than one turn of B-DNA.

223 ector plot and inclination values typical of B-DNA, but has the crystal packing, helical twist, groov

224 ally significant, and the model was based on B-DNA helices and thus cannot directly treat RNA helices

225 mulations including water and counterions on B-DNA oligomers containing all 136 unique tetranucleotid

226 mulations including water and counterions on B-DNA oligomers containing all 136 unique tetranucleotid

227 extension is close to 1.7 times the original B-DNA length, we find l ?

228 fdG adduct revealed that though the overall B-DNA structure is maintained, this lesion can disrupt W

229 a DNA duplex with alternating AT base pairs (B DNA, d[5'-G(3)(AT)(5)C(3)-3']) and with almost 3 order

230 ver, in cells stably expressing a PR-A or PR-B DNA-binding domain mutant (PRmDBD), P4-mediated transr

231 by PR/c-Src interactions and required the PR-B DNA-binding domain (DBD).

232 A-form DNA, whereas AA steps strongly prefer B-DNA and inhibit A-structures.

233 the octamer and similar to that in previous B-DNA structures (its inverse sixth root is about 2.40 A

234 ith structural variability observed in prior B-DNA structures.

235 camer (DDD: d(CGCGAATTGCGC)2) a prototypical B-DNA duplex.

236 nodeficiency virus type 1 (HIV-1) PENNVAX(R)-B DNA vaccine (PV) is a mixture of 3 expression plasmids

237 s to date been crystallized only as resolved B-DNA duplexes.

238 at the C-terminus can invade mixed-sequence B-DNA in a sequence-specific manner.

239 l properties that extend features of shorter B-DNA fragments with respect to double helical parameter

240 in the backbone, we observed that the simple B-DNA structure was able to insert into the water-chloro

241 ealed a functionally important Spi-1 and Spi-B DNA binding element located in the downstream promoter

242 In the SRY.B/DNA complex, both HMG boxes bind in the minor groove a

243 ked-X form junction with two sets of stacked B-DNA-type arms that coaxially stack to form semicontinu

244 d of a CCCC/GGGG sequence within the stacked B-DNA arms of this 1.9 A resolution structure.

245 multiple domains of half-turn-long, standard B-DNA duplexes.

246 at were predicted to stabilize this standard B-DNA, had the unexpected effect of causing a conformati

247 ion of an alternate conformation to standard B-DNA known as B'-DNA.

248 es in local structure compared with standard B-DNA, including pinching of the minor groove at the 3'

249 ems representing single- and double-stranded B-DNA are characterized using electronic structure theor

250 a 1.2 A X-ray structure of a double-stranded B-DNA dodecamer (the Dickerson Dodecamer, DDD, [d(CGCGAA

251 A and RNA that can recognize double-stranded B-DNA through direct Watson-Crick base-pairing.

252 d RNA can also be applied to double-stranded B-DNA.

253 form right-handed double helical structures (B-DNA) in standard phosphate buffer with 115 mM Na(+) at

254 tendency of the central bases to assume the B'-DNA state.

255 ctures suggests that the transition from the B-DNA to non-B-DNA conformation may play an important ro

256 omers energetically favor positioning in the B-DNA major groove, with minor groove conformers also lo

257 to the damaged cytosine, are located in the B-DNA major or minor groove, with the modified cytosine

258 P]-N(2)-dG adduct (G*), which resides in the B-DNA minor groove 5'-oriented along the modified strand

259 5'-directed along the modified strand in the B-DNA minor groove in both sequence contexts.

260 P-dG) in which the B[a]P rings reside in the B-DNA minor groove on the 3'-side of the modifed deoxygu

261 While the BP ring system is in the B-DNA minor groove, 5' directed along the modified stran

262 ons generally agreed with the results of the B-DNA (Bayer) viral load assays.

263 The 1.7 A X-ray crystal structure of the B-DNA dodecamer, [d(CGCGAATTCGCG)] (DDD)-bound non-coval

264 nce-dependent conformational features of the B-DNA duplexes and the associated patterns of hydration

265 ding small molecules in the AT region of the B-DNA minor groove.

266 This concerns both the ratio of the B-DNA substates B(I) and B(II) associated with the backb

267 hat although each duplex structure is of the B-DNA type, there are subtle conformational dissimilarit

268 Finally, the importance of preserving the B-DNA conformation for the diagnosis of cancer is put fo

269 luated first on its ability to reproduce the B-DNA decamer d(CGATTAATCG)(2) in solution with simulati

270 y supercoiling of pUC19, indicating that the B-DNA structure is largely conserved under moderate supe

271 unction can accommodate perturbations to the B-DNA conformation of the stacked duplex arms associated

272 energy for the PX molecules compared to the B-DNA molecules of the same length and sequence.

273 ibrium, which is essential to understand the B-DNA properties.

274 ycin, an aminoglycoside antibiotic, with the B-DNA minor groove binding ligand Hoechst 33258.

275 ycin, an aminoglycoside antibiotic, with the B-DNA minor groove binding ligand Hoechst 33258.

276 ing of the aminofluorene rings: B is in the "B-DNA" major groove, S is "stacked" into the helix with

277 The free energy of the transition from B- to B'-DNA is known to depend on the sequence.

278 ion of the noncontacted region from B-DNA to B'-DNA.

279 mpled the conformational space accessible to B-DNA at room temperature.

280 , both isomers bind with similar affinity to B-DNA and have enhanced luminescence.

281 buted to a conformational change from B'- to B-DNA.

282 i DNA topoisomerase I inhibition, binding to B-DNA duplex, and antibacterial activity has been evalua

283 and the utility of aminoglycoside binding to B-DNA structures by conjugating neomycin, an aminoglycos

284 and the utility of aminoglycoside binding to B-DNA structures by conjugating neomycin, an aminoglycos

285 inhibits the complete relaxation of A-DNA to B-DNA within the time scale of the simulations.

286 n is essential for the low-linking number to B-DNA transition and hence for the deactivation of repli

287 The subtle structural perturbations to B-DNA induced by moderate supercoiling are consistent wi

288 tion of the adjacent duplex arms relative to B-DNA, and this is discussed in terms of the conserved i

289 ooperative structural transitions similar to B-DNA, although less torque is required to disrupt stran

290 Docking these structures to B-DNA followed by unrestrained MD simulations led to a s

291 gth, we observe that almost all DNA tends to B-DNA and becomes less flexible.

292 at TBK1 rescued IFN responses to transfected B-DNA to a much stronger degree than IKK-i.

293 Likewise, the force required to transform B-DNA into the overstretched form is also similar for al

294 e endonuclease, encode a protein-primed type B DNA polymerase (PolB) and hence break this pattern.

295 e helicoidal parameters similar to a typical B-DNA of similar length and base sequence.

296 nt manner associated with direct ultraviolet B DNA damage.

297 pair embedded within undistorted, unmodified B-DNA.

298 ticipates in programmed cell death in the UV-B DNA damage response.

299 pecificity of HIV-1 integrase (IN) and viral B-DNA forms through ligand-receptor docking studies by m

300 for exploring the recognition potential with B-DNA.