ライフサイエンスコーパス: TBP

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

2 TBP binds several TATA-less promoters with apparent high

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

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

5 TBP recruits condensin onto RNA polymerase III-transcrib

6 TBP-associated factor (TAF) family proteins, including T

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

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

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

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

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

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

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

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

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

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

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

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

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

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

21 In contrast, Spt16 did not affect TBP recruitment.

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

23 loop sequences present in two high-affinity TBPs (K(D) values of 4.2 +/- 0.3 and 3.0 +/- 0.3 nm).

24 TBP* species to Ti(4+)-based SBUs to afford TBP(*+) ligands and Ti(3+) centers, thus propagating the

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

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

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

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

29 s of specific DmSNAPc subunits with Bdp1 and TBP.

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

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

32 and Normfinder, UBC, RPLP0, HMBS, GUSB, and TBP are the most suitable endogenous control genes for b

33 ng MACs, and what phenotypic effect MACs and TBP have on other larval species.

34 cea genomes genetically encode both MACs and TBP.

35 ed to recombinant histone octamers, NF1, and TBP in complex with DNA, our method is highly specific f

36 expansions in other TFs (HOXA13, RUNX2, and TBP) were similarly found to alter their phase separatio

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

38 n28, thus revealing an uncoupling of Taf and TBP occupancy during the transcription cycle.

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

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

41 We found that WDR5 and TBP, which bind active interphase promoters(6,7), recrui

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

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

44 more limiting essential components, such as TBP and Mediator, create a competitive transcriptional e

45 in-based polymorphism (TBP) and a new assay, TBP light, have been optimized for the authentication of

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

47 epeat length (at ATXN1, ATXN2, ATXN3, ATXN7, TBP, ATN1, HTT, JPH3, AR, and DMPK) was assessed by sing

48 0% after progression compared with baseline (TBP>30% group).

49 more comprehensive model of the DmSNAPc-Bdp1-TBP complex on the U6 promoter that includes nearly all

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

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

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

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

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

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

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

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

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

59 rp TSS selection, in contrast with canonical TBP/TFIID-driven TATA-less promoters that have broader T

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

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

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

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

64 In contrast, TBP occupancy is unaffected by depletion of Kin28, thus

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

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

67 ogy were the reference standard for definite TBP.

68 ne triphosphate (ATP) hydrolysis to displace TBP from DNA and various models for how this activity is

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

70 s work, the interaction of Mot1 with the DNA/TBP complex was investigated by single-pair Forster reso

71 Upon Mot1 binding to the DNA/TBP complex, a transition in the DNA/TBP conformation wa

72 the DNA/TBP complex, a transition in the DNA/TBP conformation was observed.

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

74 morphosis of the tubeworm Hydroides elegans, TBP biosynthesis genes had no effect under the condition

75 epigenetic complexes, including the elusive TBP-associated-factor complex as well as two distinct GC

76 fier of transcription 1 (Mot1), an essential TBP-associated ATPase.

77 At various times in evolution, TBP has acquired multiple interaction partners and diffe

78 artners and different organisms have evolved TBP paralogs with additional protein regions.

79 n, but also transfers electrons from excited TBP* species to Ti(4+)-based SBUs to afford TBP(*+) liga

80 links the enzymatic modules, and facilitates TBP loading onto TATA promoters.

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

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

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

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

85 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

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

87 additional Mot1 in solution is necessary for TBP unbinding.

88 tify a region of Bdp1 that is sufficient for TBP recruitment.

89 thout interfering with stable and functional TBP-containing complexes.

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

91 Based on these data, we find the HDPCR TBP to be a useful adjunct for the diagnosis of tick-bor

92 specimens, were used to challenge the HDPCR TBP.

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

94 ment and factor-binding analysis for Pol II, TBP, TAF1, and Sp1 to assess the effect genome replicati

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

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

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

98 quantify the impact of genetic variation in TBP and drug class variation targeting the ATP-binding r

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

100 at loss of O-GlcNAcylation at T114 increases TBP binding to BTAF1 and directly impacts expression of

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

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

103 The octamer-like fold and its TBP-interacting region are similar in TFIID, whereas Taf

104 f polycomb-silenced genes apparently lacking TBP.

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

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

107 By expressing mutant TBP in different brain regions in adult wild-type mice v

108 In SCA17 knock-in mice, mutant TBP inhibits SP1-mediated gene transcription to down-reg

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

110 eurons are particularly vulnerable to mutant TBP.

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

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

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

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

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

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

117 ts (i.e. key residues) led to the ability of TBP to acquire new interactions, resulting in an increas

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

119 Transcriptomic and metabolomic analyses of TBP(T114A) CRISPR/Cas9-edited cells showed that loss of

120 enome replication resulted in the binding of TBP, TAF1, and Pol II to previously silent late promoter

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

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

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

124 ssed by depletion of TBP, while depletion of TBP in the presence of Kin28 has little effect on Taf1 o

125 in28 depletion is suppressed by depletion of TBP, while depletion of TBP in the presence of Kin28 has

126 tivity but high specificity for diagnosis of TBP.

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

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

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

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

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

132 transcription by dynamic O-GlcNAcylation of TBP.

133 hensive study of the evolutionary history of TBP and its interaction partners across all domains of l

134 system factor that is largely independent of TBP.

135 nary model for the functional innovations of TBP.

136 er that does not correlate with the level of TBP occupancy.

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

138 The lifetime of TBP at the promoter site is controlled by several cofact

139 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

140 companied by reduced promoter occupancies of TBP, and diminished transcription; and Ino80 is enriched

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

142 vity is tuned to establish a dynamic pool of TBP without interfering with stable and functional TBP-c

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

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

145 portion of Bdp1, and the conserved region of TBP.

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

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

148 0(3) to 10(5) copies/PCR, the sensitivity of TBP was 100% for all targets, with a combined specificit

149 interaction with the DNA binding surface of TBP.

150 We show that O-GlcNAcylation at T114 of TBP blocks its interaction with BTAF1, hence the formati

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

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

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

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

155 ATPase activity primes incorrectly oriented TBP for dissociation from DNA and additional Mot1 in sol

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

157 high-definition PCR (HDPCR) Tickborne Panel (TBP) assay (ChromaCode, Carlsbad, CA) for the detection

158 -definition PCR (HDPCR) tick-borne pathogen (TBP) panel using 379 retrospective, remnant whole-blood

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

160 mer dots (PDs) by doping tributyl phosphate (TBP) in a semiconducting polymer poly[9,9-dioctylfluoren

161 (aq)) concentration with tributyl phosphate (TBP) in dodecane was the focus of this microscale study

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

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

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

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

166 printing through tubulin-based polymorphism (TBP) and a new assay, TBP light, have been optimized for

167 izing 5,10,15,20-tetra(p-benzoato)porphyrin (TBP) ligands, cationic W-TBP mediates PDT to release tum

168 zing 5,10,15,20-tetra( p-benzoato)porphyrin (TBP) ligands, for hypoxia-tolerant type I PDT.

169 Then, the prepared TBP@PFBT PDs were used to develop a very high sensitive

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

171 rical simulations, a time-bandwidth product (TBP) exceeding the 'fundamental' limit of ordinary reson

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

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

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

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

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

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

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

179 The TATA-binding protein (TBP) and a transcription factor (TF) IIB-like factor are

180 nitiation factors, the TATA-binding protein (TBP) and core factor (CF).

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

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

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

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

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

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

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

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

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

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

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

192 l transcription factor TATA binding protein (TBP) is replaced by its paralogue, TBPL2 (TBP2 or TRF3),

193 TATA-box binding protein (TBP) is required for every single transcription event in

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

195 The TATA-box Binding Protein (TBP) plays a central role in regulating gene expression

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

197 ed in yeast cells, the TATA-binding protein (TBP) typically displays rapid turnover at RNA polymerase

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

199 interact with the TATA box-binding protein (TBP)(2,7,15-17).

200 the TFIID complex with TATA-binding protein (TBP), and PRO-seq experiments revealed widespread disrup

201 common factor, the TATA-box binding protein (TBP), is thought to serve as a platform to assemble pre-

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

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

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

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

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

207 ) expansion in the TATA box-binding protein (TBP).

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

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

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

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

212 transcription requires TATA binding protein (TBP).

213 amics in ubiquitin and TATA-binding protein (TBP).

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

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

216 uctures of lab-evolved TAR-binding proteins (TBPs) in complex with HIV-1 TAR.

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

218 Here, we show that DmSNAPc-Bdp1 can recruit TBP to the U6 promoter, and we identify a region of Bdp1

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

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

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

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

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

224 Human Pol II promoters with slow TBP dissociation preferentially contain a TATA consensus

225 hese properties of human promoters with slow TBP turnover differ from those of yeast promoters with s

226 ergy of metallacyclobutane intermediates (SP/TBP isomers), whereas aryloxides with pendant ortho aryl

227 lication resulted in reduced binding of Sp1, TBP, and Pol II to early promoters.

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

229 nsitive and TFIIB is sufficient to stabilise TBP on a strained promoter.

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

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

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

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

234 Br heavy atoms in 1,3,5,8-tetrabromopyrene (TBP), and the photoinduced electron transfer in a TBPCEx

235 ile structures (MACs) and tetrabromopyrrole (TBP) respectively.

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

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

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

239 oved to be significantly more efficient than TBP and ExBox(+4) , confirming the importance of the new

240 We demonstrate that TBP-DNA complexes are force-sensitive and TFIIB is suffi

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 observations suggest that TBP binding dynamics differentially affect promoter func

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

245 The TBP panel detected three coinfections, with two of Babes

246 The TBP@PFBT PDs is a simple, one-step, fast, non-invasive,

247 study reveals that interactions between the TBP-binding module of SAGA and the spliceosomal ATPase P

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

249 onsists of a TATA sequence recognized by the TBP subunit of the Pol III basal transcription factor II

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

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

252 nt resolution, the final PPA and NPA for the TBP panel were 97.7% (95% confidence interval [CI], 95.2

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

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

255 Such excellent features make the TBP@PFBT PDs an excellent probe for successful apoptosis

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

257 geted testing, we identify components of the TBP-binding module of the Spt-Ada-Gcn5 Acetyltransferase

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

259 t state (T(1) , 1.89 eV) is localized on the TBP and is close in energy with the charge separated sta

260 which were resolved by repeat testing on the TBP panel and bidirectional sequencing.

261 perimental constraints limit our scheme, the TBP can be arbitrarily large, simply dictated by the fin

262 Among clinical specimens the TBP demonstrated 100% sensitivity for the identification

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

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

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

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

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

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

269 Upon light irradiation, Ti-TBP not only sensitizes singlet oxygen production, but a

270 Here we report the design of a new nMOF, Ti-TBP, composed of Ti-oxo chain secondary building units (

271 By generating four distinct ROSs, Ti-TBP-mediated PDT elicits superb anticancer efficacy with

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

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

274 that this overlapping function is linked to TBP-DNA recruitment.

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

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

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

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

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

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

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

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

283 benzoato)porphyrin (TBP) ligands, cationic W-TBP mediates PDT to release tumor associated antigens an

284 ationic nanoscale metal-organic framework, W-TBP, is used to facilitate tumor antigen presentation by

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

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

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 the SAGA subunits and its interactions with TBP.

292 09 through September 2012, 151 patients with TBP were enrolled.

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

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

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

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

297 Arabidopsis to a premature stop codon within TBP-ASSOCIATED FACTOR 4b (TAF4b), which encodes a subuni

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