ライフサイエンスコーパス: open complex

1 losed complex to the RNA polymerase promoter open complex).

2 e bound to P(RM) transition from a closed to open complex.

3 of RNAP with promoter DNA in the closed and open complex.

4 DNA melting and allows the transition to the open complex.

5 into a catalytically competent RNAP-promoter open complex.

6 sequent steps on the way to formation of the open complex.

7 e region that becomes single-stranded in the open complex.

8 moter complex to a transcriptional competent open complex.

9 se pairs near the initiation site to form an open complex.

10 x but bent more sharply by 86 degrees in the open complex.

11 romoter opening or to stabilize a productive open complex.

12 A did not affect dissociation rates from the open complex.

13 and the highest for the constructs mimicking open complex.

14 y interactions of RNA polymerase with DNA in open complex.

15 erization of a closed promoter complex to an open complex.

16 the leuV promoter that is unwound within the open complex.

17 duplex DNA promoter to form a pre-initiation open complex.

18 n 1.1 differs dramatically in holoenzyme and open complex.

19 uggesting their role in stabilization of the open complex.

20 tween the enzyme and the promoter DNA in the open complex.

21 2, 2, 3, and 4 are similar in holoenzyme and open complex.

22 t as a key player directing formation of the open complex.

23 sely interacts with the promoter only in the open complex.

24 tro by decreasing the lifetime of the rrn P1 open complex.

25 he transcription start site, as in the final open complex.

26 ming an antiparallel heteroduplex inside the open complex.

27 to the rns promoter and the formation of an open complex.

28 oter, is not limited by the stability of the open complex.

29 nwinds promoter DNA to form an RNAP-promoter open complex.

30 eam double-stranded DNA of the RNAP-promoter open complex.

31 ization of the initial closed complex to the open complex.

32 bent DNA results in the catalytically active open complex.

33 DksA for RNAP decreases almost 10-fold in an open complex.

34 is initiated earlier in the pathway, in the open complex.

35 s that ultimately result in formation of the open complex.

36 rt varsigma(54) closed promoter complexes to open complexes.

37 of the formation of RNA polymerase-promoter open complexes.

38 its amino acids are used to form functional open complexes.

39 isomerises into transcriptionally competent open complexes.

40 promoters like rrnB P1 that make short-lived open complexes.

41 gy ppGpp, generally decrease the lifetime of open complexes.

42 owly and were much longer-lived than rrnB P1 open complexes.

43 ng interconversions between the dead-end and open complexes.

44 lpha subunits in transcriptionally competent open complexes.

45 s on the intrinsic catalytic capacity of the open complex and also on the partitioning between produc

46 Both the open complex and an abortive complex containing a short

47 s in region 1.2 can affect promoter binding, open complex and initiated complex formation and the tra

48 a plays an essential role in stabilizing the open complex and interacts specifically with the N-termi

49 The low temperature-trapped open complex and its isothermally formed state are shown

50 s in the TRTG motif of amyP destabilized the open complex and prevented the maintenance of open compl

51 , the detailed mechanism of formation of the open complex and the high resolution structures of these

52 that is close to the promoter spacer in the open complex and to the upstream boundary of the transcr

53 omoter DNA but only undergo transition to an open complex and transcription initiation when acted on

54 achieve promoter escape nevertheless formed open complexes and extended bubbles, which collapsed bac

55 s show an unexpected architecture of minimal open complexes and the regulation of activity by TFIIF a

56 attempts for each successful formation of an open complex, and efficient release of sigma(54) from th

57 containing the lambdaP(R) promoter, form an open complex, and initiate transcription in a temperatur

58 olymerase to its promoters, formation of the open complex, and synthesis of the first few phosphodies

59 otides there is a distribution of closed and open complexes, and the promoter DNA is bent slightly by

60 Open complexes are committed to transcription, suggestin

61 and quantified the overall bend angle in the open complex as well as in the +3 abortive complex: a be

62 the rate of isomerisation from the closed to open complex at a Class II CRP-dependent promoter.

63 howed a smaller amount of the pre-initiation open complex at equilibrium, indicating that the individ

64 A, preventing RNA polymerase from forming an open complex at nlpAp.

65 se results indicate that establishment of an open complex at P(R) directly prevents formation of an R

66 M) transcription requires the presence of an open complex at P(R).

67 eplication by inhibiting the formation of an open complex at the replication origin, thus elucidating

68 o KMnO(4) indicated that in about 20% of the open complexes at 20 degrees C the DNA strands are not f

69 contrast, ppGpp decreased the half-lives of open complexes at all promoters, whether the half-life w

70 led kinetic analysis in vitro indicated that open complexes at amino acid promoters formed much more

71 pen complex and prevented the maintenance of open complexes at low temperatures.

72 of CAP and AraC in stimulating formation of open complexes at p(FGH).

73 and forked DNA, similar to the formation of open complexes at promoters, is a multistep process, and

74 , remodel the polymerase so that it can form open complexes at promoters.

75 stability, the mutant enzyme forms partially open complexes at temperatures as low as 0 degrees C whe

76 ur mutant enzymes are shown to form unstable open complexes at the lambdacro promoter.

77 lymerase (RNAP), leading to the formation of open complexes at the promoter.

78 R) promoter, it does prevent it from forming open complexes at this promoter.

79 ription factor form an initiation-competent "open" complex at a promoter by disruption of about 14 ba

80 oters region 1.1 stimulates the formation of open complexes; at the P(minor) promoter, region 1.1 inh

81 To form a functional open complex, bacteriophage T7 RNA polymerase (RNAP) bin

82 Formation of the strand-separated, open complex between RNA polymerase and a promoter invol

83 yme couple ATP hydrolysis to formation of an open complex between the promoter and RNA polymerase.

84 Formation of the stable, strand separated, 'open' complex between RNA polymerase and a promoter invo

85 it catalyzes ATP-dependent formation of the open complex, but also in efficient promoter escape, whe

86 at subtle changes in the conformation of the open complex can profoundly affect its function.

87 GreA effects on rrnB P1 open complex conformation reveal a new feature of GreA d

88 ce of nucleotides: a dead-end complex and an open complex, constituting a branched interaction pathwa

89 in the size of the transcription bubble: the open complex contains a 10.4 +/- 0.1 bp bubble, while th

90 e overall equilibrium constant for closed to open complex conversion is 0.5 and the net rate of open

91 te, and Bpa cross-linking to map the path of open complex DNA at amino acid and nucleotide resolution

92 NAP binding to the promoter and formation of open complexes do not reflect a large-scale qualitative

93 ransient state kinetic studies show that the open complex, ED(o), is formed via an intermediate ED(c)

94 This complex isomerizes to an open complex, ED(o1), in an energetically unfavorable re

95 e ED(o1) further isomerizes to a more stable open complex, ED(o2), with a rate constant around 300 s(

96 F unexpectedly modulates the activity of the open complexes, either repressing or stimulating initiat

97 sA in vitro, including shifting the promoter-open complex equilibrium in the dissociation direction,

98 eavage pattern reveals structures similar to open complex, except for notable changes to region 3 of

99 We find that the scrunched open complex exhibits reduced abortive product synthesis

100 D helicases involved in promoter melting and open complex extension.

101 Open complexes form in a concerted manner at pflgM, whil

102 The defect in pre-initiation open complex formation affected downstream steps such as

103 hibit replication, while monomers facilitate open complex formation and activate the ori.

104 rgenic region, we have demonstrated in vitro open complex formation and activation of transcription i

105 on of the upstream footprint did not require open complex formation and also occurred in reactions in

106 a DNase I footprint downstream of Mor due to open complex formation and generation of a second footpr

107 urface-exposed residues in the regulation of open complex formation and promoter DNA binding to be be

108 These data refine the structural model for open complex formation and reveal a novel interaction in

109 en sigma(2) and the DNA during both promoter open complex formation and sigma(70)-dependent early elo

110 moter binding properties and low-temperature open complex formation are similar for pfliC, pfliD, and

111 that these substitutions slowed the rate of open complex formation at 37 degrees C as well.

112 However, the rate of open complex formation at P(R-GA) in vitro was roughly o

113 We have examined the kinetics of open complex formation at the lacP1 promoter using trypt

114 ffects the RNA polymerase-mediated closed to open complex formation at the rob promoter.

115 as an ideal probe to measure the kinetics of open complex formation because its fluorescence is sensi

116 Analysis of open complex formation by a three-step pathway that incl

117 develop the first quantitative model of the open complex formation by bacterial RNAP.

118 IHF stimulates open complex formation by DnaA on supercoiled oriC in ce

119 rwinding the operator-promoter DNA to permit open complex formation by pre-bound RNA polymerase.

120 o drive conformational changes necessary for open complex formation by sigma(54)-RNA polymerase.

121 are required for NorR-dependent catalysis of open complex formation by sigma(54)-RNAP holoenzyme (Esi

122 e ATPase domain to oligomerize and stimulate open complex formation by the s54 form of RNA polymerase

123 g--to activator and ATP hydrolysis-dependent open complex formation by the sigma(54)-RNAP.

124 de of bacterial sporulation and inhibits the open complex formation due to steric clash with sigma re

125 has been implicated in the stabilization of open complex formation during nucleotide excision repair

126 rigin, ATP hydrolysis may be unnecessary for open complex formation facilitated by His-pi.F107S.

127 d suggests that DnaD and DnaB do not require open complex formation for the stable association with D

128 The kinetics of promoter binding and open complex formation in bacteriophage T7 RNA polymeras

129 P enhances RNA polymerase binding as well as open complex formation in both promoters.

130 hese variants retain the ability to activate open complex formation in vitro.

131 of the dMyx action and a stepwise pathway of open complex formation in which core enzyme mediates the

132 Our results show that open complex formation is completely dependent on FNR an

133 nal energy source is used and the energy for open complex formation is derived from the free energy o

134 te that the linking number change induced by open complex formation is essentially all due to bubble

135 omplex conversion is 0.5 and the net rate of open complex formation is nearly 150 s(-1).

136 the template at position +2, the process of open complex formation is nearly complete.

137 , with both factors present, the kinetics of open complex formation is significantly faster than in t

138 udies reveal that the nucleotide that drives open complex formation needs to be a triphosphate and to

139 nner at pflgM, while a sequential pattern of open complex formation occurs at pfliD.

140 substitutions for Y430 and W433 also affect open complex formation on promoter DNA lacking the -11A

141 The results suggest that open complex formation only occurs efficiently on replac

142 s also demonstrate that ATP and pi stimulate open complex formation over a wide range of temperatures

143 The dynamics of open complex formation provides unique insights into the

144 We derive how the open complex formation rate depends on DNA duplex meltin

145 Open complex formation requires both transcription facto

146 nitiation pathway provides insights into how open complex formation steps that are sensitive to the p

147 ding and the observed rate of pre-initiation open complex formation that corresponds to the sum of DN

148 tor re-organises the centre to favour stable open complex formation through adjustments in sigma(54)-

149 NA polymerase binding and directly stimulate open complex formation to activate transcription.

150 e (T429A) results in the largest decrease in open complex formation yet observed for any single subst

151 (CR) in terms of the three step mechanism of open complex formation yields the equilibrium constant K

152 o, His-pi.F107S-dependent local DNA melting (open complex formation) occurs in the absence of host pr

153 (R), the mutation with the largest effect on open complex formation, --10G (T:A --> G:C), substantial

154 , using permanganate footprinting to measure open complex formation, and DNase I footprinting to moni

155 e RNA polymerase alpha subunit is needed for open complex formation, and we describe two experiments

156 ects of the substitutions on the kinetics of open complex formation, as well as on the ability of the

157 d for an open intermediate on the pathway to open complex formation, in which these 2-APs are no long

158 I and the DNA fork junction structure during open complex formation, is communicated to the AAA activ

159 olymerase, remains competent for stimulating open complex formation, suggesting that this DNA superco

160 nd trp EDCBA promoters as in vitro models of open complex formation, we have identified the sites ins

161 rent conformations adopted by the DNA during open complex formation, we investigated the contribution

162 igin of plasmid R6K, yet monomers facilitate open complex formation, while dimers, the predominant fo

163 consider a more complex two-step view of the open complex formation.

164 sequences of the promoter, thus facilitating open complex formation.

165 e of an isomerization step on the pathway to open complex formation.

166 NA binding determinants of polymerase during open complex formation.

167 nce enhanced both RNA polymerase binding and open complex formation.

168 Its ATPase activity is required for open complex formation.

169 the abrB and rrnB1 promoters and facilitates open complex formation.

170 mally associated with stable DNA melting and open complex formation.

171 d to overcome the sigma(54)-imposed block on open complex formation.

172 -RNA polymerase-DNA interactions that favour open complex formation.

173 uorescence increase is assigned to the final open complex formation.

174 or RNA polymerase sequence on the process of open complex formation.

175 enzymes were observed prior to and including open complex formation.

176 Ps affect the kinetics and thermodynamics of open complex formation.

177 37 to intercalate and distort the DNA during open complex formation.

178 AP base at -4 from the guanine at -5, during open complex formation.

179 oriV, do not bind stably and fail to induce open complex formation.

180 ancer binding activator protein to stimulate open complex formation.

181 nication pathway linking changes in sigma to open complex formation.

182 Pol III recruitment but, rather, a defect in open complex formation.

183 responsible for the DksA-specific effects on open complex formation.

184 f coiled-coil tip interactions with RNAP for open complex formation.

185 oduction of the first phosphodiester bond is open complex formation.

186 e pair disruption during the early stages of open complex formation.

187 e -35 element, consequently facilitating the open complex formation.

188 on and increases the recruitment of RNAP and open complex formation; (ii) the distal UP subsite plays

189 n filament and the subsequent restoration of open-complex formation as the central mechanism of count

190 Specifically, the kinetics of open-complex formation can be explained by a model where

191 pstream promoter DNA, or both on the rate of open-complex formation with promoters that lack UP eleme

192 ation requires the melting of DNA to form an open complex, formation of the first few phosphodiester

193 le the unstable, transcriptionally competent open complexes formed at ribosomal promoters.

194 Open complexes formed at the three mutant promoters are

195 The open complexes formed by the mutant and wild-type RNAPs

196 ing effect observed in bandshift analysis of open complexes formed on this set of constructs provided

197 Dissociation kinetics of open complexes formed with DeltaJAW RNAP and/or DT+12 DN

198 egion (TATA to TAAA) decreased the extent of open complex generated at equilibrium.

199 The open complex half-life was up to 26-fold shorter in the

200 rties of the DNA bubble in the transcription open complex have been characterized by topological anal

201 NA bubble, creating the relatively unstable (open) complex I(2).

202 , which rapidly converts to much more stable open complexes (I(3), RP(o)).

203 k of transition from the intermediate to the open complex, identifying the sigma subunit as a key pla

204 s for the structure of DNA in the functional open complex in solution, and provide an important compl

205 me and the bacterial RNA polymerase-promoter open complex in solution.

206 and initiates the formation of a prepriming open complex in the absence of DnaA protein.

207 formation of the preinitiation open complex (open complex in the absence of initiating nucleotide).

208 e probing shows that the conformation of the open complex in the presence of CRP appears qualitativel

209 ion of the holoenzyme from the closed to the open complex in the presence of the activator protein.

210 ormation of a fully open initiation complex (open complex in the presence of the initiating nucleotid

211 ator prevents RNA polymerase from forming an open complex in vitro.

212 sed complex, which is then converted into an open complex in which the promoter is both sharply bent

213 (RNAP) and double-stranded promoter DNA, to open complexes, in which the enzyme is able to access th

214 disrupting eIF2alpha contacts favored in the open complex increase initiation at suboptimal sites, an

215 amyP TRTG motif dramatically stabilizes the open complex intermediate during transcription initiatio

216 Formation of a transcriptionally competent open complex is a highly regulated multistep process inv

217 However, a question of how the open complex is formed still remains open, and several q

218 Our results suggest that once the open complex is formed, TFIIH decays into an inactive co

219 Even though the open complex is less stable in the mutant promoters, the

220 that the conformation of RNAP present in an open complex is not optimal for DksA binding and that DN

221 nary activator--RNA polymerase--aer promoter open complex is organized differently from complexes at

222 indicate that the melted template DNA in the open complex is positioned to bind the +2 NTP.

223 model for the overall path of the DNA in the open complex is presented that is consistent with the me

224 the formation of transcriptionally-competent open complexes is affected by changing the length of the

225 ectly by reducing the lifetime of the rrn P1 open complex, liberating enough RNAP to stimulate transc

226 In vitro, DksA binds to RNAP, reduces open complex lifetime, inhibits rRNA promoter activity,

227 ed, resulting in a 4- to 30-fold decrease in open complex longevity at an rRNA promoter and a approxi

228 ement for DNA unwinding, reminiscent of the 'open complex' model of RNA polymerase-promoter DNA inter

229 ition of +1 NTP alone does not stabilize the open complex; nor is it required for +2 NTP binding.

230 ree-dimensional architecture of the complete open complex (OC) composed of the promoter DNA, TATA box

231 o investigate roles of the discriminator and open complex (OC) lifetime in transcription initiation b

232 Formation of the RNA polymerase II (Pol II) open complex (OC) requires DNA unwinding mediated by the

233 te of the RNA polymerase (RNAP), forming the open complex (OC).

234 nges increase lifetimes of lambdaPR and T7A1 open complexes (OCs) by >10(5)-fold and >10(2)-fold, res

235 h is not sufficient to melt and stabilize an open complex of a non-specific DNA.

236 Isomerization of a closed to open complex of a promoter upon RNA polymerase binding i

237 her stringent promoters investigated so far, open complex of rrnB P1 has been shown to be intrinsical

238 location and size of the DNA bubble in this open complex of the mtRNAP closely resembles that of the

239 The single-stranded region of DNA within the open complex of transcriptionally active genes provides

240 te an 8-oxoG template started from partially open complexes of pol beta.

241 Stable open complexes of Pol II are largely absent from the tra

242 nformation of promoter DNA in the closed and open complexes of T7 RNAP.

243 er, Rpo41 alone was able to form a competent open complex on a pre-melted promoter.

244 promoter melting and/or stabilization of the open complex on LSP.

245 In contrast to other efflux conduits, the open complex only displays a slight preference for catio

246 t inhibit the formation of the preinitiation open complex (open complex in the absence of initiating

247 helix, as expected, and a relatively mobile "open complex" or undocked state.

248 del where nucleotide selection occurs in the open complex prior to the formation of a closed ternary

249 rving as a "molecular mimic" of DNA, but, in open complex, region 1.1 is located outside the active c

250 The conversion into open complexes requires the ATPase activity of activator

251 d bubbles, which collapsed back to closed or open complexes, resulting in repeated futile scanning.

252 under conditions that favor formation of the open complex results in destabilization of the preinitia

253 nges to form the transcriptionally competent open complex RP(o).

254 formation of the transcriptionally competent open complex (RP(o)) by Escherichia coli RNA polymerase

255 ficant effect of Sp1 on the apparent rate of open complex (RP(o)) formation (k(2)) of the pAS8 promot

256 ase (R) and promoter DNA (P) that create the open complex (RP(o)).

257 conformational changes required to form the open complex (RP(O)).

258 bble" within a catalytically active RNAP-DNA open complex (RP(o)).

259 or conversion of closed complexes (RP(c)) to open complexes (RP(o)) but do not affect K(B), the equil

260 ate a burst of I(2) by rapidly destabilizing open complexes (RP(o)) with 1.1 M NaCl.

261 rmation of this transcriptionally competent "open" complex (RP(o)) by Escherichia coli RNAP at the la

262 of the open region to form the highly stable open complex, RP(o).

263 ne another, to produce a polymerase/promoter open complex (RPo) competent for transcription.

264 nwinds promoter DNA to form an RNAP-promoter open complex (RPo) containing a single-stranded 'transcr

265 bp of promoter DNA, forming an RNAP-promoter open complex (RPo) containing a single-stranded transcri

266 ficant effect of Sp1 on the apparent rate of open complex (RPo) formation (k2) or on the apparent rat

267 Mechanistic analyses of promoter open complex (RPo) formation establish that RbpA and Car

268 in the catalytically competent RNAP-promoter open complex (RPo).

269 the approach by showing that the DNA path in open complexes (RPO) is the same as in high-resolution X

270 and show that RbpA stabilizes RNAP-promoter open complexes (RPo) via a distinct mechanism from that

271 5 base pairs of the promoter DNA to form an 'open' complex; scanning downstream to a transcription st

272 However, in the rrnB P1 open complex, scrunching occurs before RNA synthesis beg

273 Migration retardation assays of open complexes showed that RNA polymerase binds exceptio

274 great flexibility in the position of active open complexes, spanning 30 to 80 bp downstream from TAT

275 The kinetics and open-complex stabilities of CarD mutants further clarify

276 n shown to be intrinsically unstable, making open complex stability a potential regulatory step in tr

277 reported on the energetics of CarD-mediated open complex stabilization on the Mycobacterium tubercul

278 stigate the function and architecture of the open complex state of RNA polymerase II (Pol II), Saccha

279 domain, thereby allowing acquisition of the open complex status.

280 mation of the RNA polymerase (RNAP)-promoter open complex step to the productive elongation complex s

281 1 preinitiation complexes, presumably at the open complex step, contributes prominently to transcript

282 ivity, implying that it is predominantly the open complex that is sensitive.

283 We find that in stable DeltaJAW open complexes the downstream boundary of hydroxyl radic

284 In this initial unstable "open" complex the template strand appears correctly posi

285 ator form shifts the interactions toward the open complex to activate transcription.

286 site, pronounced in the promoter DNA of the open complex, was not present.

287 enerate the pre-initiation DNA bubble in the open complex, we estimate that one half (3.5-4 kcal mol(

288 Here, using a fluorescent reporter of open complex, we quantitate RPo formation in real time a

289 I (Pol II), Saccharomyces cerevisiae minimal open complexes were assembled by using a series of heter

290 on formation of transcriptionally competent open complexes were studied by DNAse I footprinting, KMn

291 ssays using DNA probes that mimic closed and open complexes were used to explore the determinants of

292 ce establish the transcriptionally competent open complex, where full promoter melting occurs.

293 IC resulted in quantitative conversion to an open complex, which retained all 31 proteins, contrary t

294 9 degrees +/- 7 degrees was measured for the open complex, while a bend of 47 degrees +/- 11 degrees

295 and Promoter) is melted from -4 to +1 in the open complex with all three proteins and from -4 to +3 w

296 s, i.e. open and closed, of apoFgFCO1 and an open complex with product fucose at atomic resolution.

297 potentiating the formation of the productive open complex with RNA polymerase.

298 Probing of the architecture of the minimal open complexes with TFIIB-FeBABE [TFIIB-p-bromoacetamido

299 dicates that when polymerase is in a stable (open) complex with P(minor), the DNA is single stranded

300 inds to free GK (super-open) and GK-glucose (open) complexes with comparable affinities (Kd = 0.23 +/