ライフサイエンスコーパス: elongation complex

1 the RNA strand of the RNA-DNA hybrid in the elongation complex.

2 es forming an unstable RNA-DNA hybrid in the elongation complex.

3 ate may serve to reduce back-tracking of the elongation complex.

4 active and stable polymerase-primer-template elongation complex.

5 1A proteome contained MED26-associated super elongation complex.

6 eras and their oncogenic cofactor, the super elongation complex.

7 tween Mpk1 and the Paf1 subunit of the Paf1C elongation complex.

8 ural model of Tgt bound to the transcription elongation complex.

9 n structural interaction that stabilizes the elongation complex.

10 independently of the DNA-RNA scaffold of the elongation complex.

11 pathway for the formation of a transcription elongation complex.

12 the nascent RNA as the RNA emerges from the elongation complex.

13 tion initiation complex into a transcription elongation complex.

14 an 18 nt to stably associate with the Pol II elongation complex.

15 adenylation site triggers disassembly of the elongation complex.

16 trand at the catalytic center of the pol III elongation complex.

17 NA hybrid as a part of a stably transcribing elongation complex.

18 ce for the formation of an active telomerase elongation complex.

19 ion state equilibrium of Pol II in a stalled elongation complex.

20 with one of its interacting partners in the elongation complex.

21 AP in the context of a specific paused early elongation complex.

22 s as a stable component of the transcription elongation complex.

23 with elongating Pol II and components of the elongation complex.

24 iprocally aids in recruitment of Rat1 to the elongation complex.

25 which binds nascent RNA and dissociates the elongation complex.

26 esidues increase the affinity of NusG to the elongation complex.

27 promoting forward translocated states of the elongation complex.

28 ition between the exonuclease and the pol II elongation complex.

29 cids accepted and produced by the fatty acid elongation complex.

30 ocation of RNAP along the DNA template in an elongation complex.

31 rial transcription factor (MTF1), and of the elongation complex.

32 anscription to initiate a discrete "wave" of elongation complexes.

33 tive synthesis and the formation of arrested elongation complexes.

34 observed are nascent RNAs held within early elongation complexes.

35 nd facilitate cleavage of the nascent RNA in elongation complexes.

36 s and the high stability and processivity of elongation complexes.

37 o 65% of NS5B could be converted into active elongation complexes.

38 on in aborting "divergent" promoter-proximal elongation complexes.

39 to increase the sigma content of downstream elongation complexes.

40 on complex formation rates but form unstable elongation complexes.

41 PCI2 is required for directing CE to Pol II elongation complexes.

42 e components of transcriptional mediator and elongation complexes.

43 ssembly of Pol V transcription initiation or elongation complexes.

44 DNA and RNA strands from individual ternary elongation complexes.

45 tigation of factor interactions with RNAP II elongation complexes.

46 g the accessibility of elongation factors to elongation complexes.

47 s virtually identical in both initiation and elongation complexes.

48 distinct from those described previously for elongation complexes.

49 ng a role for the proteasome in dissociating elongation complexes.

50 version of early transcribing complexes into elongation complexes.

51 erved the dynamics of GreB interactions with elongation complexes.

52 ch mimics sigmaR2 is retained throughout the elongation complexes.

53 n the crystal structures of different 3D-RNA elongation complexes.

54 H2B dimers and the presence of queued Pol II elongation complexes.

55 f the transcription bubble in initiation and elongation complexes.

56 erase II elongation by reactivating arrested elongation complexes.

57 oniae is to prevent formation of backtracked elongation complexes.

58 , purified, and then crystallized poliovirus elongation complexes after multiple rounds of nucleotide

59 ercomplex" structure within a punctate where elongation complexes aggregate through entanglement of D

60 tal structures of the T7 RNAP initiation and elongation complexes allowed us to predict major rearran

61 ich encodes a subunit of the Spt4-Spt5 early elongation complex, also suppresses ssu72-2, whereas the

62 of the divisome, the MreB-directed cell wall elongation complex, alternate peptidoglycan synthases, t

63 multiple interactions between the transcript elongation complex and factors involved in mRNA splicing

64 ntrolled by direct interactions with the PAF elongation complex and H3K4Me2/3.

65 n physically interact with the transcription elongation complex and influence transcription elongatio

66 TFIIB is normally associated with the early elongation complex and is only destabilized at +12 to +1

67 etd2 histone methyltransferase to the RNAPII elongation complex and is required for H3K36 trimethylat

68 ation, Spt4/5 can displace TFE from the RNAP elongation complex and stimulate processivity.

69 utR sites of phage HK022 bind the transcript elongation complex and suppress termination at downstrea

70 t assembly and modification status of Pol II elongation complexes and by favoring efficient nucleosom

71 cription elongation factor DSIF with RNAP II elongation complexes and discovered that the nascent tra

72 -Not increases the recruitment of TFIIS into elongation complexes and enhances the cleavage of the di

73 iation complexes also occur in transcription elongation complexes and facilitate pause read-through b

74 the upstream fork junction of transcription elongation complexes and modulate RNA synthesis in respo

75 Collisions between paused transcription elongation complexes and replication forks inevitably ha

76 is important for Ccr4-Not to associate with elongation complexes and stimulate elongation.

77 on 5 progressively decrease the stability of elongation complexes and their processivity on genome-le

78 pt core RNA polymerase, holoenzymes, stalled elongation complexes and transcribing RNA polymerases in

79 ation sequencing, we identified locations of elongation complexes and transcription-repair coupling e

80 cally associates with the PAF1 transcription elongation complex, and inhibition of PAF1 phenocopies t

81 osomes, a central component of transcription elongation complexes, and is required for recruitment of

82 ription bubble in the T7 RNAP initiation and elongation complexes, and to define the function of the

83 n, but not all important Bur1 targets in the elongation complex are known.

84 We also found that productive elongation complexes are completely resistant to negativ

85 First, Pol II elongation complexes are isolated with specific phospho-

86 J-Gtpbp2(nmf205)(-/-) mice in which neuronal elongation complexes are stalled at AGA codons due to de

87 the signaling pathways triggered by stalled elongation complexes are unknown.

88 Our results envision the elongation complex as a flexible structure, not a rigid

89 induction, vesicle nucleation, and membrane elongation complexes as key signaling intermediates driv

90 osphorylated factor does not bind to stalled elongation complexes as measured in a gel mobility shift

91 The elongation complex assembly is 6 times slower at 30 degr

92 The elongation complex assembly is slow, following a one-ste

93 Rapid release of pyrophosphate from the elongation complex at a rate consistent with productive

94 transcripts during transcription by stalling elongation complexes at catalytically dead EcoRIE111Q ro

95 ss-linking strategy to isolate transcription elongation complexes at early steps of elongation, we fo

96 thesized transcripts dictates the release of elongation complexes at the end of genes.

97 motes proofreading by transcript cleavage in elongation complexes backtracked by nucleotide misincorp

98 nd Py-Im polyamides, we find that the pol II elongation complex becomes arrested immediately upstream

99 hing the unique resistance activities of the elongation complexes before and after P-TEFb function.

100 port for the residence time of paused Pol II elongation complexes being much shorter than estimated f

101 res of Spt5 required for it to interact with elongation complexes, bind nucleic acids, and promote tr

102 kely a general mechanism for dissociation of elongation complexes, both in the presence and absence o

103 on of Spt5 did not prevent Spt4/5 binding to elongation complexes, but abrogated the cross-linking of

104 inct role before its assembly into the super elongation complex by stabilizing Pol II recruitment/ini

105 Arresting the elongation complexes by a quick removal of NTPs leads to

106 , we show that, unexpectedly, the polymerase elongation complex can use NTPs to excise the terminal n

107 Here, we demonstrate that paused elongation complexes can be remarkably stable, with half

108 d DNA templates to form active initiation or elongation complexes can be resolved and monitored by th

109 ghly stable lambdaQ-containing transcription elongation complex capable of traversing the entire late

110 esence of inorganic pyrophosphate (PPi), the elongation complex catalyzes the reverse pyrophosphoroly

111 While not essential for its interaction with elongation complexes, Ccr4-Not interacts with the emergi

112 The catalytic component of the elongation complex, CDK9, was important for the transcri

113 t changes in properties of the transcription elongation complex closely correlate with utilization of

114 e before recruitment of AFF4 and other super elongation complex components.

115 nding and recruitment of the transcriptional elongation complex containing cyclin dependent kinase-9

116 diated phosphorylation events, targeting the elongation complex containing DSIF and NELF, reverse the

117 end itself to structural studies of an early elongation complex containing sigma(70).

118 We measured the kinetics of formation of the elongation complex containing the polymerase and a doubl

119 s, this study reveals that T7 RNA polymerase elongation complexes containing only a 4-base pair hybri

120 expression by recruiting human transcription elongation complexes containing P-TEFb, AFF4, ELL2, and

121 By monitoring the response of elongation complexes containing RNAPII and combinations

122 We also show that elongation complexes containing sigma(70) manifest enhan

123 Recent advances have identified the super elongation complex, containing the eleven-nineteen lysin

124 in vivo, the lambdaQ-modified transcription elongation complex contains Q as a stably associated sub

125 several components of the PAF1 transcription elongation complex contribute to Chd1 recruitment to hig

126 using, including backtracking of the ternary elongation complex, delay of translocation of the enzyme

127 Crystal structures of the elongation complex do include downstream DNA and provide

128 These results indicate that individual elongation complexes do not engage in multiple rounds of

129 iption complexes by moving the transcription elongation complex downstream on the DNA template in the

130 ci, Spt4/5 is recruited to the transcription elongation complex during early elongation within 500 ba

131 ssory proteins and antibiotics can alter the elongation complex dynamics.

132 d in rapid dissociation of the transcription elongation complex (EC) at termination points located 7-

133 The RNA polymerase elongation complex (EC) is both highly stable and proces

134 chanism by which it reaches and disrupts the elongation complex (EC) is unknown.

135 solid matrices, we have determined that a T7 elongation complex (EC) may be advanced past a halted T3

136 The T7RNA polymerase (RNAP) elongation complex (EC) pauses and is destabilized at a

137 nthesis initiation, rates of RNA elongation, elongation complex (EC) stability, and virus growth.

138 ution structures of the Thermus thermophilus elongation complex (EC) with a non-hydrolysable substrat

139 ier that in the absence of the transcription elongation complex (EC), N interacts with the C-terminal

140 transition from an initiation complex to an elongation complex (EC), T7 RNA polymerase undergoes maj

141 inators (his, t500, and tR2) destabilize the elongation complex (EC).

142 tRNAP and the nucleic acid components of the elongation complex (EC).

143 llance mechanisms that target mRNAs on which elongation complexes (ECs) are stalled by, for example,

144 nascent RNAs from all actively transcribing elongation complexes (ECs) in Escherichia coli and Sacch

145 the binding of pyrophosphate to well-defined elongation complexes (ECs) indicate that the intrinsic o

146 erved regulatory protein that interacts with elongation complexes (ECs) of RNA polymerase, DNA, and R

147 Studies of halted T7 RNA polymerase (T7RNAP) elongation complexes (ECs) or of T7RNAP transcription ag

148 as GreB facilitates RNA cleavage in arrested elongation complexes (ECs).

149 nds on the productive state of transcription elongation complexes (ECs).

150 elongation complexes on native gels, namely elongation complex electrophoretic mobility shift assay

151 ugh protein-primed initiation and RNA-primed elongation complexes employ the same polymerase active s

152 structures of Thermus RNAP elemental paused elongation complexes (ePECs).

153 longation Complex (SEC), the transcriptional elongation complex essential for HIV-1 long terminal rep

154 In the structural model of the Pol II elongation complex, fork loop 2 directly interacts with

155 longation rates, RNA binding affinities, and elongation complex formation rates but form unstable elo

156 s the formation of an artificially assembled elongation complex from its component DNA and RNA strand

157 able of promoting the dissociation of Pol II elongation complexes from DNA.

158 pletely displaces TFIIF from free pol II and elongation complexes, Gdown1 does not functionally assoc

159 of TFIIF, TTF2, TFIIS, DSIF and P-TEFb with elongation complexes generated from a natural promoter u

160 ses and base-pairs at these positions as the elongation complex goes through the various steps of the

161 ructures of T7 RNA polymerase initiation and elongation complexes have provided a wealth of detailed

162 es, measurements of the stability of stalled elongation complexes have shown lifetimes that are much

163 ose that dynamic interactions between RNAPII elongation complexes help regulate polymerase traffic an

164 scriptional stalling by rendering polymerase elongation complexes highly susceptible to backtracking

165 virus to target the human PAF1 transcription elongation complex (hPAF1C).

166 sition of Pol II into a mature transcription elongation complex in vivo.

167 s question, we determine the structure of an elongation complex in which the tip complex assembly com

168 decreases in the total mass of transcription elongation complexes in the same experiments.

169 abilizes paused mitochondrial RNA polymerase elongation complexes in vitro and favors the posttranslo

170 at domain (CTD) both in vivo and in isolated elongation complexes in vitro.

171 phosphorylates Proteins in the transcription elongation complex, including RNA polymerase II (pol II)

172 The assembled elongation complex incorporates a correct nucleotide, GT

173 ision entails a transient state in which the elongation complexes interact, followed by substantial b

174 ers undergo signal-induced release of paused elongation complexes into productive RNA synthesis.

175 We propose that RNA anchoring to the elongation complex is a widespread mechanism of pause re

176 The upstream DNA in the elongation complex is also found to be sharply bent at t

177 al modification conferred by putL RNA on the elongation complex is also long-lived: the efficiency of

178 ination, a process wherein the transcription elongation complex is altered by accessory factors to be

179 The resultant lambdaQ-modified transcription elongation complex is competent to read through downstre

180 We show that the clamp in elongation complexes is modulated by the nontemplate str

181 l III bound to preinitiation complexes or in elongation complexes is protected from repression by Maf

182 anti-CTD antibody, which also dismantles the elongation complex, is found to bridge the CTD to RNA.

183 PICs, but once polymerase enters transcript elongation, complexes lacking TFIIF quantitatively bind

184 actor that, in collaboration with the little elongation complex (LEC) comprising ELL, Ice1, Ice2, and

185 Recently, we identified the little elongation complex (LEC) in Drosophila that is required

186 Recently, the little elongation complex (LEC)-which contains the transcriptio

187 nd other components of SEC named the "little elongation complex" (LEC).

188 ion response in the RNA polymerase (RNAP) of elongation complexes located at terminators far downstre

189 Spt4/5, becomes an integral component of the elongation complex, making direct contact with the 'jaws

190 (pol)-RNA interactions within the polymerase elongation complex might increase and/or decrease the ma

191 The transcription elongation complex model reveals that the Spt4/5 is an u

192 shes a novel way to generate a highly active elongation complex of the medically important NS5B polym

193 The current study demonstrates that halted elongation complexes of T7 RNA polymerase in the absence

194 Mutations associated with the elongation complex often alter cell width, though it is

195 However, the status of the elongation complex on the HIV long terminal repeat (LTR)

196 -RNA interactions facilitate assembly of the elongation complex on transcribed genes when RNA emerges

197 the effect of incorporating Spt4/5 into the elongation complex on transcription through the 601R nuc

198 lyzing direct factor interactions to RNAP II elongation complexes on native gels, namely elongation c

199 id is maintained, we assembled transcription elongation complexes on synthetic nucleic acid scaffolds

200 le transferal of the downstream DNA from the elongation complex onto the initiation complex.

201 DksA/ppGpp do not destabilise transcription elongation complexes or inhibit their backtracking, as w

202 e is known about the dynamics of these early elongation complexes or the fate of the short transcript

203 d functional properties of the transcription elongation complex over distances of at least 700 base p

204 ed recruitment of the positive transcription-elongation complex P-TEFb and thereby prevented phosphor

205 Thus, the transcription elongation complex Paf1, the histone methylase Set1-COMP

206 Instead, GreB binds rapidly and randomly to elongation complexes, patrolling for those requiring nuc

207 when it is a component of the transcription elongation complex, perhaps, in part, by blocking intera

208 the local concentrations of boxB-bound N at elongation complexes poised at terminators, and are comb

209 -alpha signaling 2D10 T cells and leaves the elongation complex prior to the termination site.

210 typical Escherichia coli message because the elongation complex protects this RNA from degradation.

211 e interaction of TRCF with the transcription elongation complex, provide mechanistic insights into TR

212 boundary of the transcription bubble in the elongation complex, providing a possible explanation of

213 Elongation complexes remain stable on DNA, with their ac

214 Therefore, the RNAPII transcript elongation complex represents a platform for interaction

215 tors ELL1/2 are core components of the super elongation complex required for HIV-1 proviral transcrip

216 .0038 s(-1)); a substantial subpopulation of elongation complexes retained sigma(70) throughout trans

217 ependently of thermodynamic stability of the elongation complex, RNA polymerase directly 'senses' the

218 family protein AFF3 within the transcription elongation complex SEC-L3.

219 purified the AFF1- and AFF4-containing super elongation complex (SEC) as a major regulator of develop

220 We have identified super elongation complex (SEC) associated with all chimeras pu

221 by the recruitment of the Ser2P kinase super elongation complex (SEC) effecting increased release of

222 The super elongation complex (SEC) governs this process by mobiliz

223 cription elongation factor)-containing super elongation complex (SEC) in the regulation of gene expre

224 lectively recruits P-TEFb as part of a super elongation complex (SEC) organized on a flexible AFF1 or

225 LL were found recently to coexist in a super elongation complex (SEC) that includes known transcripti

226 AFF4 act as a scaffold to assemble the Super Elongation Complex (SEC) that strongly activates transcr

227 use release by directly recruiting the super elongation complex (SEC) to chromatin.

228 is required to engage and recruit the super elongation complex (SEC) to EGF-responsive genes to allo

229 The viral Tat protein recruits human Super Elongation Complex (SEC) to paused Pol II to overcome th

230 d by a positive feedback loop with the super elongation complex (SEC) to quickly differentiate betwee

231 d genes and for the recruitment of the super elongation complex (SEC) to these loci following differe

232 lin T1 heterodimer that is part of the super elongation complex (SEC) used by the viral encoded Tat p

233 romodomain-containing protein Brd4 and super elongation complex (SEC) via different recruitment mecha

234 ich leukemia (ELL) participates in the super elongation complex (SEC) with the RNA polymerase II (Pol

235 MLL-fusion partners are members of the super elongation complex (SEC), a critical regulator of transc

236 duces binding of CDK8-Mediator and the super elongation complex (SEC), containing AFF4 and CDK9, to a

237 The Super Elongation Complex (SEC), containing transcription elong

238 CDK9, as part of P-TEFb and the super elongation complex (SEC), is by far the best characteriz

239 ated histone H3 specifically recruited Super Elongation Complex (SEC), the transcriptional elongation

240 ia transcription factors, BRD4, or the super elongation complex (SEC).

241 on elongation components including the super elongation complex (SEC).

242 Pol II correlates with recruitment of super-elongation complexes (SECs) containing ELL/EAF family me

243 The viral Tat protein recruits human super elongation complexes (SECs) to paused Pol II to overcome

244 upstream fork junction of the transcription elongation complex, similar to sigma2 in the transcripti

245 nitin are added to a human RNA polymerase II elongation complex simultaneously, the reaction becomes

246 ator RNA directly modifies the transcription elongation complex so that it terminates less efficientl

247 ative effects on transcription initiation or elongation complex stability but reduced the rate of tra

248 x:polymerase interactions that contribute to elongation complex stability.

249 A majority of Pol II elongation complexes stall after successful addition of

250 o generate a productive NS5B.primer.template elongation complex stalled after formation of a 9-nucleo

251 Furthermore, selecting for transcription elongation complexes stalled near the codon that suffers

252 promoter open complex step to the productive elongation complex step involves "promoter escape" of RN

253 RNA segment in the backtracked transcription elongation complex strongly promotes transcript hydrolyt

254 upstream of the transcription bubble in the elongation complex structure means that our picture of t

255 rmination hairpin combine to destabilize the elongation complex sufficiently to permit significant tr

256 ructures of multiple picornavirus polymerase elongation complexes suggest that these enzymes use a di

257 f the complete NusG-associated transcription elongation complex, suggesting that the NGN domain binds

258 However, the stability of RNA Pol II elongation complexes suggests that such complexes are no

259 ins remain associated with the transcription elongation complex (TEC) as it escapes the pause and tra

260 ry RNA molecule but, rather, a transcription elongation complex (TEC) comprising the growing nascent

261 o by loading directly onto the transcription elongation complex (TEC) in trans.

262 ive and off-pathway states of the transcript elongation complex (TEC), and this complicates modeling

263 ctor capable of disrupting the transcription elongation complex (TEC), detail the rate of and require

264 mRNA export factor Yra1 to the transcription elongation complex (TEC).

265 RNAP that comprise the ternary transcription elongation complex (TEC).

266 ks RNA in an RNA:DNA hybrid within a ternary elongation complex (TEC).

267 and the nucleic acid scaffold of the ternary elongation complex (TEC, RNAP-DNA-RNA).

268 is impeded by collisions with transcription elongation complexes (TEC).

269 We tested the activity of Nun on ternary elongation complexes (TECs) assembled with templates lac

270 structures of Escherichia coli RNAP ternary elongation complexes (TECs) with and without Nun by sing

271 iometrically limiting component of the super-elongation complex that drives secretory-specific immuno

272 TEFb and ELL2 combine to form a bifunctional elongation complex that greatly activates HIV-1 transcri

273 In other organisms, MreB is part of an elongation complex that requires RodZ for proper functio

274 sults have uncovered important properties of elongation complexes that allow a more complete understa

275 p7 stabilizes the upstream DNA duplex of the elongation complex thus disfavouring backtracking and pr

276 e stability of the pre-translocated state of elongation complex, thus slowing down addition of the fo

277 ntermediate that reflects transition from an elongation complex to a true termination event.

278 Mis-incorporation causes the transcription elongation complex to backtrack, releasing a single stra

279 NELF, and a reconstituted Drosophila Pol II elongation complex to gain insight into the mechanism of

280 lated by DNA-encoded elements that cause the elongation complex to pause.

281 ne tails via their bromodomain, bringing the elongation complex to the promoter region.

282 Before P-TEFb function, early elongation complexes under the control of negative facto

283 Isolated elongation complexes undergo termination in a PAS-depend

284 While effective, the distribution of elongation complexes using EcoRIE111Q requires laborious

285 ide a possible model by which DSIF binds the elongation complex via association with the nascent tran

286 The elongation complex was extremely stable, allowing purifi

287 When binding to the elongation complex was prevented by mutation of either p

288 und that, at the dose used, a single wave of elongation complexes was blocked within the first 25 kb

289 sigma(70) release from mature elongation complexes was slow (0.0038 s(-1)); a substant

290 sh the overall architecture of the HIV-1 Tat elongation complex, we mapped the binding sites that med

291 reover, by analyzing stepwise initiation and elongation complexes, we demonstrate that P-TEFb activit

292 ur structures of picornaviral polymerase-RNA elongation complexes, we have previously engineered more

293 TCR occurred where the elongation complexes were blocked, and repair was associ

294 stabilizing the association with the RNAPII elongation complex, which also requires the presence of

295 is "locked" in the active center of a Pol II elongation complex, which is stabilized by the coordinat

296 n function in the ribosome or the transcript elongation complex with minimal structural change, provi

297 he transcribed strand arrested 60-90% POLRMT elongation complexes with greater arrest by the adduct w

298 s, indicating an ability to form more stable elongation complexes with long primer-template RNAs.

299 to prevention of collisions of transcription elongation complexes with replication forks.

300 factor Spt16, a subunit of the transcription elongation complex yFACT.