ライフサイエンスコーパス: elongation complex

1 promoting forward translocated states of the elongation complex.

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

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

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

5 polymerase II (Pol II) is carried out by an elongation complex.

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

7 several DNA lesions within the transcription elongation complex.

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

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

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

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

12 1A proteome contained MED26-associated super elongation complex.

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

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

15 n structural interaction that stabilizes the elongation complex.

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

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

18 tion initiation complex into a transcription elongation complex.

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

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

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

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

23 rms a ternary complex with it and the RNAPII elongation complex.

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

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

26 pathway for the formation of a transcription elongation complex.

27 adenylation site triggers disassembly of the elongation complex.

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

29 h and disengages when needed to generate the elongation complex.

30 which binds nascent RNA and dissociates the elongation complex.

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

32 oter as initiating complexes transition into elongation complexes.

33 ch mimics sigmaR2 is retained throughout the elongation complexes.

34 bly of abnormally long-lived (i.e., stalled) elongation complexes.

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

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

37 f the transcription bubble in initiation and elongation complexes.

38 erase II elongation by reactivating arrested elongation complexes.

39 oniae is to prevent formation of backtracked elongation complexes.

40 tive synthesis and the formation of arrested elongation complexes.

41 observed are nascent RNAs held within early elongation complexes.

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

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

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

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

46 to increase the sigma content of downstream elongation complexes.

47 on complex formation rates but form unstable elongation complexes.

48 monstrating specificity of Spt4/5 binding to elongation complexes.

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

50 a pathway to terminating NusA/NusG-modified elongation complexes.

51 e components of transcriptional mediator and elongation complexes.

52 ssembly of Pol V transcription initiation or elongation complexes.

53 DNA and RNA strands from individual ternary elongation complexes.

54 tigation of factor interactions with RNAP II elongation complexes.

55 g the accessibility of elongation factors to elongation complexes.

56 s virtually identical in both initiation and elongation complexes.

57 n is not inhibited by arrested transcription elongation complexes.

58 nd DNA and dissociates stalled transcription elongation complexes.

59 erved the dynamics of GreB interactions with elongation complexes.

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

61 s differences between priming/initiation and elongation complexes.

62 n initiation complex, and a transition to an elongation complex(1-4).

63 hat only a complete ops-paused transcription elongation complex activates RfaH, probably via a transi

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

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

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

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

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

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

70 Vaccinia vRNAP in the form of a transcribing elongation complex and in the form of a co-transcription

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

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

73 3 functions upstream of modifications to the elongation complex and provides an entry site for the XR

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

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

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

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

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

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

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

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

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

83 riven mechanism that reactivates backtracked elongation complexes and thus helps suppress their inter

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

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

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

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

88 gation complexes are less stable than Pol II elongation complexes, and Pol I is more error prone than

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

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

91 Pol I elongation complexes are less stable than Pol II elongat

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

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

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

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

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

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

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

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

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

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

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

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

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

105 that stalled Escherichia coli transcription elongation complexes block reconstituted replisomes.

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

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

108 ranslocase that is thought to dissociate the elongation complex by exerting torque on a stalled RNAP.

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

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

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

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

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

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

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

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

117 drive the dynamic exchange of initiation and elongation complex components over the transcription cyc

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

119 sibility that it controls the degradation of elongation complex components.

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

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

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

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

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

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

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

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

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

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

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

131 studies implicate NELF functioning in early elongation complexes distinct from RNA Pol II pause-rele

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

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

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

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

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

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

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

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

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

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

142 a fide initially transcribing complex (ITC), elongation complex (EC), and reinitiation complex (EC+IT

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

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

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

146 viously reported an activated porcine Pol II elongation complex, EC*, encompassing the human elongati

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

148 we present cryo-EM structures of yeast Pol I elongation complexes (ECs) bound to the nucleotide analo

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

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

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

152 RNA polymerase II elongation complexes (ECs) were assembled from nuclear e

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

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

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

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

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

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

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

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

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

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

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

164 copy (EM) structures of Pol I initiation and elongation complexes have given first insights into the

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

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

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

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

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

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

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

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

173 The assembled elongation complex incorporates a correct nucleotide, GT

174 ption elongation defects seen with the super elongation complex inhibitor KL-2 are exacerbated in DOT

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

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

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

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

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

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

185 of Super Elongation Complex (SEC) or Little Elongation Complex (LEC) to regulate the expression of c

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

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

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

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

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

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

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

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

201 CDK9 - a component of the transcription elongation complex P-TEFb - bound to the MYCN-amplicon s

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

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

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

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

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

207 Elongation complexes remain stable on DNA, with their ac

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

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

210 .0038 s(-1)); a substantial subpopulation of elongation complexes retained sigma(70) throughout trans

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

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

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

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

215 Among all of the Super Elongation Complex (SEC) components, ELL1 (also known as

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

217 nal elongation and is a subunit of the Super Elongation Complex (SEC) essential for HIV-1 transactiva

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

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

220 D26 plays a role in the recruitment of Super Elongation Complex (SEC) or Little Elongation Complex (L

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

222 show that site-specific acetylation of super elongation complex (SEC) subunit AFF1 by p300 reduces it

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

224 details are used to model the TAR-Tat-super-elongation complex (SEC) that is essential for efficient

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

246 es in dinucleotide production, transcription elongation complex stability, and Pol I pausing in vitro

247 palm and thumb domains coordinately control elongation complex stability.

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

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

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

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

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

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

254 minal region that interacts with other super-elongation complex subunits and a C-terminal homology do

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

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

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

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

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

260 ) to a nascent transcript in a transcription elongation complex (TEC) promotes tethering but not dire

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

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

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

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

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

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

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

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

269 l, multisubunit RNA polymerase transcription elongation complexes (TECs).

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

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

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

273 also demonstrate that upon release from the elongation complex, the CTD transforms back into the aut

274 nt triggered by recruitment to transcription elongation complexes through a specific DNA element.

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 Isolated elongation complexes undergo termination in a PAS-depend

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

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

285 The elongation complex was extremely stable, allowing purifi

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

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

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

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

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

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

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

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

294 e scaffold protein of the multisubunit super-elongation complex, which plays key roles in the release

295 nt kinase targets replication initiation and elongation complexes, which may be relevant to human dis

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.