ライフサイエンスコーパス: strand transfer

1 A end to a target DNA (a reaction called DNA strand transfer).

2 3'-viral DNA ends into host chromosomal DNA (strand transfer).

3 ed successively by HIV-1 for efficient minus strand transfer.

4 s eliminated both the associated pausing and strand transfer.

5 inetics of inhibition of integrase-catalyzed strand transfer.

6 ion site has a limited range of influence on strand transfer.

7 ymerase activity thereby promoting increased strand transfer.

8 anism of NC-dependent and -independent minus-strand transfer.

9 nealing is significantly higher than that of strand transfer.

10 action that resembled reversal of target DNA strand transfer.

11 d BIV IN was equally active in both types of strand transfer.

12 ion of D520 to facilitate steps that promote strand transfer.

13 e invasion site, correlating with defects in strand transfer.

14 e integrase residue Gln-148 are critical for strand transfer.

15 reaction that provides the motive force for strand transfer.

16 nding to captured targets immediately before strand transfer.

17 a dead-end reaction that competes with minus-strand transfer.

18 ocesses referred to as 3' processing and DNA strand transfer.

19 ugh stable secondary structures and reducing strand transfer.

20 apsis, also appear to serve as hot spots for strand transfer.

21 essing site inhibited both 3'-processing and strand transfer.

22 position: DNA binding, DNA cleavage, and DNA strand transfer.

23 eptor invasion-initiated mechanism for minus strand transfer.

24 molecules that are cleaved also complete DNA strand transfer.

25 egions of homology was observed during minus strand transfer.

26 effective at blocking 3' processing but not strand transfer.

27 the conformation that normally promotes DNA strand transfer.

28 ess the role of nucleocapsid protein (NC) in strand transfer.

29 ts role as a nucleic acid chaperone in minus-strand transfer.

30 occurred readily during both minus and plus strand transfer.

31 egrase-mediated reactions: 3'-processing and strand transfer.

32 ces on a DNA acceptor template to enable (+) strand transfer.

33 activity of the RT, subsequently leading to strand transfer.

34 ct HIV-1 reverse transcriptase (RT)-mediated strand transfer.

35 tivated state competent for DNA cleavage and strand transfer.

36 he components necessary for 3'-processing or strand transfer.

37 e showed that a polymer trap still prevented strand transfer.

38 This confirms that RT dissociates during strand transfer.

39 ts before the hairpin base and their role in strand transfers.

40 HIV-1 nucleocapsid (NC) protein stimulated strand transfers.

41 nstrate that for efficient NC-mediated minus-strand transfer, a delicate thermodynamic balance betwee

42 in both disintegration and 3'-end-processing-strand transfer activities in vitro.

43 minal fragments effectively stimulate MLV IN strand transfer activities in vitro.

44 2-33, 51, and 53) inhibited 3'-processing or strand transfer activities of IN with IC(50) < or = 25 m

45 may be required for stimulation of in vitro strand transfer activities of IN.

46 from the post-drug RT abolished the elevated strand transfer activity and RNase H activity, in additi

47 uggest that the dipeptide insertion elevates strand transfer activity by increasing the interaction o

48 First, the post-drug RT displayed elevated strand transfer activity compared to the pre-drug RT, wi

49 All the variants examined were impaired for strand transfer activity compared with the wild type enz

50 n approach is described wherein the specific strand transfer activity for each integrase/LTR variant

51 LEDGF/p75 is known to enhance the integrase strand transfer activity in vitro, but the underlying me

52 ells moreover supported normal levels of DNA strand transfer activity in vitro.

53 ion, and the B' subunit stimulates concerted strand transfer activity of delta-retroviral INs in vitr

54 LEDGF potently stimulated strand transfer activity of divergent lentiviral INs in

55 of the 27 compounds, 13 compounds inhibited strand transfer activity of IN with an IC50 value less t

56 egrase/LTR variant is derived by normalizing strand transfer activity to the concentration of active

57 peptide fingers domain insertion mutation on strand transfer activity using two clinical RT variants

58 t, with a K219S substitution showing loss in strand transfer activity while maintaining 3' processing

59 r Arg-322 reduce both hairpin resolution and strand transfer activity within protein-DNA complexes.

60 of the HIV LTR on complex assembly, specific strand transfer activity, and inhibitor binding.

61 ower rate of primer extension, and increased strand transfer activity, can all be explained by a defe

62 binding to and stimulating HTLV-1 and -2 IN strand transfer activity.

63 Finally, reduced DNA strand-transfer activity together with increased vinylog

64 heir IC(50) values for 3'-end processing and strand transfer against recombinant HIV-1 IN were determ

65 that provides the nick required to initiate strand transfer and a processive 5'-to-3' helicase react

66 pha-Hydroxytropolones preferentially inhibit strand transfer and are inhibitory both in the presence

67 s that mimic tRNA primer removal during plus-strand transfer and degradation of genomic RNA fragments

68 3) The strand transfer and inhibitor binding defects of a Q148R

69 trate interaction mechanistically influences strand transfer and recombination of HIV-1 RT.

70 ptor RNA constructs were used to assay minus-strand transfer and self-priming in vitro.

71 d HIV-1 IN with IC50 values below 100 nM for strand transfer and showed a 2 order of magnitude select

72 C to chaperone "reverse annealing" in single-strand transfer and the first observation of partially a

73 I24Q/N27D all showed defects in DNA binding, strand transfer, and helix destabilization, suggesting t

74 e compound inhibits HIV-1 integrase-mediated strand transfer, and its antiviral activity in vitro is

75 including DNA polymerization, RNA cleavage, strand transfer, and strand displacement synthesis.

76 ic role, nonetheless its presence stimulates strand transfer approximately 30-fold.

77 Donor cleavage and strand transfer are two functions performed by transposa

78 ecular mechanisms coupling 3'-processing and strand transfer as well as for the molecular pharmacolog

79 An in vitro strand transfer assay that mimicked recombinational even

80 50) values were achieved in an HIV-integrase strand transfer assay with both carboxylic ester and car

81 determined by using a reconstituted in vitro strand transfer assay.

82 Strand transfer assays in vitro revealed that three paus

83 Strand transfer assays were performed with cations that

84 melanogaster and Ae. aegypti and by in vitro strand transfer assays.

85 at one of these positions and for efficient strand transfer at the other.

86 oducts were produced as a result of frequent strand transfer between RNA templates, averaging at leas

87 s on translocation, dNTP binding, and primer strand transfer between the polymerase and exonuclease s

88 ip between the translocation step and primer strand transfer between the polymerase and exonuclease s

89 se the fidelity of recombination by reducing strand transfers between segments that have limited comp

90 riptase is known to promote recombination by strand transfer both in vivo and in vitro.

91 cDNA into the host genome, 3' processing and strand transfer, but the dynamic behavior of the active

92 g synthesis and these cuts can contribute to strand transfer by creation of an invasion site.

93 to the inhibition of divalent ion dependent strand transfer by HIV integrase in antiviral therapy.

94 uctures within RNA templates in facilitating strand transfer by HIV-1 RT (reverse transcriptase).

95 ow that the low mobility bands formed during strand transfer by Rad51 (or Escherichia coli RecA) repr

96 ted, the mechanics of target DNA capture and strand transfer by these enzymes remained unclear.

97 required to re-constitute position-specific strand transfer by Ty3 integrase are defined.

98 important and overlapping roles in assembly, strand transfer catalysis and high affinity inhibitor bi

99 Integrase complex assembly and subsequent strand transfer catalysis are mediated by specific inter

100 se/donor DNA complex or its rate constant of strand transfer catalysis was observed.

101 We previously analyzed strand transfers catalyzed by human immunodeficiency vir

102 ficantly different from that observed in the strand transfer complex (0.07+/-0.02).

103 st chromatin results in the formation of the strand transfer complex (STC) containing catalytically j

104 ciated with target DNA and progressed to the strand transfer complex (STC), the nucleoprotein product

105 The synaptic complex and strand transfer complex can be isolated by native agaros

106 hown that diketo acid inhibitors bind to the strand transfer complex of integrase and are competitive

107 altered transposase configuration in the Mu strand transfer complex that inhibits reversal, thereby

108 Accordingly, when the Mu or Tn10 strand transfer complex was produced in vitro through tr

109 he concerted integration product, termed the strand transfer complex.

110 s a need to develop a model representing the strand transfer complex.

111 In contrast, when the Mu or Tn10 strand transfer complexes were assembled from DNA alread

112 tic complexes associated with target, termed strand transfer complexes, are resistant to disruption b

113 gression coefficients (r(2)) of up to 0.932 (strand transfer CoMSIA, Conf-d) were obtained, with the

114 alidated coefficients (q(2)) of up to 0.719 (strand transfer CoMSIA, Conf-s) regression coefficients

115 Transposase also catalysed strand transfer, covalently joining the transposon 3' en

116 acceptor had a large effect on the level of strand transfer despite very few crossovers mapping to t

117 Various studies have revealed that double-stranded transfer DNA (T-DNA) intermediates can serve as

118 grobacterium tumefaciens delivers its single-stranded transferred DNA (T-strand) into the host cell n

119 Strand transfer drives recombination between the co-pack

120 The proposed invasion-mediated mechanism of strand transfer during HIV-1 reverse transcription has t

121 Strand transfer during reverse transcription can produce

122 The origin of the reduced strand transfer efficiencies of the variant enzymes was

123 r with the influence of MuB filament size on strand-transfer efficiency, lead to a model in which MuB

124 get site is identified, the time between PFV strand transfer events is 470 ms.

125 A polymerase (RdRp), which recapitulates the strand transfer events of the recombination process.

126 removing a bulge increases the proportion of strand transfer events to an acceptor template that occu

127 Human immunodeficiency virus-1 employs strand transfer for recombination between two viral geno

128 secondary structure (for example, the first strand transfers for viruses whose genomes have consider

129 noncomplementary nucleotides promotes primer strand transfer from the polymerase site to the exonucle

130 We demonstrate that the pathway for primer strand transfer from the polymerase to exonuclease site

131 essential for both helix destabilization and strand transfer functions.

132 molabile properties for 3' OH processing and strand transfer (half-site and full-site integration) ac

133 Strand transfer has been linked to "pausing" occurring a

134 Two of the compounds that inhibited strand transfer have no effect on DNA cleavage.

135 icantly, NC may not be required for in vitro strand transfer if (-) SSDNA and acceptor RNA are small,

136 translocation rates and the rates of primer strand transfer in both directions between the polymeras

137 Strand transfer in highly structured nucleic acid specie

138 Only I24Q and N27D showed reduced strand transfer in in vitro assays.

139 s suppressed both the associated pausing and strand transfer in vitro.

140 e nucleocapsid protein (NC), including minus-strand transfer, in which the DNA transactivation respon

141 The strand transfer inhibition properties of various DKA com

142 ing pharmacophore required for HIV integrase strand transfer inhibition represents a vibrant area of

143 oxypyrone MBG were found to display superior strand-transfer inhibition when compared to an abbreviat

144 r boosted drug, which should be an integrase strand transfer inhibitor (dolutegravir, elvitegravir, o

145 utegravir (DTG), a next-generation integrase strand transfer inhibitor (INSTI), was recently approved

146 ase case prevalence of transmitted integrase strand transfer inhibitor (INSTI)-resistant (INSTI-R) vi

147 The prevalence of integrase strand transfer inhibitor (INSTI)-transmitted drug resis

148 riptase inhibitors (NRTIs) plus an integrase strand transfer inhibitor (InSTI).

149 r (atazanavir or darunavir), or an integrase strand transfer inhibitor (raltegravir).

150 In phase 1 trials, the HIV-1 integrase strand transfer inhibitor cabotegravir (GSK1265744) was

151 The HIV integrase strand transfer inhibitor elvitegravir (EVG) has been co

152 cribes the kinetics of binding of a specific strand transfer inhibitor to integrase variants assemble

153 n to be due to lower affinity binding of the strand transfer inhibitor to the integrase complex, a co

154 Dolutegravir is a once-daily integrase strand transfer inhibitor with no need for pharmacokinet

155 otegravir (GSK1265744) is an HIV-1 integrase strand transfer inhibitor with potent antiviral activity

156 fovir alafenamide is a once-daily, integrase strand transfer inhibitor-based regimen approved in the

157 Resistance to raltegravir in integrase strand transfer inhibitor-naive patients remains today a

158 se proteins containing mutations observed in strand transfer inhibitor-resistant viruses were express

159 GSK1265744 (GSK744) is an integrase strand-transfer inhibitor that has been formulated as a

160 nd safety of raltegravir, an HIV-1 integrase strand-transfer inhibitor.

161 e (RT) inhibitors (NNRTI) and integrase (IN) strand transfer inhibitors (INSTI) are key components of

162 ere are currently three HIV-1 integrase (IN) strand transfer inhibitors (INSTIs) approved by the FDA

163 Integrase strand transfer inhibitors (INSTIs) are highly effective

164 Integrase strand transfer inhibitors (INSTIs) are recommended comp

165 ent treatment guidelines recommend integrase strand transfer inhibitors (INSTIs) as components of ini

166 Integrase strand transfer inhibitors (INSTIs) coadministered with

167 uted quinolinonyl derivatives were proven IN strand transfer inhibitors (INSTIs) that also displayed

168 the first-generation FDA-approved integrase strand transfer inhibitors (INSTIs), raltegravir (RAL) a

169 egravir (EVG) (August 2012), which act as IN strand transfer inhibitors (INSTIs), were the first anti

170 The synaptic complex is inactivated by strand transfer inhibitors (STI) with IC(50) values of a

171 c complex that is kinetically trapped by HIV strand transfer inhibitors (STIs).

172 HIV-1 integrase strand transfer inhibitors are an important class of com

173 viral DNA integration and explain why HIV IN strand transfer inhibitors are ineffective against the 3

174 Specific HIV integrase strand transfer inhibitors are thought to bind to the in

175 he discovery of a new class of HIV integrase strand transfer inhibitors based on the 2-pyridinone cor

176 itors that are structurally distinct from IN strand transfer inhibitors but analogous to LEDGINs.

177 ated the mechanisms associated with multiple strand transfer inhibitors capable of inhibiting concert

178 Strand transfer inhibitors L-870,810, L-870,812, and L-8

179 mes with human immunodeficiency virus type 1 strand transfer inhibitors that interact simultaneously

180 the IN-viral DNA complex is "trapped" by the strand transfer inhibitors via a transient intermediate

181 ration and how clinically relevant integrase strand transfer inhibitors work.

182 ranscriptase inhibitors [NNRTIs]), integrase strand transfer inhibitors, and virus entry inhibitors.

183 counterpart, PFV IN was sensitive to HIV IN strand transfer inhibitors, suggesting that this class o

184 ls of the inhibitor binding site of specific strand transfer inhibitors.

185 te architecture, which has high affinity for strand transfer inhibitors.

186 These IN strand-transfer inhibitors (INSTIs) were evaluated in vi

187 The binding of strand-transfer inhibitors displaces the reactive viral

188 One of these complexes also binds strand-transfer inhibitors of HIV antiviral drugs, makin

189 ave designed and synthesized a new integrase strand transfer (INST) inhibitor type featuring a 5-N-be

190 VirB9) form close contacts with the VirD2-T-strand transfer intermediate during export, as shown rec

191 A common strand transfer intermediate is resolved differentially

192 ration target DNA capture and post-catalytic strand transfer intermediates of the retroviral integrat

193 repair (MMR) to allow efficient detection of strand-transfer intermediates, and the results reveal st

194 ioned for nucleophilic attack and subsequent strand transfer into another DNA duplex (target or chrom

195 NA hairpin formation, hairpin resolution and strand transfer into target DNA) resulting in the integr

196 within a target capture complex to carry out strand transfer, irreversibly joining the viral and cell

197 rand (NTS) 5' phosphate in Tn5 transposition strand transfer is analyzed.

198 the other that was unmodified, to show that strand transfer is decreased in a dose-dependent manner.

199 hat the conformation of the target DNA after strand transfer is involved in preventing accidental cat

200 One mechanism proposed for strand transfer is strand exchange in which a homologous

201 Strand transfer is unique; the DNA strand being made by

202 at although the drug did not stimulate minus-strand transfer, it did stimulate minus-strand strong-st

203 of NC on recombination and illustrates that strand transfer may occur by several different mechanism

204 The minus strand transfer mechanism in human immunodeficiency viru

205 rocess is similar to the process of obligate strand transfers mediated by the repeat and primer bindi

206 rus assembly, both of which are required for strand transfer-mediated recombination during reverse tr

207 mes during virus assembly, a requirement for strand-transfer-mediated recombination during reverse tr

208 d RNA genome, both of which are utilized for strand-transfer-mediated recombination during reverse tr

209 eptor RNA was also crucial, and little or no strand transfer occurred if the RNA was highly stable.

210 Retroviral recombinants are generated by strand transfers occurring within internal regions of th

211 We previously proposed that HIV-1 minus strand transfer occurs by an acceptor invasion-initiated

212 DNA annealing and strand transfer occurs within large oligomeric filaments

213 ts, Brf1 and TBP, mediated position-specific strand transfer of duplex oligonucleotides representing

214 that uracilation of target DNA inhibits the strand transfer of HIV DNA ends by IN, thereby inhibitin

215 ro were designed to test mechanisms of minus strand transfer of human immunodeficiency virus 1 (HIV-1

216 ithin the transpososome through cleavage and strand transfer of Mu ends to target DNA.

217 Naphthyridine 7 inhibits the strand transfer of the integration process catalyzed by

218 due to the higher efficiency of cleavage and strand transfer of the preferred transposon end.

219 ssing of the viral DNA ends, followed by the strand transfer of the processed ends into host cell chr

220 nucleotides from both LTR ends and catalyses strand transfer of the recessed 3'-hydroxyls into the ta

221 h DNA strands, and participates in the three-strand transfers of DNA synthesis, with all steps after

222 MutS inhibited strand transfer on such substrates in a concentration-de

223 to the molecular mechanism insuring that DNA strand transfer ordinarily occurs rather than inappropri

224 Absent Me(2+), the primer strand transfer pathway between the polymerase and exonu

225 We have previously provided evidence that strand transfer proceeds by an invasion-mediated mechani

226 p structures, but its ability to inhibit the strand transfer process has only been implied.

227 ction mimics the annealing step of the minus-strand transfer process in reverse transcription.

228 from DNA already having the structure of the strand transfer product, we detected a reaction that res

229 tably associated with the transpososome, the strand transfer products undergo neither the reverse rea

230 ncentrations for effective inhibition of all strand transfer products.

231 ation in bacteria is facilitated by the RecA strand transfer protein and strongly depends on the homo

232 The strand transfer reaction can be blocked by the action of

233 processivity, RT stimulated the IN-mediated strand transfer reaction in a dose-dependent manner up t

234 8 and 20 showed a 5-fold selectivity for the strand transfer reaction over 3'-processing.

235 Integrase inhibitors of the strand transfer reaction remained active in the presence

236 The final step, a DNA strand transfer reaction that joins the transposon ends

237 roM and 15 microM, respectively, against the strand transfer reaction were the most potent.

238 ssing of the viral DNA ends, followed by the strand transfer reaction, which inserts the viral DNA in

239 two of them showed IC50 < or = 10 microM for strand transfer reaction.

240 3' processing and selectively inhibited the strand transfer reaction.

241 rget recognition and in the chemistry of the strand transfer reaction.

242 e HIV-1 NC, HTLV-1 NC does not chaperone the strand-transfer reaction involving TAR DNA.

243 compounds showed selective inhibition of the strand-transfer reaction over 3'-processing, suggesting

244 case, the efficiencies of both annealing and strand transfer reactions are similar.

245 ding activity and the catalysis of other DNA strand transfer reactions, such as transposition, are no

246 the branch migration phase of RecA-mediated strand transfer reactions.

247 oth the integrase-mediated 3'-processing and strand transfer reactions.

248 has differential effects on the cleavage and strand transfer reactions.

249 The general inability of strand transfer-related substitutions to diminish 3' pro

250 We propose that strand transfer requires a conformational change of the

251 roteins, each with specific DNA recognition, strand transfer, resolution, or other functions.

252 These strand transfer selective inhibitors also inhibited HIV-

253 In contrast, strand transfer-selective inhibitors provide weak cross-

254 fferent chemical families and with different strand transfer selectivities.

255 ates indicated that the adducts both inhibit strand transfer specifically at the minor groove bound s

256 ctive inhibitors of 3'-processing (3'-P) and strand transfer (ST) functions of HIV-1 integrase (IN),

257 over RT polymerase (pol) and integrase (IN) strand transfer (ST) inhibitions.

258 G), act as interfacial inhibitors during the strand transfer (ST) integration step.

259 IN-mediated reactions, 3'-processing (3'-P), strand transfer (ST), and disintegration, (2) to determi

260 quential reactions, 3'-processing (3'-P) and strand transfer (ST).

261 3'-processing (3'-P) but severely inactivate strand transfer (ST).

262 ity, is a critical determinant for the minus-strand transfer step (annealing of acceptor RNA to (-) s

263 c acid rearrangements that precede the minus-strand transfer step in reverse transcription.

264 The minus-strand transfer step of HIV-1 reverse transcription is c

265 f the nucleocapsid protein (NC) in the minus-strand transfer step of HIV-1 reverse transcription, in

266 In the minus-strand transfer step of HIV-1 reverse transcription, the

267 d with the G118R substitution, mostly at the strand transfer step of integration, compared to either

268 ation reaction, and are able to catalyze the strand transfer step of retroviral integration.

269 NA hairpin is an essential step in the minus-strand transfer step of reverse transcription.

270 ir duplex, is an essential step in the minus-strand transfer step of reverse transcription.

271 ad, this LEDGF/p75 added at the start of the strand transfer step was able to promote the formation o

272 ase in the rate constant of catalysis of the strand transfer step when 150 nM LEDGF/p75 was present d

273 LEDGF/p75 was added at the beginning of the strand transfer step, no increase in either the concentr

274 the pseudoreversal of the normal target DNA strand transfer step.

275 ity for the target DNA during the subsequent strand transfer step.

276 e transposon end cleavage reaction after the strand transfer step.

277 es in Ty1 reverse transcription at the minus-strand transfer step.

278 rful inhibitor of both the 3'-processing and strand transfer steps of HIV-1 integrase.

279 t of LEDGF/p75 on both the 3'-processing and strand transfer steps was analyzed.

280 eptor invasion initiation site using a minus strand transfer system in vitro, containing the 97-nucle

281 hich efficiently inhibited 3' processing and strand transfer targeted the LTR sequences through posit

282 s, several of which were more potent against strand transfer than 3'-end processing, a phenomenon pre

283 rate constants for both DNA cleavage and DNA strand transfer (the joining reaction) are unaffected by

284 Finally, all six compounds inhibit strand transfer, the final step of Tn5 transposition.

285 ng human immunodeficiency virus type 1 minus-strand transfer, the nucleocapsid protein (NC) facilitat

286 In minus-strand transfer, the transactivation response region (TA

287 of TAR DNA was not sufficient for successful strand transfer: the stability of acceptor RNA was also

288 omolar potency against 3'-end processing and strand transfer, though only with modest antiviral activ

289 NC (nucleocapsid) increased the strand transfer throughout the whole template.

290 t provided good selectivity for IN-catalyzed strand transfer versus the 3'-processing reactions as we

291 human immunodeficiency virus 1 (HIV-1) minus strand transfer was examined using a genomic RNA sequenc

292 Strand transfer was measured in vitro, in reactions invo

293 Human immunodeficiency virus type 1 minus strand transfer was measured using a genomic donor-accep

294 Surprisingly, in the presence of MnCl(2), strand transfer was TFIIIB-independent and targeted sequ

295 ates proposed to occur during recombination (strand transfer) were investigated.

296 They improve strand transfer when the target DNA contains a mismatch

297 This suggests that NC facilitates strand transfer where the nucleic acids have considerabl

298 transcription including tRNA initiation and strand transfer, which may be mediated through interacti

299 d a differential role for the two fingers in strand transfer with finger 1 (N-terminal) being more im

300 esigned a primer-template system that allows strand transfer without RNase H activity.