ライフサイエンスコーパス: transcription complex

1 uitment of DNA repair factors to the stalled transcription complex.

2 y assemble the Notch1/Rbpj/Maml trimolecular transcription complex.

3 c segment that in turn is linked to a single transcription complex.

4 mponent in a newly defined, HOXA9-containing transcription complex.

5 inhibit progression of the RNA polymerase I transcription complex.

6 regulators recognize distinct states of the transcription complex.

7 motif, that were occupied by the NOTCH3/CSL transcription complex.

8 NGN2 simultaneously, forming a multi-protein transcription complex.

9 clear proteins and assembly of the NF-kappaB transcription complex.

10 the viral core, in proximity to the reverse transcription complex.

11 ng a pivotal role in regulation of the Notch transcription complex.

12 erves to bring RNA-processing enzymes to the transcription complex.

13 the assembly of a functional MHV replication-transcription complex.

14 l I-associated transcripts destabilizing the transcription complex.

15 y, is an integral part of the RNA polymerase transcription complex.

16 ith constitutive activation of the NF-kappaB transcription complex.

17 assembly and initiation of the mitochondrial transcription complex.

18 e necessary for the sigma recruitment to the transcription complex.

19 required for formation of a stable Met4-Cbf1 transcription complex.

20 ate that P-TEFb activity is regulated in the transcription complex.

21 hat Mist1 and Sp1 were found within the same transcription complex.

22 titermination-proficient modification of the transcription complex.

23 globulin genes, possibly via the spliceosome transcription complex.

24 isplacement activity when bound to a stalled transcription complex.

25 mily members and associating with CBP in the transcription complex.

26 uitment and anti-pausing modification of the transcription complex.

27 nstitutive activity of the beta-catenin-Tcf4 transcription complex.

28 al role for the CTD in CE recruitment to the transcription complex.

29 of nucleic acids at the upstream edge of the transcription complex.

30 a subunit is a part of RNA binding domain in transcription complex.

31 is an essential component of the early gene transcription complex.

32 rily conserved IDR within the metazoan TFIID transcription complex.

33 IL-23-induced SOCS1 binding to the IFN-gamma transcription complex.

34 multiple strategies for the assembly of the transcription complex.

35 one chaperone FACT (facilitator of chromatin transcription) complex.

36 addition cycles and destabilize the initial transcription complexes.

37 those halted by protein-DNA barriers such as transcription complexes.

38 t of RNA- and chromatin-modifying factors to transcription complexes.

39 cleavage reactions in the context of stable transcription complexes.

40 nnel, restricting DksA action to a subset of transcription complexes.

41 age complexes (Top1cc) up- and downstream of transcription complexes.

42 the yeast genome that interact with Pol III transcription complexes.

43 se, which is an enzyme that disrupts stalled transcription complexes.

44 ) prior to its ATP-dependent dissociation of transcription complexes.

45 relevant mode of interaction within dimeric transcription complexes.

46 artially colocalize to the viral replication-transcription complexes.

47 , a DNA translocase that removes the stalled transcription complexes.

48 eleases newly synthesized RNA molecules from transcription complexes.

49 orks are arrested by encounters with head-on transcription complexes.

50 sites can be combined to form high affinity transcription complexes.

51 with coactivators, aids in the formation of transcription complexes.

52 intrinsically disordered regions to remodel transcription complexes.

53 he RapA-mediated remodeling of nonproductive transcription complexes.

54 s, thereby permitting assembly of functional transcription complexes.

55 cessing factors are stored for assembly into transcription complexes.

56 ssion and increasing the processivity of LTR transcription complexes.

57 in the recruitment of PCAF/P-TEFb-containing transcription complexes.

58 hey assemble with nuclear partners into NFAT transcription complexes.

59 rfering with the assembly of ATF1-containing transcription complexes.

60 al species and, probably, different types of transcription complexes.

61 an bind to emerging transcripts and displace transcription complexes.

62 xtracellular antagonists and destruction and transcription complexes.

63 bservations of DNA scrunching on immobilized transcription complexes.

64 genes by forming chromatin-associated Notch transcription complexes.

65 ding acetylated histone tails and recruiting transcription complexes.

66 oteins bound to the template DNA, especially transcription complexes.

67 NAP affects the activity and distribution of transcription complexes across the genome, and ultimatel

68 cule techniques now permit the tracking of a transcription complex along a DNA template in real time

69 The DNA in transcription complexes also has a more open structure,

70 inst decapentaplegic homolog 3 (Smad3)/Smad4 transcription complex and by interfering with p300, a co

71 tDNAs by displacing the stable multi-protein transcription complex and by removing R-loops.

72 PAF1C interacts with the pol III transcription complex and causes pol III loss from the g

73 by promoting assembly of an Olig2-dependent transcription complex and define a nucleoporin as a key

74 roteins that interact first with the reverse transcription complex and later with the preintegration

75 nent of the transcription factor IIH (TFIIH) transcription complex and plays essential roles in trans

76 ggers the dissociation of the CREB-CBP-TORC2 transcription complex and reduces gluconeogenic enzyme g

77 with Notch signaling by disrupting the Notch transcription complex and shows therapeutic potential fo

78 ermination via conformational changes in the transcription complex and the latter proposes that degra

79 rminator is flexibly accommodated within the transcription complex and, unexpectedly, plays a major s

80 have identified proteins that bind tRNA gene transcription complexes and are required for tgm silenci

81 dels for communication between the tRNA gene transcription complexes and local chromatin are discusse

82 Barriers can include transcription complexes and R-loops that form when RNA h

83 have investigated replisome collisions with transcription complexes and R-loops using a reconstitute

84 SRY competitively displaces SOX10 in such transcription complexes and represses their regulatory f

85 romote the local assembly of tissue-specific transcription complexes and show how nuclear pore compos

86 interact with the nontemplate DNA strand in transcription complexes and thus may interfere with each

87 targets include histones, components of the transcription complex, and components of the spliceosome

88 ion of the nuclear factor-kappaB (NF-kappaB) transcription complex, and its effect on apoE was elimin

89 he energy from ATP hydrolysis to disrupt the transcription complex, and stimulates DNA repair by recr

90 ions among TIF1gamma, the blood-specific SCL transcription complex, and the positive elongation facto

91 roach to identify Spt7, a member of the SAGA transcription complex, and the RP transactivator Ifh1 as

92 se similarity between the Pol II and Pol III transcription complexes, and additionally explain previo

93 s lacking components of chromatin modifiers, transcription complexes, and modulators of translation.

94 dynamics of recruitment of these proteins to transcription complexes, and of the transitions between

95 l machinery, the kinetics of assembly of the transcription complexes, and the synthesis and degradati

96 In the nucleus, ErbB3 interacts with transcription complexes, and thereby has a role in trans

97 ase III (Pol III) is one of three eukaryotic transcription complexes, and was identified as the compl

98 ast two-hybrid screen, we identified a novel transcription complex AR-p44-Smad1, confirmed for physic

99 he results suggest that intergenic and genic transcription complexes are independent and possibly dif

100 about how collisions between replisomes and transcription complexes are minimized and the mechanisms

101 Transcription complexes are recruited not only to the gl

102 do not lead to replisome inactivation, that transcription complexes are the primary sources of this

103 ct early enhancers, each requiring different transcription complexes, are required for full activatio

104 s, including the FACT (facilitates chromatin transcription) complex, are central for these processes

105 dentify MAML1 and other members of the Notch transcription complex as high-confidence cellular intera

106 1 is not involved in interactions within the transcription complex as suggested by X-ray analysis.

107 important molecular insights into how Notch transcription complexes assemble at different target gen

108 Pol II factors that we tested suggests that transcription complexes assemble via stochastic multiste

109 , these results suggest that the identity of transcription complex assembled in the core promoter-dep

110 binding regulates nucleosome positioning and transcription complex assembly >300 bp away and how core

111 omplex regulates the formation of the active transcription complex assembly (and, hence, transcriptio

112 t an early stage of chromatin remodeling and transcription complex assembly after binding of androgen

113 of both their unique and shared functions in transcription complex assembly and chromatin structure r

114 inding protein (TBP) plays a central role in transcription complex assembly and is regulated by a var

115 re, we demonstrate that the formation of the transcription complex assembly at the promoter is depend

116 In particular, we examine transcription complex assembly by the stress-directed SA

117 data suggest that MMS-induced genes undergo transcription complex assembly sequentially, first invol

118 nd suggest possible roles for this domain in transcription complex assembly.

119 r proteins to remodel chromatin and regulate transcription complex assembly.

120 at influence genomic occupancy of GR as well transcription complex assembly.

121 y ensure lambdaQ is recruited exclusively to transcription complexes associated with P(R').

122 enhancer elements regulate the assembly of a transcription complex at a promoter remains poorly under

123 genes in mouse ES cells and suggest that the transcription complex at developmental genes is differen

124 s a central role in both the assembly of the transcription complex at gene promoters and also in the

125 ntiation by assembling Olig2 and Brd7 into a transcription complex at nuclear periphery.

126 oss of SRC-2 leads to destabilization of the transcription complex at the peroxisome proliferator res

127 26p is not due to the defect in formation of transcription complex at the promoter.

128 the association of MARE-binding proteins and transcription complexes at LCR HS2 and the adult betamaj

129 ERK phosphorylates additional substrates in transcription complexes at mitogen-responsive promoters.

130 hat modulate the association and activity of transcription complexes at specific genes.

131 the source of the ssDNA cofactor within the transcription complex because removal of the non-templat

132 n is transient, as Brd4 is released from the transcription complex between positions +14 and +36.

133 an intricate network of interactions within transcription complexes between RNAP, transcription fact

134 cleotide transcripts that remain part of the transcription complex but cannot be further elongated.

135 into the assembly of a Notch pathway active transcription complex but have also raised several intri

136 parently dispensable for RfaH binding to the transcription complex but is required for the antitermin

137 plisome stalls upon collision with a head-on transcription complex, but instead of collapsing, the re

138 of SF3b RNA splicing complex and STAGA/TFTC transcription complexes, but its specific function withi

139 d, in the nucleus, disrupts functional Smad3 transcription complexes by competing with coregulators.

140 fd releases transcripts and rescues arrested transcription complexes by moving the transcription elon

141 oped a method to visualize HIV-1 DNA reverse transcription complexes by the incorporation and fluores

142 lear translocator (ARNT), to form functional transcription complexes capable of DNA binding and gene

143 Moreover, the master circadian transcription complex CLK/CYC directly regulates Mef2 tr

144 RNA polymerase transcription complexes co-directionally oriented with t

145 for promoter chromatin remodeling and basal transcription complex communication.

146 Transcription complex components frequently show coupled

147 ng regulates gene expression by inhibiting a transcription complex consisting of the transcriptional

148 malignant renal proximal tumor cells, that a transcription complex, consisting of NF-kappaB p65 and m

149 Nevertheless, the long-persisting transcription complex containing RNA and all of the GTFs

150 itochondrial transcription and distinct from transcription complexes containing POLRMT and h-mtTFB2.

151 X-ray crystal structures of transcription complexes containing short RNAs reveal thr

152 veral direct targets of the beta-catenin/TCF transcription complex (cyclin D1, c-MYC, c-MYC-binding p

153 tions between sigma and the remainder of the transcription complex decreases.

154 rmutation requires RNA polymerase II (polII) transcription complex-dependent targeting of the DNA mut

155 enhanced retention of a U5 snRNP subunit on transcription complexes downstream of the gene.

156 RfaH is recruited to the transcription complex during RNA chain elongation throug

157 and chromatin immunoprecipitation to analyze transcription complex dynamics in gene regulation during

158 disassembly of the highly stable elongating transcription complex (EC) over windows of two to three

159 In bacteria, disassembly of elongating transcription complexes (ECs) can occur at intrinsic ter

160 obal analysis reveals that the TFIIIB-TFIIIC transcription complex exhibits remarkable structural ela

161 This transcription complex facilitates generation of both pro

162 data indicate that the facilitates chromatin transcription complex (FACT) interacts with CKII and may

163 rimeric IFN-stimulated gene factor 3 (ISGF3) transcription complex for induction of IFN-stimulated ge

164 strate a general strategy of using embryonic transcription complexes for producing specific cell type

165 nt data arguing that sigma-dependent stalled transcription complexes form frequently in vivo, where t

166 inct mechanisms, including protein turnover, transcription complex formation and selective enzyme rec

167 The role of these proteins during transcription complex formation and the importance of pr

168 comitantly disrupted myocardin/SRF and Notch transcription complex formation at respective CArG and C

169 promoter interactions, thereby facilitating transcription complex formation.

170 olymerase to the promoter and the productive transcription complex formation.

171 similar to the orientation and occupancy of transcription complexes formed with TFB1.

172 icated that the orientation and occupancy of transcription complexes formed with TFB2 at the strong g

173 1 on the silencer, P-TEFb interacts with the transcription complex, forming a different chromatin loo

174 matin immunoprecipitation analysis of apo A1 transcription complexes from control and ligand-activate

175 to RNA polymerase (RNAP) and removes stalled transcription complexes from DNA.

176 kinase and the polymerase associated factor transcription complex function upstream of the Spt6-Ctk1

177 Gdown1 can enter the transcription complex immediately after initiation.

178 that another major role for the Nus-modified transcription complex in rrn operons is as an RNA chaper

179 of the Hap complex human homologue NF-YA/B/C transcription complex in SURF1-deficient fibroblasts fro

180 Thus, glyco-Gag rendered the reverse transcription complex in the viral core resistant to APO

181 PKCalpha, a component of the transcription complex in tumors, is up-regulated in beni

182 BEC3 in vivo--namely, protecting the reverse transcription complex in viral cores from APOBEC3.

183 19 was not required for incorporation of the transcription complex in virus particles, the transcript

184 analogous strategies to allosterically trap transcription complexes in a moribund state.

185 to regulate the recruitment and activity of transcription complexes in a tissue-specific chromatin d

186 We demonstrate that RECQ5 associates with transcription complexes in DNA replication foci and coun

187 nd tightly packed with a conserved number of transcription complexes in icosahedral capsids.

188 Thus, acetate directly alters transcription complexes in vitro in ways that lead to si

189 t promote replisome movement through stalled transcription complexes in vitro.

190 However, the nature of mitochondrial transcription complexes in vivo and the potential involv

191 ith the highly dynamic behavior of RNA Pol I transcription complexes in vivo, which undergo cycles of

192 We hypothesize that DksA binds to transcription complexes in which i6 becomes mobile, for

193 myces cerevisiae FACT (facilitates chromatin transcription) complex in assembling chromatin within op

194 required to clear protein blocks (primarily transcription complexes) in vivo, and that a polarity of

195 tails where they facilitate the assembly of transcription complexes including transcription factors

196 ed by mass spectrometry as components of the transcription complex, including RNA polymerase subunits

197 Recently, Brd4 has been found in several transcription complexes, including the general cofactor

198 R-loops, but not normal transcription complexes, induce DNA breaks and orientati

199 perative interactions of PspF with the basal transcription complex influence dynamics of the PspF hex

200 The evolutionarily conserved Six1-Eya1 transcription complex is central to mammalian organogene

201 ever, the source of this cofactor within the transcription complex is not known.

202 thways, one of which, involving the Mediator transcription complex, is associated with the shift from

203 Based on available structures of transcription complexes it has been hypothesized that th

204 We characterized transcription complexes made with RNA polymerase and the

205 DNA synthesis was inhibited, suggesting that transcription complexes may be formed early on L promote

206 PUFA-sensing PPARG-retinoid X receptor (RXR) transcription complex, may influence neovascularization

207 Within Hox transcription complexes, Meis binds directly to Pbx and

208 tor of the major histocompatibility class II transcription complex (MHC-II) and is critical for initi

209 als underlying cutaneous inflammation is the transcription complex NF-kappaB, its upstream modulators

210 The replication/transcription complex of severe acute respiratory syndro

211 -pair crosslinking (CPX) analyses of various transcription complexes of a bacterial RNAP and crystall

212 ur length were ideal for analysis of T7 RNAP transcription complexes on bound single template DNAs.

213 that STAT5 is an early step in establishing transcription complexes on genes specifically expressed

214 that cooperative formation of dimeric Notch transcription complexes on promoters with paired sites i

215 and analysis, which enabled localization of transcription complexes on templates at kilobase resolut

216 fected cells is crucial for the formation of transcription complexes on these promoters.

217 e to unwrap the RNA by disrupting either the transcription complex or the anchoring structure.

218 -centric look at the coronavirus replication transcription complex organelle in the context of the wi

219 the nucleus, as previously described for the transcription complex Paf1.

220 vivo, Spt5-CTR phosphorylation decreases as transcription complexes pass the cleavage and polyadenyl

221 The RNA Pol II transcription complex pauses just downstream of the prom

222 lunt RANK activation and as a component of a transcription complex promoting FHL2 expression.

223 Reconstitution of the his paused transcription complex provides a valuable tool for futur

224 th EKLF-dependent processes by destabilizing transcription complexes, providing a rational explanatio

225 ts, we propose that YvrHa is situated in the transcription complex proximal to the -10 element of the

226 TFS-enhanced cleavage of RNAs in backtracked transcription complexes reactivates stalled RNAPs and dr

227 ythropoiesis, suggesting that Ldb1-nucleated transcription complexes regulate key steps during erythr

228 lar context: recruitment of Mfd to a stalled transcription complex relieves the autoinhibition and un

229 functional architecture of T7 RNA polymerase transcription complexes remains incomplete.

230 pite the importance of CarD, its function at transcription complexes remains unclear.

231 ef1 and beta-catenin, which form a bipartite transcription complex required for initiation of the hai

232 K and core components of the Notch-dependent transcription complex, respectively.

233 by evoking MAPK cascades and activating AP-1 transcription complex resulting in alterations of gene e

234 kinase 3 (Plk3) signaling and the c-Jun.AP-1 transcription complex, resulting in apoptosis of corneal

235 We further identify a novel FHL2-AR-filamin transcription complex, revealing how deregulation of thi

236 ands to be made continuously and replication-transcription complex (RTC) activity to be unstable.

237 biotin ligase into a coronaviral replication/transcription complex (RTC) and identified >500 host pro

238 e transcription, but whether any are reverse transcription complex (RTC) cofactors or affect reverse

239 ity and limits APOBEC3 access to the reverse transcription complex (RTC).

240 gation studies reveal that these replication-transcription complexes (RTCs) are associated with cellu

241 y decreasing RNAP pausing and increasing the transcription complex stability, in cooperation with hos

242 ry complex interacts with the RNA polymerase transcription complex, stabilizing it and allowing trans

243 dependent DNA translocase activity to remove transcription complexes stalled at sites of DNA damage,

244 o occurs via modulation of the efficiency of transcription complex subunit capture and assembly.

245 e novo missense variant in the gene CCR4-NOT transcription complex, subunit 1 (CNOT1).

246 RNA cleavage in certain types of backtracked transcription complexes, suggesting that these complexes

247 omponents of the FACT (facilitates chromatin transcription) complex, SUPT16H and SSRP1, as top host f

248 eviously, raising a question of what makes a transcription complex susceptible to DksA.

249 functioning as component of a multi-subunit transcription complex that includes the ubiquitous adapt

250 RNA synthesis is performed by a replication-transcription complex that includes viral and cell prote

251 s the only factor within the multimegadalton transcription complex that is obligatorily required to u

252 in the formation of a functional GATA4/FOG2 transcription complex that is required for Sox9 expressi

253 pes suggest a difference in the N74D reverse transcription complex that manifests early after infecti

254 is an important component of the replication transcription complex that plays a crucial role in viral

255 ed a genetic pathway involving the Six1/Eya1 transcription complex that regulates cardiovascular and

256 ed that c-Myb, GATA-3, and Menin form a core transcription complex that regulates GATA-3 expression a

257 refore, c-Myb, GATA-3, and Menin form a core transcription complex that regulates GATA-3 expression a

258 the MluI cell cycle box-binding factor (MBF) transcription complex that regulates the G1/S progressio

259 Transcription complexes that assemble at the HIV-1 promo

260 mation of beta-catenin-T-cell factor (TCF)-4 transcription complexes that bind to the promoter of the

261 in the assembly of inappropriate multimeric transcription complexes that deregulate hematopoietic pr

262 ption permits Mfd to act indiscriminately at transcription complexes that lack the usual determinants

263 unctions as a core component of multiprotein transcription complexes that regulate differentiation in

264 fined by the release of product RNA from the transcription complex, the subsequent retention of RNAP

265 in ATP hydrolysis but fully remodels target transcription complexes, the RNAP-sigma(54) holoenzyme,

266 ation factors, guides the nontemplate DNA in transcription complexes, thereby modulating their regula

267 ed regions and assists in the passage of the transcription complex through chromatin, and it provides

268 The ability to deliver inhibitors to transcription complexes through the use of targeting/loc

269 competition and permits binding of the basal transcription complex to activate transcription.

270 rfaces with critical components of the Notch transcription complex to affect Notch-dependent lineage

271 it RelA and RelB components of the NF-kappaB transcription complex to chromatin, and these transcript

272 endent standard free energy variation of the transcription complex to model the experimentally observ

273 Recruitment of the RNA polymerase II transcription complex to the promoter of the Ifng gene h

274 s remodel substrates such as nucleosomes and transcription complexes to control a wide range of DNA-a

275 Furthermore, we show that failure of transcription complexes to escape the pause results in b

276 interact with advancing replication forks or transcription complexes to generate lethal lesions.

277 4-serves an essential role in three distinct transcription complexes to regulate cell cycle gene expr

278 and promoter interaction, and recruitment of transcription complexes to the active beta-globin promot

279 LCR HS2 is important for the recruitment of transcription complexes to the adult betamajor-globin ge

280 ricted activator NF-E2 in the recruitment of transcription complexes to the beta-globin gene locus.

281 and directly by mediating the recruitment of transcription complexes to the globin gene locus.

282 complexes that are precursors for functional transcription complexes upon addition of the remaining f

283 protein family, are required to remodel the transcription complex using energy derived from ATP hydr

284 approaches to identify an upstream sequence transcription complex (USTC) that is essential for piRNA

285 the heterotrimeric STAT1-STAT2-IRF9 (ISGF3) transcription complex, utilized the GR cofactor GRIP1/TI

286 vering its essential cognate receptor to the transcription complex via an alternative route.

287 engagement of a multimeric bEBP with a basal transcription complex via several L1s.

288 When nuclear import of the HIV-1 reverse transcription complex was blocked by expressing a trunca

289 Spt4/5 association with transcription complexes was slowly reversible, with DNA-

290 basis for such distinct temporal assembly of transcription complexes, we examined the role of core pr

291 characterize proteins associated with active transcription complexes, we purified RNA polymerase II (

292 Functional transcription complexes were assembled directly by mixin

293 tor 1 (HIF-1) and activator protein 1 (AP-1) transcription complexes were found to be responsible for

294 of reconstituting hairpin-stabilized paused transcription complexes when incubated with RNAP either

295 failure to downregulate Ldb1/Lmo2-nucleated transcription complexes which normally function to enfor

296 lear Rel/A p65, a component of the NF-kappaB transcription complex, which mediates the repression of

297 ation of its C-terminal domain with relevant transcription complexes, which promotes the stable assem

298 hybrid formation, and promote collisions of transcription complexes with replisomes.

299 Zeppo1 regulates transcription, complexing with Groucho and repressing E-

300 Intrinsic terminators dissociate transcription complexes without the assistance of auxili