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

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

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

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

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

13 al' RNA triple helix, analogous to A-RNA and B-DNA double helices.

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

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

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

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

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

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

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

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

22 ly, the Gibbs free energy difference between B-DNA and P-DNA, and the galactic virial mass.

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

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

25 30% DNA extension is sufficient for breaking B-DNA around and significantly above cellular supercoili

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

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

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

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

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

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

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

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

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

44 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

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

46 Family B DNA polymerases from archaea such as Pyrococcus furios

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

81 seemingly simple process of base flipping in B-DNA.

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

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

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

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

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

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

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

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

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

91 e structure of the DNA outside the intrinsic B-DNA envelope.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

113 atson-Crick and HG base pairs for both naked B-DNA and A-RNA duplexes.

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

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

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

117 Non-B DNA-forming sequences are highly enriched at transloca

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

119 8 is a fragile site, because it adopts a non-B DNA conformation that can be cleaved by the RAG comple

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

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

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

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

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

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

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

127 res are a prevalent class of alternative non-B DNA structures that form during transcription upon inv

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

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

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

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

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

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

134 n adopt alternative DNA structures (i.e. non-B DNA, such as H-DNA).

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

136 Expanded TA repeats form non-B DNA secondary structures that stall replication forks,

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

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

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

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

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

142 erstanding of the mechanisms involved in non-B DNA-induced genetic instability is needed.

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

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

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

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

147 time- and length-dependent formation of non-B DNA structures at chromosomal termini participates in

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 R-loops are a prevalent class of non-B DNA structures that have been associated with both pos

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

152 can modulate the formation/stability of non-B DNA structures, and therefore the subsequent mutagenic

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

170 R-loops are prevalent three-stranded non-B DNA structures composed of an RNA-DNA hybrid and a sin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

190 Regardless of their topologies, non-B DNA structures exhibited impaired binding to Cdc13 in

191 sity of G-rich sequences to form various non-B DNA structures.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

224 ansition timescales much longer than that of B-DNA.

225 between intercalation sites remains that of B-DNA.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

262 5'-directed along the modified strand in the B-DNA minor groove in both sequence contexts.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

295 nt manner associated with direct ultraviolet B DNA damage.

296 Unlike B-DNA, the transition pathway primarily involved base pa

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

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

299 for exploring the recognition potential with B-DNA.

300 Hfq hexamer as parallel, straight rods with B-DNA like conformational properties.