ライフサイエンスコーパス: TBP

1 TBP (TATA-box binding protein) is a central transcriptio

2 TBP also increased steroid receptor co-activator 1 (SRC-

3 TBP and TFB/TF(II)B are highly conserved in structure an

4 TBP binds several TATA-less promoters with apparent high

5 TBP binds to core promoter DNA, recognizing the TATA-box

6 TBP occurs in Archaea and eukaryotes, but TRF2 evolved p

7 TBP recruits condensin onto RNA polymerase III-transcrib

8 prises the TATA-binding protein (TBP) and 13 TBP-associated factors (TAF1-13), which specifically int

9 sed of the TATA-binding protein (TBP) and 13 TBP-associated factors (TAFs)-assembles into a functiona

10 sed of TATA box-binding protein (TBP) and 13 TBP-associated factors (Tafs).

11 comprising TATA-binding protein (TBP) and 13 TBP-associated factors (TAFs).

12 x-binding protein (TBP) and approximately 14 TBP-associated factors (TAFs).

13 ity constants were determined for [UO2(NO3)2(TBP)2], [UO2(NO3)2(H2O)(TBP)2], and [UO2(NO3)2(TBP)3].

14 P)2], [UO2(NO3)2(H2O)(TBP)2], and [UO2(NO3)2(TBP)3].

15 nced disease progression, including 85 (28%) TBP patients and 221 (72%) non-TBP patients.

16 Strikingly, we find a median value of 5 TBP-chromatin binding events associated with the synthes

17 n cat food for 6-OH-BDE47 (p < 0.002), 2,4,6-TBP (p < 0.035), and BB-209 (p < 0.007).

18 ncies of both substrates 2,4,6-TCP and 2,4,6-TBP deviate from Michaelis-Menten kinetics at high conce

19 logue because of the low solubility of 2,4,6-TBP in an aqueous buffer solution.

20 s), hydroxylated PBDEs (OH-PBDEs), and 2,4,6-TBP in order to study differences in body burden between

21 with substrate, 2,4,6-tribromophenol (2,4,6-TBP), in buffer solvent with added methanol (MeOH), 2-pr

22 ethane (DBDPE), 2,4,6-tribromophenol (2,4,6-TBP), OH-PBDEs) and organochlorines (polychlorinated bip

23 At the time of this analysis, 65 (76%) TBP patients and 21 (87%) TBP>30% patients were still al

24 analysis, 65 (76%) TBP patients and 21 (87%) TBP>30% patients were still alive; 27 (32%) and 11 (46%)

25 Here, we report that TAF3, a TBP-associated core promoter factor, is highly enriched

26 timulated mechanism and to euchromatin via a TBP-stimulated mechanism.

27 es ATP hydrolysis to redistribute accessible TBP away from intrinsically preferred sites to other sit

28 In contrast, Spt16 did not affect TBP recruitment.

29 Mot1 dissociation of a stable, high affinity TBP-DNA interaction is surprisingly inefficient, suggest

30 u increased N. europaea inhibition, although TBP alone did not substantially alter activity.

31 ibed complex comprising TAFs 2, 6, 7, 11 and TBP.

32 VDUP1 [vitamin D upregulated protein 1] and TBP-2 [thioredoxin binding protein 2]) was regulated by

33 spinocerebellar ataxia type 6; and ATXN3 and TBP in spinocerebellar ataxia type 7.

34 BRF1 associates with BDP1 and TBP to form the transcription factor IIIB (TFIIIB), whic

35 transcription factor IIIB subunits, Brf1 and TBP, mediated position-specific strand transfer of duple

36 TBP-DNA interaction is extremely dynamic and TBP from the archaeal organism Sulfolobus acidocaldarius

37 ely prior to LT was the primary endpoint and TBP measurements were repeated 10, 30, 90, 180, and 360

38 it interacts with PPARgamma at enhancers and TBP/Pol II at core promoters.

39 revealed that the Ring1b subunit of PRC1 and TBP co-enrich at developmental genes.

40 Further, genes enriched for Ring1b and TBP are expressed at significantly lower levels than tho

41 s into a transcriptionally paused state, and TBP and TFIIB remain at the promoter.

42 While TFIID subunits and TBP are downregulated during myoblast differentiation, r

43 d factor 7l (Taf7l; a paralogue of Taf7) and TBP-related factor 2 (Trf2) are components of the core p

44 al initiation of TFIID (a complex of TBP and TBP-associated factors [TAFs])-dependent ribosomal prote

45 -a complex of TATA-binding protein (TBP) and TBP-associated factors (TAFs)-is a central component of

46 In contrast, the archaeal TBP-DNA interaction is extremely dynamic and TBP from th

47 tored DNA bending by eukaryotic and archaeal TBPs in the absence and presence of TFB in real-time.

48 Nucleotide expansions in JPH3, ATN1, TBP, and C9ORF72 and mutations in PRNP, as well as acqui

49 hanges did not reduce the occupancy of ATX1, TBP, or Pol II at promoters.

50 axia (SCA) genes ATXN1, ATXN2, ATXN3, ATXN7, TBP and CACNA1A and the CAG repeat expansion gene PPP2R2

51 0% after progression compared with baseline (TBP>30% group).

52 (II)B specifically stabilizes the fully bent TBP-promoter DNA complex and we identify this step as a

53 ules that are involved in activator binding, TBP binding, histone acetylation (HAT) and deubiquitinat

54 lated IL1B displayed very low levels of both TBP and paused Pol II, requiring the lineage-specific Sp

55 nfirmed that TAF7L forms complexes with both TBP and PPARgamma.

56 of H3S28ph by mutant H3S28A repressed Brf1, TBP and tRNA(Leu) and 5S rRNA expression and decreased o

57 TFIIIB, a complex formed by Brf1 (or Brf2), TBP (TATA-binding protein), and Bdp1.

58 uires TFIIIB, a complex formed by Brf1/Brf2, TBP and Bdp1.

59 ors describe the crystal structure of a Brf2-TBP-Bdp1 complex bound to a DNA promoter and characteriz

60 re, we present a crystal structure of a Brf2-TBP-Bdp1 complex bound to DNA at 2.7 A resolution, integ

61 ve solved crystal structures of a human Brf2-TBP complex bound to natural promoters, obtaining a deta

62 n of alkylphenols (APs), 4-tert-butylphenol (TBP), 4-pentylphenol (PP), 4-hexylphenol (HP), 4-tert-oc

63 he model for the mechanism of DNA binding by TBP and for how DNA bending is affected by TATA sequence

64 reas the remaining active genes are bound by TBP and all six hESC TAFs.

65 rease the fraction of DNA molecules bound by TBP.

66 We identified a ternary complex formed by TBP and the histone fold (HF) domain-containing TFIID su

67 RNA gene promoters are occupied primarily by TBP in cells and that knockdown of TBP, but not TRF1, in

68 Here, we report on a non-canonical TBP family-insensitive (TFI) mechanism of transcription

69 ion have been proposed, but how it catalyzes TBP removal from DNA is unknown.

70 ion, but not other conserved regions, caused TBP to redistribute away from a subset of Mot1-inhibited

71 We propose that the Cnd2-TBP interaction coordinates transcription with chromosom

72 Inhibition of the Cnd2-TBP interaction disrupts condensin localization across t

73 Gli proteins and a transcription coactivator TBP-associated factor 9 (TAF9), and validated its functi

74 Oxidation of the Fe(III) complex (TBP(8)Cz)Fe(III) [TBP(8)Cz = octakis(4-tert-butylphenyl)

75 ives the reactive high-valent Fe(O) complex (TBP(8)Cz(+*))Fe(IV)(O) (2).

76 The direct conversion of a Mn(III) complex [(TBP(8)Cz)Mn(III) (1)] to a Mn(V)-oxo complex [(TBP(8)Cz)

77 P(8)Cz)Mn(III) (1)] to a Mn(V)-oxo complex [(TBP(8)Cz)Mn(V)(O) (2)] with O(2) and visible light is re

78 TFI genes are part of a densely connected TBP family-insensitive T-box-Otx2-Gsc interaction networ

79 As expected, Mot1 was found to control TBP levels at co-regulated promoters.

80 days after LT (P < 0.0001) and, at 360 days, TBP had not increased significantly (IMN: 0.08 +/- 0.19

81 ogy were the reference standard for definite TBP.

82 ion lifetime is limited by the ATP-dependent TBP displacement activity of the Snf2/Swi2 ATPase Mot1.

83 We show that the eukaryotic DNA-TBP interaction is characterized by a linear, stepwise b

84 ation approach and identified the Drosophila TBP (TATA-box-binding protein)-related factor 2 (TRF2) a

85 (a Fab fragment and the transcription factor TBP) with low nanomolar detection limits and no detectab

86 [TATA box binding protein-associated factor (TBP)] and third-trimester [Testis-expressed sequence 15

87 CTCF, RAD21, a general transcription factor (TBP) and activating chromatin marks are important determ

88 We demonstrate that TAF11/TAF13 competes for TBP binding with TATA-box DNA, and also with the N-termi

89 contains two conserved regions important for TBP interactions, another conserved region that hydrolyz

90 e of treatment was 4.7 (1.4-25.8) months for TBP patients and 7.6 (2.4-19.4) months for TBP>30% patie

91 r TBP patients and 7.6 (2.4-19.4) months for TBP>30% patients.

92 acids 327-428), similar to that required for TBP-induced folding, was required for functional respons

93 mined for [UO2(NO3)2(TBP)2], [UO2(NO3)2(H2O)(TBP)2], and [UO2(NO3)2(TBP)3].

94 nsfer (smFRET) to study DNA bending by human TBP on consensus and mutant TATA boxes in the absence an

95 stem to study the stepwise assembly of human TBP, TFIIA, TFIIB, Pol II, TFIIF, TFIIE and TFIIH onto p

96 cation of ChIP-nexus to four proteins--human TBP and Drosophila NFkB, Twist and Max--shows that it ou

97 Our smFRET studies reveal that human TBP bends DNA in a largely uniform manner under a variet

98 on of the Fe(III) complex (TBP(8)Cz)Fe(III) [TBP(8)Cz = octakis(4-tert-butylphenyl)corrolazinate] wit

99 Preoperative changes in TBP were not significant (IMN: 0.06 +/- 0.15 [SEM]; CON:

100 able to distinguish between metallacycles in TBP (trigonal-bipyramidal) and SP (square-pyramidal) geo

101 Tumor response and safety in TBP and non-TBP patients.

102 associated with reduced H3 levels, increased TBP binding and tri-methylation of H3K4 and is independe

103 ies have demonstrated that alcohol increases TBP expression and Pol III gene transcription to promote

104 Here, we report that ethanol induces TBP promoter activity and the induction is ethanol dose

105 f Huwe1 expression during myogenesis induces TBP degradation and myotube differentiation.

106 For instance, TBP activates TATA-box-dependent core promoters, whereas

107 f polycomb-silenced genes apparently lacking TBP.

108 ICs by interfering with Mediator, but leaves TBP and perhaps TFIID intact, highlighting a specific me

109 continue to investigate how ethanol mediates TBP expression.

110 wer levels than those enriched for Mediator, TBP, and Ring1b.

111 In positive ion mode, TBP produced a strong signal with and without complexati

112 ely associated with the DNA in a stable Mot1-TBP-DNA ternary complex.

113 Mutant TBP shows decreased association with XBP1s, resulting in

114 nd overexpression of MANF ameliorates mutant TBP-mediated Purkinje cell degeneration via protein kina

115 We find that more mutant TBP accumulates in older mouse and that this accumulatio

116 on to U or Pu, but, in negative ion mode, no TBP, U-TBP, or Pu-TBP complexes were observed.

117 ding 85 (28%) TBP patients and 221 (72%) non-TBP patients.

118 verse events were similar in the TBP and non-TBP groups (5 [6%] and 9 [4%], respectively).

119 Tumor response and safety in TBP and non-TBP patients.

120 olumab therapy before or at progression (non-TBP group).

121 inding protein)-related factor TRF2, but not TBP, is required for transcription of the TCT-dependent

122 in the morphology of the dendrites, nuclear TBP-positive immunoreactivity, and axonal torpedos were

123 1088 operator binding even in the absence of TBP.

124 first time to our knowledge, the activity of TBP with poly-T stretches by presenting an elegant stepw

125 ent property of variable binding affinity of TBP for different promoter sequences, competition betwee

126 elta med3Delta yeast, whereas association of TBP, Pol II, and other Mediator modules with TFIID-depen

127 density, ensuring an accurate comparison of TBP activity with both types of DNA.

128 criptional initiation of TFIID (a complex of TBP and TBP-associated factors [TAFs])-dependent ribosom

129 We further investigate the correlation of TBP activity with various lengths of DNA and find that t

130 rs to fine-tune the requisite degradation of TBP during myogenesis.

131 ene promoters is increased upon depletion of TBP family factors.

132 tivity but high specificity for diagnosis of TBP.

133 the origin and phylogenetic distribution of TBP, TFB, and TFE transcription factors, and

134 ons as a molecular switch in the exchange of TBP-associated factor 7 (TAF7) for LEC to facilitate the

135 ved in targeting the TAF-independent form of TBP to the promoters of ribosomal protein genes for tran

136 of TBP) but not the TAF-independent form of TBP to the promoters of ribosomal protein genes.

137 ecruitment of TFIID (a TAF-dependent form of TBP) but not the TAF-independent form of TBP to the prom

138 system factor that is largely independent of TBP.

139 marily by TBP in cells and that knockdown of TBP, but not TRF1, inhibits U6 transcription in cells.

140 In contrast, high levels of TBP did not complement Taf1 depletion in vivo and instea

141 mpared to baseline, a 0.7 +/- 0.2 kg loss of TBP was seen in both groups at 30 days after LT (P < 0.0

142 Furthermore, overexpression of TBP alone causes the hallmarks of oncogene-induced repli

143 Overexpression of TBP in cells enhanced transcriptional activity mediated

144 box two kinetically distinct populations of TBP-DNA complexes exist; however, the bent state of the

145 state of the bent DNA within populations of TBP-DNA complexes is homogeneous; partially bent interme

146 Provision of TBP with Eu increased N. europaea inhibition, although T

147 iometry was directly related to the ratio of TBP to DBP.

148 d factors resulted in de novo recruitment of TBP and Pol II to IL1B in concert with a permissive stat

149 ion of Rad14p facilitates the recruitment of TBP, TFIIH, and RNA polymerase II to the GAL1 promoter.

150 Ptr2, mediates activation by recruitment of TBP.

151 reveal cooperation of negative regulation of TBP with specific chromatin regulators to inhibit intrag

152 r, how ATP hydrolysis facilitates removal of TBP from DNA is not well understood, and several models

153 interaction with the DNA binding surface of TBP.

154 initiation) and variable residence times of TBP complexes at a promoter.

155 s lengths of DNA and find that the number of TBPs bound to DNA increases >7-fold as the oligomer leng

156 omerization, resulting in the formation of [(TBP(8)Cz(+*))Mn(IV)(O)-Zn(2+)].

157 We found that Huwe1 activity on TBP is antagonized by the deubiquitinase USP10, which pr

158 raction partners to bind the same surface on TBP (to either promote or disrupt transcription initiati

159 f transcription that does not require TBP or TBP-related factors.

160 nd protein complexes TFIIA, TFIIB, TFIID (or TBP), TFIIE, TFIIF, TFIIH and TFIIK were positioned with

161 Here, we report that the orphan TBP-associated factor TAF9B is selectively up-regulated

162 an (LAM) assays in tuberculous pericarditis (TBP).

163 tively stripped from 30% tributyl phosphate (TBP) in kerosene into 1 M HNO3 with H2A.

164 tyl phosphate (DBP), and tributyl phosphate (TBP).

165 ppm), and the extractant tributyl phosphate (TBP, at 0.1 g/L).

166 ESCs, the proteins bind to active and poised TBP-bound promoters along with promoters of polycomb-sil

167 Instead, a highly stable, preloaded TBP/TFIIA "pioneer" complex primes the rapid initiation

168 P:DNA:NC2 state, suggesting that Mot1 primes TBP:NC2 displacement in an ATP-independent manner.

169 volumab more than 6 weeks after progression (TBP group); and patients not treated beyond progression,

170 by the deubiquitinase USP10, which protects TBP from degradation.

171 ription factors and the TATA-binding protein TBP.

172 or residence time for TATA-binding protein (TBP) across the yeast genome from competition ChIP data.

173 TFIID comprises the TATA-binding protein (TBP) and 13 TBP-associated factors (TAF1-13), which spec

174 omplex composed of the TATA-binding protein (TBP) and 13 TBP-associated factors (TAFs)-assembles into

175 lex is composed of TATA box-binding protein (TBP) and 13 TBP-associated factors (Tafs).

176 zed complex comprising TATA-binding protein (TBP) and 13 TBP-associated factors (TAFs).

177 FIID comprises the TATA-box-binding protein (TBP) and approximately 14 TBP-associated factors (TAFs).

178 ditions identified TATA-Box Binding Protein (TBP) and Importin 8 (IPO8) to be stable in non-small cel

179 NF exhibited pre-bound TATA Binding Protein (TBP) and paused RNA Polymerase II (Pol II), hallmarks of

180 ng with the binding of TATA binding protein (TBP) and POLR2E to the CDKN1A promoter.

181 , ATX1 is required for TATA binding protein (TBP) and RNA Polymerase II (Pol II) recruitment.

182 and recruitment of TATA box binding protein (TBP) and RNA polymerase II, but not recruitment of the a

183 TFIID-a complex of TATA-binding protein (TBP) and TBP-associated factors (TAFs)-is a central comp

184 nscription factors TATA box-binding protein (TBP) and TFB.

185 core promoter includes TATA-binding protein (TBP) and two TBP-related factors.

186 one copy of mutant TATA box binding protein (TBP) at different ages by tamoxifen-mediated Cre recombi

187 additional recombinant TATA binding protein (TBP) at only the TATA-containing promoters.

188 upon the canonical TATA box-binding protein (TBP) but instead upon the TBP-related factor 1 (TRF1).

189 der the concept of TATA-box-binding protein (TBP) family proteins as "system factors" that each suppo

190 ATPase that can remove TATA-binding protein (TBP) from DNA using ATP hydrolysis and in so doing exert

191 on the thiamine periplasmic binding protein (TBP) from Escherichia coli for thiamine biorecognition a

192 tions, and apply it to TATA binding protein (TBP) interactions with oligonucleotides.

193 , we show that the TATA box-binding protein (TBP) interacts with the Cnd2 kleisin subunit of condensi

194 The TATA box binding protein (TBP) is a central component of the transcription preinit

195 TATA binding protein (TBP) is a key component of the eukaryotic RNA polymerase

196 TATA-box binding protein (TBP) is an essential factor that is required at virtuall

197 anscription factor TATA-box binding protein (TBP) leads to increased RNA synthesis, which together wi

198 TATA binding protein (TBP) plays a central role in transcription complex assem

199 Although the TATA-binding protein (TBP) subunit of TFIID is necessary and sufficient for in

200 (TRF2) rather than the TATA-binding protein (TBP) was found to function in transcription of RP genes

201 ng the PIC components, Tata Binding Protein (TBP) was the most resistant to eviction by PRC1.

202 the interaction of the TATA-binding protein (TBP) with the NTD of the progesterone receptor (PR) and

203 , II, or III), the TATA box-binding protein (TBP), and transcription factors TFIIB, TFIIE, and TFIIF

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

205 CP4 interacts with TATA box-binding protein (TBP), TFIIB, and the TBP-associated factor 1 (TAF1) in v

206 the promoter DNA, TATA box-binding protein (TBP), transcription factor B (TFB), transcription factor

207 initiation factors TATA box binding protein (TBP), transcription factor IIB (TFIIB) and RNA polymeras

208 ot1p-NC2 regulators of TATA-binding protein (TBP), we detected synthetic genetic interactions indicat

209 iptional initiation of TATA-binding protein (TBP)-associated factor (TAF)-dependent ribosomal protein

210 of the analyzed TSTRs, TATA-binding protein (TBP)-associated factor 7-like (TAF7L).

211 TATA-binding protein (TBP)-associated factor 7l (Taf7l; a paralogue of Taf7) a

212 TATA box-binding protein (TBP)-associated factors (TAFs), evolutionarily conserved

213 replacing cellular TATA-box-binding protein (TBP).

214 or USF, TFIIB, and TATA box binding protein (TBP).

215 l transcription factor TATA-binding protein (TBP).

216 transcription requires TATA binding protein (TBP).

217 lyQ) repeat in the TATA-box-binding protein (TBP).

218 on and activity of the TATA-binding protein (TBP).

219 ion 1) dissociates TATA box-binding protein (TBP):DNA complexes, offering a useful system to address

220 The change in total body protein (TBP) measured by neutron activation from study entry unt

221 vious FRAP studies of TATA binding proteins (TBP) and also as a tool to minimize the contribution of

222 , in negative ion mode, no TBP, U-TBP, or Pu-TBP complexes were observed.

223 ase and a deubiquitinating enzyme regulating TBP levels during cellular differentiation.

224 nserved region that hydrolyzes ATP to remove TBP from DNA, and a fourth conserved region with unknown

225 ence demonstrates that TBP2 does not replace TBP during muscle differentiation, as previously propose

226 anism of transcription that does not require TBP or TBP-related factors.

227 SAGA-TBP binding involves a network of interactions between s

228 rmine the molecular architecture of the SAGA-TBP complex.

229 istent with the model that sequence-specific TBP-DNA contacts are not important at yeast TATA-less ge

230 tion factors (GTFs), such as testis-specific TBP-related factor 2 (TRF2), enables the spatiotemporal

231 ription and that Spt3 functions to stimulate TBP recruitment at all tested genes.

232 to the results of previous ensemble studies, TBP was found to bend a mutant TATA box to the same exte

233 st transcription factor IID (TFIID) subunit, TBP-associated factor 1 (TAF1), possesses protein kinase

234 etermine the architecture of the TAF11/TAF13/TBP complex, revealing TAF11/TAF13 interaction with the

235 e identified Huwe1 as an E3 ligase targeting TBP for K48-linked ubiquitination and proteasome-mediate

236 We identify a highly conserved C-terminal TBP-interaction domain (CTID) in TAF13, which is essenti

237 ranscription program regulated by the testis TBP-associated factor (tTAF) or meiosis arrest complex (

238 Replacement of the canonical TFIID-TBP complex with TRF3/TBP2 was reported to be required f

239 sly proposed, with limiting amounts of TFIID-TBP being required to promote muscle-specific gene expre

240 In particular, we find that TBP binds tightly to single-stranded DNA, especially to

241 Here, we report that TBP protein levels are tightly regulated by the ubiquiti

242 Here we show that TBP (TATA box-binding protein)-related factor TRF2, but

243 These data suggest that TBP can mediate structural reorganization of the NTD to

244 Taken together, these results suggest that TBP-DNA affinity as well as other aspects of promoter se

245 The TBP-promoter DNA complex contains sharply bent DNA and i

246 TA box-binding protein (TBP), TFIIB, and the TBP-associated factor 1 (TAF1) in vitro.

247 TFIIA bridges the TBP-TATA complex with lobe B of TFIID.

248 TFS4 destabilises the TBP-TFB-RNAP pre-initiation complex and inhibits transcr

249 and can use ATP hydrolysis to dissociate the TBP-DNA complex.

250 Expression of Hsc70 improves the TBP-XBP1s interaction and MANF transcription, and overex

251 de 3 to 4 adverse events were similar in the TBP and non-TBP groups (5 [6%] and 9 [4%], respectively)

252 ow Mot1 affects the trajectory of DNA in the TBP-DNA complex.

253 at carries a full human cDNA fragment of the TBP gene with 64 CAA/CAG repeats (TBPQ64).

254 Twenty-four (28%) of the TBP patients had a target lesion reduction of greater th

255 erlapping Elk1 and AP-1 binding sites of the TBP promoter and affected by alcohol.

256 ing G>A at a -46 bp Elk1 binding site of the TBP promoter or mutating AP-1 binding site at -37 bp (A>

257 We observed that the lifetime of the TBP-DNA interaction differs significantly between the ar

258 at -37 bp (A>G) and -38 bp (C>T) reduces the TBP promoter activity.

259 Transcription factor IID (TFIID), the TBP-containing coactivator that functions at most TATA-l

260 eractions and unbends DNA as compared to the TBP:DNA:NC2 state, suggesting that Mot1 primes TBP:NC2 d

261 d sufficient for in vitro transcription, the TBP-associated factor (TAF) subunits recognize downstrea

262 x-binding protein (TBP) but instead upon the TBP-related factor 1 (TRF1).

263 While the TBP-TATA interaction is critical for transcription at TA

264 ion of transcription factor B (TFB) with the TBP-DNA complex is followed by the recruitment of the ri

265 In Xenopus embryos, the three TBP family factors are all essential for development and

266 how other transcription factors that bind to TBP may compete with Mot1.

267 constants were determined for U complexed to TBP and DBP.

268 quired for structural folding in response to TBP interaction.

269 from drug-resistant tumors were sensitive to TBP when grown in vitro, but exhibited resistance when p

270 Addition of the Lewis acid Zn(2+) to (TBP(8)Cz)Mn(V)(O) induces valence tautomerization, resul

271 includes TATA-binding protein (TBP) and two TBP-related factors.

272 or Pu, but, in negative ion mode, no TBP, U-TBP, or Pu-TBP complexes were observed.

273 Unlike TBP, TRF2 does not bind to the TATA box and could thus f

274 Unlike TBP, TRF2 lacks sequence-specific DNA binding activity,

275 It was previously shown that, unlike TBP, TRF2 fails to bind DNA containing TATA-boxes.

276 Using TBP family single- and triple-knockdown experiments, alp

277 Thirty-eight percent were detected using TBP and 39% with SDDI.

278 ymerase III promoters differentially utilize TBP and TRF1 for the initiation of transcription.

279 transcription in vitro effectively utilizes TBP, whereas TBP cannot substitute for TRF1 to promote t

280 and biochemical studies have shown that when TBP binds DNA, it sharply bends the DNA.

281 INR also reside at Pol III promoters, where TBP makes similar contacts.

282 nce of ATP, Mot1 acts to unbend DNA, whereas TBP remains closely associated with the DNA in a stable

283 s TATA-box-dependent core promoters, whereas TBP-related factor 2 (TRF2) activates TATA-less core pro

284 n in vitro effectively utilizes TBP, whereas TBP cannot substitute for TRF1 to promote tRNA transcrip

285 ining promoters, it has been unclear whether TBP sequence-specific DNA contacts are required for tran

286 es are bound by only TAFs 3 and 5 along with TBP, whereas the remaining active genes are bound by TBP

287 ix-month full-body examination compared with TBP.

288 and nitrification shut down completely with TBP addition.

289 In vitro, Mot1 forms a ternary complex with TBP and DNA and can use ATP hydrolysis to dissociate the

290 he N-terminal domain of Mot1 in complex with TBP, DNA, and the transcription regulator negative cofac

291 N-oxide or through a direct interaction with TBP.

292 the SAGA subunits and its interactions with TBP.

293 09 through September 2012, 151 patients with TBP were enrolled.

294 Analyzing mixtures of U or Pu with TBP and DBP yielded the formation of ternary complexes w

295 to evaluate the speciation of U and Pu with TBP and DBP.

296 the eukaryotic OC, the TATA DNA region with TBP and TFB is positioned closer to the surface of the R

297 Monitoring patients at extreme risk with TBP and SDDI assisted with early diagnosis of primary me

298 in the model, we are able to estimate yeast TBP-chromatin residence times as short as 1.3 minutes, d

299 We generated a set of mutations in the yeast TBP DNA binding surface and found that most support grow

300 Our results also explain why yeast TBP derivatives defective for TATA binding appear defect