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 stabilizes an early initiation complex, containing

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 best conserved in polymerases that require a TFIIB-like factor.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 rincipal site of interaction between TBP and TFIIB.

45 ption factors TATA-binding protein (TBP) and TFIIB, as well as hyperacetylation of histones H3 and H4

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

47 ecruit a complex containing TFIID, TFIIA and TFIIB.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

63 markedly stabilizing the interaction between TFIIB and transcription factor TFIIF and activating tran

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

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

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

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

68 enome without having been recruited there by TFIIB.

69 Both recombinant and cellular TFIIB can autoacetylate, markedly stabilizing the intera

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

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

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

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

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

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

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

77 hared surface to interact with two different TFIIB family members--TFIIB and Brf2--to initiate transc

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

79 ion has specific and diverse effects on each TFIIB family member.

80 ormed a comprehensive analysis of eukaryotic TFIIB gene families.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

99 nd to the yeast general transcription factor TFIIB.

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

101 the additional general transcription factors TFIIB and TFIIA.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 ure of the general transcription factor IIB (TFIIB) in a complex with RNA polymerase II reveals three

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

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

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

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

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

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

142 cription, requires transcription factor IIB (TFIIB).

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

144 2 both have a C-terminal extension absent in TFIIB, but their C-terminal extensions are unrelated.

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

146 am shifts that are conferred by mutations in TFIIB.

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

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

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

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

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

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

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

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

155 act with two different TFIIB family members--TFIIB and Brf2--to initiate transcription by different R

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

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

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

159 egulatory pathway controlling acetylation of TFIIB, and they link acetyl-CoA with basal gene transcri

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

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

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

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

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

165 tiation: an N-terminal zinc ribbon domain of TFIIB that contacts the "dock" domain of the polymerase,

166 a transcribing enzyme; a "finger" domain of TFIIB that is inserted into the polymerase active center

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

194 moters, coincident with reduced retention of TFIIB.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

217 Stable TFIIB-promoter association and progression beyond this a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

241 s assembly of a complex containing TBP:TFIIA:TFIIB, which lacks TAFs, and provides a mechanism that c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

261 probing were used to map the location of the TFIIB zinc ribbon domain on Pol II within the transcript

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

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

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

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

275 t with a general role in transcription, this TFIIB(ZR) surface is directly involved in the recruitmen

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

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

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

279 ts Brf1 and Brf2 are structurally similar to TFIIB.

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

281 lar interaction when compared with wild-type TFIIB.

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

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

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

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

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

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

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

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

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

291 ves the flap loop interaction interface with TFIIB.

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

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

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

295 evealed a physical interaction of Rna15 with TFIIB.

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

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

298 Class A HSFs can also interact weakly with TFIIB.

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

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