ライフサイエンスコーパス: strand transfer

1 3'-viral DNA ends into host chromosomal DNA (strand transfer).

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

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

4 This confirms that RT dissociates during strand transfer.

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

6 s eliminated both the associated pausing and strand transfer.

7 inetics of inhibition of integrase-catalyzed strand transfer.

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

9 nd kinetic requirements for efficient primer strand transfer.

10 ymerase activity thereby promoting increased strand transfer.

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

12 nealing is significantly higher than that of strand transfer.

13 action that resembled reversal of target DNA strand transfer.

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

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

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

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

18 reaction that provides the motive force for strand transfer.

19 nding to captured targets immediately before strand transfer.

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

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

22 ugh stable secondary structures and reducing strand transfer.

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

24 quence followed by C as the dominant site of strand transfer.

25 tivated state competent for DNA cleavage and strand transfer.

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

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

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

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

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

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

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

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

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

35 The LEDGF also stimulates HIV-1 IN DNA strand transfer activity and improves its solubility in

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

51 e DNA 3'-hydroxyl group that is required for strand transfer activity.

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

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

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

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

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

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

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

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

60 xplain the asymmetric outcome of the initial strand transfer and show how DNA binding is modulated by

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

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

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

64 dyl transferase reactions, 3' processing and strand transfer, and INSTIs tightly bind the divalent me

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

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

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

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

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

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

71 Strand transfer assays in vitro revealed that three paus

72 Strand transfer assays were performed with cations that

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

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

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

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

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

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

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

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

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

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

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

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

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

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

87 We previously analyzed strand transfers catalyzed by human immunodeficiency vir

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

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

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

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

92 complex with hairpin DNA intermediates and a strand transfer complex capturing the integration step.

93 iously determined the structure of the HIV-1 strand transfer complex intasome.

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

95 ocytes, we determined the structure of a DNA-strand transfer complex of mouse RAG at 3.1- angstrom re

96 et capture complex) and two forms of the RAG strand transfer complex that differ based on whether tar

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

98 ture of the Drosophila P element transposase strand transfer complex using cryo-EM.

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

100 process from the apo enzyme to the terminal strand transfer complex with transposon ends covalently

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

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

103 In contrast to strand transfer complexes of genuine transposases, where

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

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

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

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

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

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

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

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

112 Strand transfer drives recombination between the co-pack

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

114 Strand transfer during reverse transcription can produce

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

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

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

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

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

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

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

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

123 essential for both helix destabilization and strand transfer functions.

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

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

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

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

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

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

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

131 The strand transfer inhibition properties of various DKA com

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

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

134 riptase inhibitor (43%), NRTI plus integrase strand transfer inhibitor (25%), and NRTI plus protease

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

136 enced VF without resistance to the integrase strand transfer inhibitor (INSTI) class; 1 patient disco

137 bination therapy that includes the integrase strand transfer inhibitor (INSTI) dolutegravir (DTG).

138 ong-acting injectable (CAB LA), an integrase strand transfer inhibitor (INSTI), reduces dosing freque

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

140 Integrase strand transfer inhibitor (INSTI)-based combination anti

141 Integrase strand transfer inhibitor (InSTI)-based regimens are now

142 iretroviral therapy (ART) to newer integrase strand transfer inhibitor (INSTI)-based regimens.

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

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

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

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

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

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

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

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

151 se inhibitor (0.68 [0.51-0.90]) or integrase strand transfer inhibitor use (0.26 [0.13-0.53]) were pr

152 Integrase strand transfer inhibitor use was associated with more w

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

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

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

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

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

158 2-drug regimen, which includes an integrase strand transfer inhibitor.

159 Integrase strand-transfer inhibitor (INSTI)-based antiretroviral t

160 Integrase strand-transfer inhibitor (INSTI)-based antiretroviral t

161 Testing for transmitted integrase strand-transfer inhibitor resistance is currently not re

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

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

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

165 living with HIV who are prescribed integrase strand transfer inhibitors (INSTI).

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

167 Integrase strand transfer inhibitors (INSTIs) are crucial for the

168 Integrase strand transfer inhibitors (INSTIs) are highly effective

169 Integrase strand transfer inhibitors (INSTIs) are now recommended

170 Integrase (IN) strand transfer inhibitors (INSTIs) are recent compounds

171 Integrase strand transfer inhibitors (INSTIs) are recommended comp

172 Integrase strand transfer inhibitors (InSTIs) are recommended for

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

174 Integrase strand transfer inhibitors (INSTIs) coadministered with

175 Treatment initiation with integrase strand transfer inhibitors (INSTIs) has been associated

176 Although some integrase strand transfer inhibitors (INSTIs) promote peripheral a

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

178 Integrase strand transfer inhibitors (INSTIs) were associated with

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

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

181 e required to understand the mechanism of IN strand transfer inhibitors (INSTIs), which are front-lin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

198 Although second-generation HIV integrase strand-transfer inhibitors (INSTIs) are prescribed throu

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

200 eneration of antiretroviral drugs, integrase strand-transfer inhibitors (INSTIs).

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

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

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

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

205 A common strand transfer intermediate is resolved differentially

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

222 DNA annealing and strand transfer occurs within large oligomeric filaments

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

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

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

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

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

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

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

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

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

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

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

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

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

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

237 ncentrations for effective inhibition of all strand transfer products.

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

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

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

241 8 and 20 showed a 5-fold selectivity for the strand transfer reaction over 3'-processing.

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

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

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

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

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

247 3' processing and selectively inhibited the strand transfer reaction.

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

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

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

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

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

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

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

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

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

257 These strand transfer selective inhibitors also inhibited HIV-

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

259 fferent chemical families and with different strand transfer selectivities.

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

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

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

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

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

265 3'-processing (3'-P) but severely inactivate strand transfer (ST).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

284 s, it requires both asymmetric and symmetric strand transfer steps.

285 In the strand transfer structure, target DNA is severely bent a

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

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

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

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

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

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

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

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

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

295 Strand transfer was measured in vitro, in reactions invo

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

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

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

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

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