ライフサイエンスコーパス: TFIIB

1 TFIIB also cross-links to terminator regions and is requ

2 TFIIB bridges RNA polymerase II (Pol II) with the promot

3 TFIIB cross-linked to both the promoter and the terminat

4 TFIIB crosslinks to both the promoter and terminator reg

5 TFIIB is composed of two domains that engage in an intra

6 TFIIB is essential for transcription initiation by RNA p

7 TFIIB is normally associated with the early elongation c

8 TFIIB is phosphorylated at serine-65 at the promoters of

9 TFIIB is the only factor within the multimegadalton tran

10 TFIIB plays a pivotal role during assembly of the RNA po

11 TFIIB R78C shifts start site selection downstream of nor

12 TFIIB releases after both trigger points with similar ki

13 TFIIB-related factor 2 (Brf2) is a member of the family

14 A TFIIB R78C mutant extract was defective for promoter-spe

15 A TFIIB-like protein was not evident in the Pol I basal tr

16 to both strands of promoter DNA; and (iii) a TFIIB arginine-78 to cysteine replacement (R78C), which

17 terminal half of the CTR, and the other is a TFIIB binding domain (BD) that shows affinity for TFIIB

18 Taken together, our results show that a TFIIB conformational change is critical for the formatio

19 Therefore, a TFIIB-related protein is implicated in preinitiation com

20 egulation and localization of the acetylated TFIIB variant on the transcriptionally silent mitotic ch

21 e algae species encode one or two additional TFIIB-related protein subfamilies.

22 ection downstream of normal, does not affect TFIIB-DNA cross-links prior to promoter melting but inst

23 complex with recruitment of coactivators and TFIIB and Pol II are required for E(2)-activated transcr

24 nd yet retaining binding domains for DNA and TFIIB and nuclear localization signal (NLS).

25 uroprotective factor, was downregulated, and TFIIB occupancy of the Hspb1 promoter was decreased.

26 it is stabilized by CCCTC-binding factor and TFIIB and poises the gene for a prompt response.

27 matin where recruitment of polymerase II and TFIIB to the promoter was significantly increased.

28 preinitiation complex (RNA polymerase II and TFIIB) to the c-jun promoter.

29 cription factor, p300, RNA polymerase II and TFIIB, to both promoters during hypoxia, which traffics

30 wnstream Promoter Element (DPE) and Inr, and TFIIB recognition element (BRE) and TATA box] we propose

31 IIE) to the promoter; (ii) that Mediator and TFIIB, which both interact with pol II, are jointly requ

32 We conclude that OSTF1 and TFIIB are critical elements of osmosensory signal transd

33 Induction of OSTF1 and TFIIB increases gradually with increasing salinity.

34 Induction of OSTF1 and TFIIB is specific for osmotic stress and absent during o

35 Coinduction of OSTF1 and TFIIB may serve to recruit TFIIB preferentially to OSTF1

36 e RNA polymerase II TATA-binding protein and TFIIB.

37 RNA polymerase II, TATA-binding protein, and TFIIB of the general transcription machinery.

38 RNA polymerase II, TATA-binding protein, and TFIIB) and in a complex system, using TFIIB-immunodeplet

39 eral transcription factors TFIIF (RAP74) and TFIIB, protein kinase CK2 (CK2), and the HIV-1 transcrip

40 at TBP-DNA complexes are force-sensitive and TFIIB is sufficient to stabilise TBP on a strained promo

41 of the general transcription factors TBP and TFIIB at the reporter promoter.

42 transcriptionally paused state, and TBP and TFIIB remain at the promoter.

43 nt, but not upon recruitment of only TBP and TFIIB.

44 g protein (TBP), which then allows TFIIA and TFIIB to be recruited.

45 ecruit a complex containing TFIID, TFIIA and TFIIB.

46 The TATA-binding protein (TBP), TFIIA, and TFIIB interact with promoter DNA to form a complex requi

47 with TATA-binding protein (TBP), TFIIA, and TFIIB.

48 omoter-specific binding of TFIID, TFIIA, and TFIIB.

49 show that Isw2 can be targeted by Ume6- and TFIIB-dependent DNA looping.

50 ults suggest the interaction between VPN and TFIIB potentially initiate a network of contacts allowin

51 using locked nucleic acid-modified antisense TFIIB oligonucleotide treatment.

52 f a nonproductive complex which included AR, TFIIB, and PolII and the essential role of these coactiv

53 ore factor, and its human ortholog TAF1B are TFIIB-like factors.

54 he RNAPII transcriptional machinery, such as TFIIB and CDK7, are recruited more extensively to the p2

55 plant general transcription factors such as TFIIB have expanded in number and in some cases perform

56 The general transcription factor II B (TFIIB) plays a central role in both the assembly of the

57 ilapia homolog of transcription factor II B (TFIIB), that are rapidly and transiently induced during

58 fine a novel, functional interaction between TFIIB and Ssl2 that affects start site selection and gen

59 serine 65 regulates the interaction between TFIIB and the CstF-64 component of the CstF 3' cleavage

60 identified a functional interaction between TFIIB and the Rpb2 subunit of RNAP II and defined a nove

61 Domain swaps between TFIIB-related factors show that Rrn7 is most closely rel

62 have tested truncated Brf2, as well as Brf2/TFIIB chimeric proteins for U6 transcription and for ass

63 ordance with the function of TFIIB, T.brucei TFIIB(like) is encoded by an essential gene, localizes t

64 IID and TFIIA is stable, promoter binding by TFIIB is highly transient and dynamic (with an average r

65 enome without having been recruited there by TFIIB.

66 In Saccharomyces cerevisiae, TFIIB interacts with the BRCA1 C-terminal region domain

67 is regulated by the HIV-1 Tat protein, CK2, TFIIB, and the large subunit of TFIIF (RAP74).

68 Release is not dependent on the contacts TFIIB makes with its recognition element in promoter DNA

69 sites on the genome, which will not contain TFIIB.

70 ure (TFIIB(ZR)) and a carboxy-terminal core (TFIIB(CORE)).

71 We report a novel cell cycle TFIIB regulation and localization of the acetylated TFII

72 higher plants encode more than 10 different TFIIB-like proteins.

73 r, Arabidopsis thaliana encodes 14 different TFIIB-like proteins and predicted domain architectures o

74 recognition element (BREu), TATA, downstream TFIIB recognition element (BREd), and initiator element

75 ormed a comprehensive analysis of eukaryotic TFIIB gene families.

76 rtant regions of the well-studied eukaryotic TFIIB support conservation of a general mechanism of TFI

77 able homology to the archaeal TFB/eukaryotic TFIIB B-finger motif.

78 ATA-binding protein (TBP) and the eukaryotic TFIIB orthologue TFB.

79 ited overall sequence homology to eukaryotic TFIIB and archaeal TFB but harbors conserved residues wi

80 ble regions of Pol II and the general factor TFIIB to promote initiation and start site selection.

81 cts with the transcription initiation factor TFIIB and with the Ssu72 CTD phosphatase and Pta1 compon

82 ially resembles the Pol II initiation factor TFIIB, that the vRNAP subunit Rpo30 resembles the Pol II

83 tructural homology with transcription factor TFIIB and can bind DNA on its own.

84 ruitment of the general transcription factor TFIIB and increased overall histone occupancy at a subse

85 of TBP with the general transcription factor TFIIB and induces neurodegeneration in transgenic SCA17

86 A polymerase II-general transcription factor TFIIB complex at 4.5 angstrom resolution revealed the am

87 The general transcription factor TFIIB is a highly conserved and essential component of t

88 However, the general transcription factor TFIIB is presumed to be universally required for RNAP2 t

89 The general transcription factor TFIIB is required for accurate initiation, although the

90 The general transcription factor TFIIB plays a central role in preinitiation complex (PIC

91 t molecules such as the transcription factor TFIIB show no preference.

92 a missense mutation in transcription factor TFIIB suppresses gene looping, yet neither crumpling nor

93 surface of the general transcription factor TFIIB were used to probe the architecture of the RNA pol

94 racted with the general transcription factor TFIIB when the genes were activated and in a looped conf

95 the eukaryotic general transcription factor TFIIB) to initiate basal transcription.

96 release of the general transcription factor TFIIB, although the mechanism of release and its relatio

97 and exclude the general transcription factor TFIIB.

98 nd to the yeast general transcription factor TFIIB.

99 endent upon the general transcription factor TFIIB: the E62K (glutamic acid 62 --> lysine) form of TF

100 the additional general transcription factors TFIIB and TFIIA.

101 Transcription factors TFIIB and TFIIF are both required for RNA polymerase II

102 The transcription factors TFIIB, Brf1, and Brf2 share related N-terminal zinc ribb

103 urally related general transcription factors TFIIB, Brf1, and TFB, respectively, which are essential

104 ing protein (TBP), and transcription factors TFIIB, TFIIE, and TFIIF (for Pol II) or proteins structu

105 One of these factors, TFIIB, combines promoter recognition, recruitment of RNA

106 he minimal open complexes with TFIIB-FeBABE [TFIIB-p-bromoacetamidobenzyl-EDTA-iron(III)] derivatives

107 First, TFIIB acts as a catalytic cofactor for initial RNA bond

108 binding domain (BD) that shows affinity for TFIIB and is located C-terminally from the RD.

109 -characterized site-specific RNA aptamer for TFIIB, we were able to delineate some key features of th

110 els increase 6-fold for OSTF1 and 4-fold for TFIIB, and they reach maxima 2 h after SW transfer.

111 s increase 7.5-fold for OSTF1 and 9-fold for TFIIB, and they reach maxima 4 h after SW transfer.

112 , these results establish a new paradigm for TFIIB functionality in human gene expression, which when

113 remote homology program HHPred to search for TFIIB homologs in the plant kingdom and performed a comp

114 Furthermore, TFIIB interaction with the CF1 complex and Pap1 is cruci

115 a for the first time reveal distinct general TFIIB dynamics that regulate specialized versus housekee

116 This holo-TFIIB complex was resistant to MNase digestion.

117 urther show that in sua7-1 cells, where holo-TFIIB complex is not formed, the kinetics of activated t

118 Here we show that a six-amino acid human TFIIB tip region is needed for appropriate levels of ser

119 In this study, we describe a novel human TFIIB derivative harbouring two point mutations in the h

120 e role of the amino-terminal region of human TFIIB in transcription in vivo and in vitro.

121 Although expression of human TFIIB shifts the start site to the nearby human position

122 he highly basic DNA binding surface of human TFIIB, contains a neutral surface in the corresponding r

123 shift is directed by the C terminus of human TFIIB, in contrast to expectations from S.cerevisiae.

124 e substitutions across the B-finger of human TFIIB, made change-of-charge mutations in selected resid

125 Curiously, although the amino-terminal human TFIIB(ZR) domain can recruit both human pol II and yeast

126 domain architectures of the newly identified TFIIB-like proteins revealed that they have unique modul

127 s sharply decrease the rate at which Pol II, TFIIB, and TFIIF assemble on promoter-bound TFIID-TFIIA.

128 We find that alterations to Pol II, TFIIB, or TFIIF function widely alter the initiation lan

129 ioning is not observed in the smaller Pol II-TFIIB complex.

130 recent X-ray structure of the yeast RNAP II-TFIIB complex, these results define a functional interac

131 tic center and distal to the site of RNAP II-TFIIB interaction.

132 show that general transcription factor IIB (TFIIB) and cyclin-dependent kinase 9 are upregulated dur

133 ing protein (TBP), transcription factor IIB (TFIIB) and RNA polymerase (Pol) II.

134 se II (RNAPII) and transcription factor IIB (TFIIB) confer the distinct initiation patterns between t

135 The "B-finger" of transcription factor IIB (TFIIB) is highly conserved and believed to play a role i

136 protein (TBP) and transcription factor IIB (TFIIB) onto the promoter of these genes remained unaffec

137 hare homology with transcription factor IIB (TFIIB) or TFIIB-related proteins, key factors in the ini

138 Transcription factor IIB (TFIIB) recruits RNA polymerase II to promoters and inser

139 AR, SRC-1, Med-1, transcription factor IIB (TFIIB), and polymerase II (PolII) to GRTH ARE2 (bp -980/

140 lap loop, contacts transcription factor IIB (TFIIB), but the function of the flap loop has not been a

141 cription, requires transcription factor IIB (TFIIB).

142 P with the general transcription factor IIB (TFIIB).

143 2 both have a C-terminal extension absent in TFIIB, but their C-terminal extensions are unrelated.

144 tations in the Rpb1 subunit of Pol II and in TFIIB disrupt IMD2 regulation by altering start site sel

145 e three major TFIIB subfamilies that include TFIIB, Brf, Rrn7/TAF1B/MEE12 subfamilies, while all plan

146 The increased TFIIB binding correlates with VPN2's increased ability t

147 rescence transcription system to investigate TFIIB release in vitro.

148 d, more important, identify a step involving TFIIB as a key site of action of Mediator.

149 r-dependent, whereas Mediator recruitment is TFIIB-independent; (iii) that a high level of TFIIB can

150 Moreover, Ssl2, like TFIIB, associates with promoter and terminator regions,

151 entification of a trypanosomatid TFIIB-like (TFIIB(like)) protein which has limited overall sequence

152 fp1, and Hmo1), the transcription machinery (TFIIB, TFIID, and RNA polymerase II), and chromatin at n

153 owed that most life forms encode three major TFIIB subfamilies that include TFIIB, Brf, Rrn7/TAF1B/ME

154 This mutant, TFIIB R53E:R66E, exhibits an enhanced affinity in its in

155 Surprisingly, no TFIIB or TFIID was detectable or functionally required a

156 n caused a marked increase in the ability of TFIIB to stimulate abortive transcription ('superstimula

157 r, further genetic and biochemical assays of TFIIB chimeras revealed that TFIIB and the proposed B-fi

158 r regions, and the diminished association of TFIIB E62K with the PMA1 terminator is restored by the S

159 We have earlier demonstrated association of TFIIB with the distal ends of a gene in an activator-dep

160 These results suggest that a complex of TFIIB, CF1 subunits, and Pap1 exists in yeast cells.

161 l interaction between the B-finger domain of TFIIB and the distal lobe-jaw region of RNAP II and prov

162 r DNA determined by the C-terminal domain of TFIIB traverses sites of interaction with TFIIE, TFIIF,

163 ioinformatic analysis of data and effects of TFIIB knockdown in primary and transformed cell lines on

164 role in promoter escape and that ejection of TFIIB from the RNA exit tunnel of pol II by the growing

165 To determine the extent of TFIIB expansion in plants, I used the remote homology pr

166 factor 2 (Brf2) is a member of the family of TFIIB-like core transcription factors.

167 e sua7-1 mutation encodes an altered form of TFIIB (E62K) that is defective for both start site selec

168 e E62K (glutamic acid 62 --> lysine) form of TFIIB adversely affects looping at every gene tested, in

169 in vivo and that the phosphorylated form of TFIIB is present within (PICs).

170 In accordance with the function of TFIIB, T.brucei TFIIB(like) is encoded by an essential g

171 rate a model for the evolutionary history of TFIIB-like proteins in eukaryotes.

172 directly interacts with CstF independent of TFIIB phosphorylation, providing an alternative route to

173 Interestingly, the interaction of TFIIB with Ssu72 is compromised in rpb4Delta cells.

174 FIIB-independent; (iii) that a high level of TFIIB can bypass the Mediator requirement for basal tran

175 Accordingly, cross-linking of TFIIB to the 3' end of genes was abolished in the mutant

176 present a high-resolution genome-wide map of TFIIB locations that implicates 3' NFRs in gene looping.

177 pport conservation of a general mechanism of TFIIB function in eukaryotes.

178 d gene looping defect of sua7-1, a mutant of TFIIB.

179 orrelated with reduced promoter occupancy of TFIIB as well as TFIIF (RAP74).

180 binding to strongly reduce the occupancy of TFIIB, RNA polymerase II, and TFIIE at the silenced prom

181 We show that phosphorylation of TFIIB at serine 65 regulates the interaction between TFI

182 Our results reveal that phosphorylation of TFIIB is a critical event in transcription that links th

183 TFIIH is critical for the phosphorylation of TFIIB serine-65, but it is also dispensable for the tran

184 The presence of TFIIB at the 3' end of a gene required its interaction w

185 The presence of TFIIB on the terminator was dependent on the Rna15 compo

186 g, promoters, whereas de novo recruitment of TFIIB and polymerase II is required for specialized gene

187 ificantly reduced TSA-induced recruitment of TFIIB and RNAP II, at the promoter.

188 lution revealed the amino-terminal region of TFIIB, including a loop termed the "B finger," reaching

189 e, revealing the carboxyl-terminal region of TFIIB, located above the polymerase active center cleft,

190 gertip mediates the timing of the release of TFIIB that is associated with appropriate promoter escap

191 thus indicating a conditional restriction of TFIIB function and a key role of Mediator in overcoming

192 moters, coincident with reduced retention of TFIIB.

193 This analysis illustrates the key role of TFIIB in transcription bubble stabilization and provides

194 d by the presence of the B finger segment of TFIIB within the complex.

195 rs and/or squelching the limited supplies of TFIIB and TBP.

196 This transient-to-stable transition of TFIIB-binding dynamics has gone undetected previously an

197 e presence of RD had an inhibitory effect on TFIIB binding and transcriptional activation.

198 er order complex formation with TFIIA and/or TFIIB.

199 Overexpression of HSPB1 or TFIIB alleviated mutant TBP-induced neuritic defects.

200 initial formation of the TBP, TFIIA-TBP, or TFIIB-TBP complexes.

201 ogy with transcription factor IIB (TFIIB) or TFIIB-related proteins, key factors in the initiation me

202 ent of C/EBPbeta, ERalpha, SRC1, p300, pCAF, TFIIB, and Pol II, with no change in Sp1/Sp3.

203 ng expels Pol II, and despite the persistent TFIIB-chromatin complexes, Pol II recruitment is blocked

204 Our data reveal a mode of phospho-TFIIB-independent transcriptional regulation that priori

205 owever, if TFIIF is not retained in the PIC, TFIIB can be lost immediately after initiation.

206 aspartates that can bind magnesium, placing TFIIB within a family of proteins that insert finger dom

207 we found that Pol II, TATA-binding protein, TFIIB and TFIIF can form a quaternary complex in the abs

208 highly dependent upon TATA-binding protein, TFIIB and TFIIF.

209 tion of OSTF1 and TFIIB may serve to recruit TFIIB preferentially to OSTF1 target genes during hypero

210 y disconnected, effects on RNAP recruitment, TFIIB/RNAP complex stability and the rate of transcripti

211 l transcriptionally active complexes release TFIIB during early transcription.

212 del regarding the concerted roles of RNAPII, TFIIB, and TFIIF during mRNA 5'-end formation in S. cere

213 ICs), containing TFIIA, TFIID (and/or SAGA), TFIIB, TFIIE, and TFIIF.

214 to a reduction in the level of phospho-ser65 TFIIB that leaves the p53 transcriptional response intac

215 erefore has an important role in stabilizing TFIIB within the PIC and after transcription initiates.

216 Stable TFIIB-promoter association and progression beyond this a

217 ns: an amino-terminal zinc ribbon structure (TFIIB(ZR)) and a carboxy-terminal core (TFIIB(CORE)).

218 The identification of superstimulating TFIIB variants reveals the existence of a previously unk

219 Surprisingly, TFIIB occupancy persisted at most sites upon repression.

220 Surprisingly, TFIIB serine 65 phosphorylation is required after the ph

221 In contrast, levels of Taf1, TFIIB, and RNA polymerase II are reduced at Mot1-activat

222 Thus, by acutely targeting TFIIB, we were able to inhibit selectively the former se

223 HIS4 promoters, TATA binding protein (TBP), TFIIB, and Pol II.

224 teracts with TATA box-binding protein (TBP), TFIIB, and the TBP-associated factor 1 (TAF1) in vitro.

225 er containing all the factors (SNAP(c), TBP, TFIIB-related factor 2 (Brf2), and B double prime 1 (Bdp

226 ) and the general transcription factors TBP, TFIIB, and TFIIF on promoter DNA.

227 and is required for full recruitment of TBP, TFIIB, and RNA polymerase II (RNAP II) at a subset of th

228 cription initiates downstream of the DNA-TBP-TFIIB-RNAP II-TFIIF complex in the S. cerevisiae system;

229 e or the topology of Rpb7 within the DNA-TBP-TFIIB-RNAP II-TFIIF complex is different from that defin

230 n factor TFIIIB is bipartite; its N-terminal TFIIB-related half is principally responsible for recrui

231 through the interactions of its N-terminal, TFIIB-like domains.

232 rup of TBP forms the main interface with TFB/TFIIB.

233 en the Tfg1 mutations and mutations in Tfg2, TFIIB, and RNA polymerase II.

234 A polymerase II and protein complexes TFIIA, TFIIB, TFIID (or TBP), TFIIE, TFIIF, TFIIH and TFIIK wer

235 tiation complex (PIC), which contains TFIIA, TFIIB, TFIID, TFIIE, TFIIF, TFIIH, RNAPII, and Mediator.

236 general transcription factors (GTFs; TFIIA, TFIIB, TBP, TFIIE, TFIIF, and TFIIH) and escapes the pro

237 h as TFIIE and TFIIH, and segments of TFIIA, TFIIB and TFIIF.

238 he general transcription factors TBP, TFIIA, TFIIB and TFIIH and showed that these factors are essent

239 extremely divergent orthologs of TBP, TFIIA, TFIIB, and TFIIH which, together with the small nuclear

240 y the stepwise assembly of human TBP, TFIIA, TFIIB, Pol II, TFIIF, TFIIE and TFIIH onto promoter DNA

241 general transcription factors TFIID, TFIIA, TFIIB, TFIIF, TFIIE, and TFIIH.

242 general transcription factors (e.g., TFIID, TFIIB, and Mediator) for antisense transcription initiat

243 pol II recruitment to the promoter and that TFIIB recruitment is Mediator-dependent, whereas Mediato

244 Here we demonstrate that TFIIB phosphorylation is dispensable for the transcripti

245 Together our data support the model that TFIIB release is important for Pol II to successfully es

246 Here we report that TFIIB can be phosphorylated within the N terminus at ser

247 y and global gene expression, we report that TFIIB is dispensable for transcription of many human pro

248 mical assays of TFIIB chimeras revealed that TFIIB and the proposed B-finger/reader domain do not pla

249 Recent studies have revealed that TFIIB engages in contact with the transcription terminat

250 immunoprecipitation-sequencing reveals that TFIIB is constitutively bound to all paused, housekeepin

251 ycerol gradient centrifugation, we show that TFIIB associates with poly(A) polymerase and the entire

252 We propose a model suggesting that TFIIB binds RNAP II at the terminator, which in turn ass

253 the regulation of activity by TFIIF and the TFIIB core domain.

254 or head module binds the Pol II dock and the TFIIB ribbon and stabilizes the initiation complex.

255 ability of 381 site-directed mutants in the TFIIB 'linker domain' to stimulate abortive transcriptio

256 and +1 and trans-acting substitutions in the TFIIB B-finger.

257 Mutations in the TFIIB reader and linker region, which were inactive on d

258 ase II, and TFIIH are not a component of the TFIIB complex.

259 Specific interaction of the TFIIB core domain with Pol II positions and orients the

260 prehensive genome-wide identification of the TFIIB gene family has been conducted in the plant kingdo

261 plates, showing that a major function of the TFIIB reader and linker is in the initiation or stabiliz

262 entified a small nonconserved surface of the TFIIB(ZR) that is required for pol II transcription in v

263 correlate with increased recruitment of the TFIIB/RNAP complex because substitutions in a particular

264 In PICs, the TFIIB linker and core domains are positioned over the ce

265 ly though, an activator fails to recruit the TFIIB mutant to the promoter.

266 I, and the addition of TFIIF repositions the TFIIB core domain to the Pol II wall domain.

267 er dissociation but in addition requires the TFIIB homology domain of Brf1.

268 Second, the TFIIB fingertip mediates the timing of the release of TF

269 In addition to suppressing the TFIIB E62K growth defect, Ssl2 H508R partially restores

270 -EDTA-iron(III)] derivatives showed that the TFIIB core domain is surprisingly positioned away from P

271 These results suggest that the TFIIB-Ssu72 interaction, which is critical for gene loop

272 nit Tfg1 was found in close proximity to the TFIIB B finger, linker, and core domains, suggesting tha

273 NA pol III may be regulated by BRCA1 via the TFIIB family members Brf1 and Brf2.

274 tes that highly localized changes within the TFIIB linker have profound, yet surprisingly disconnecte

275 Furthermore, this TFIIB derivative is able to support high order preinitia

276 er for reinitiation of transcription through TFIIB-Ssu72 mediated gene looping.

277 divergent primary sequence in comparison to TFIIB in well-studied eukaryotes.

278 r protein: Its N-proximal half is related to TFIIB and binds similarly to the C-terminal stirrup of T

279 ption factor SL1, is structurally related to TFIIB/TFIIB-like proteins, through predicted amino-termi

280 ts Brf1 and Brf2 are structurally similar to TFIIB.

281 eport the identification of a trypanosomatid TFIIB-like (TFIIB(like)) protein which has limited overa

282 lar interaction when compared with wild-type TFIIB.

283 promoter is equivalent to that of wild-type TFIIB.

284 in the four core promoter elements- upstream TFIIB recognition element (BREu), TATA, downstream TFIIB

285 ch tract (SRT), and binding domains for USF, TFIIB, and TATA box binding protein (TBP).

286 n, and TFIIB) and in a complex system, using TFIIB-immunodepleted HeLa cell nuclear extract (NE).

287 Rrn7 shares many activities associated with TFIIB-like factors.

288 hitecture of the minimal open complexes with TFIIB-FeBABE [TFIIB-p-bromoacetamidobenzyl-EDTA-iron(III

289 IP to its promoter occurs concomitantly with TFIIB, a component of the RNA polymerase II complex, and

290 paused promoters through an interaction with TFIIB but for transit into elongation by histone acetyla

291 gene looping through their interaction with TFIIB during transcriptional activation of genes.

292 ves the flap loop interaction interface with TFIIB.

293 rs fall into two classes that interfere with TFIIB's interactions with either TBP or RNA polymerase I

294 co-occupies promoters with TBP, but not with TFIIB, TFIIA, or Pol II when cells are grown in normal c

295 ntal stress, Mot1 co-occupies promoters with TFIIB and elongation-competent Pol II, but not with TFII

296 evealed a physical interaction of Rna15 with TFIIB.

297 the BD region alone interacted strongly with TFIIB, and the presence of RD had an inhibitory effect o

298 tructures of eukaryotic Pol II together with TFIIB highlights significant functional similarities.

299 Class A HSFs can also interact weakly with TFIIB.

300 hemical analyses of an altered form of yeast TFIIB containing an arginine-78 --> cysteine (R78C) repl

301 (Saccharomyces cerevisiae) pol II, the yeast TFIIB amino-terminal region recruits yeast pol II but no