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1 TFIIA (tau+gamma) supported basal and activated transcri
2 TFIIA and TATA-binding protein (TBP) associate directly
3 TFIIA antagonizes these TBP repressors but may be effect
4 TFIIA bridges the TBP-TATA complex with lobe B of TFIID.
5 TFIIA induced a rapid dissociation of TFIID dimers, allo
6 TFIIA interacts with TFIID via association with TATA bin
7 TFIIA is encoded by two genes (alphabeta and gamma) that
8 TFIIA phosphorylation had little effect on the TFIIA.TBP
9 TFIIA plays a central role in loading TBP and its multis
10 TFIIA significantly enhanced the kinetic stability of TB
11 TFIIA was dispensable for ICP4 activation of a late prom
12 TFIIA-gammaY65A is defective for binding to the beta-she
14 TFIIA allows for the production of an active TFIIA-like general transcription factor throughout oogen
17 ding was not significantly changed, although TFIIA did increase the fraction of DNA molecules bound b
18 ma), formed the TFIIA-TBP-TATA DNA (T-A) and TFIIA-TFIIB-TBP-TATA DNA (TAB) complexes indistinguishab
20 y regulated reciprocal expression of ALF and TFIIA allows for the production of an active TFIIA-like
23 ealed that the interaction between TAF11 and TFIIA involves two distinct regions of TAF11: the highly
28 llowing findings: (1) In one step, TFIID and TFIIA assemble at the promoter independently of holoenzy
29 und that while promoter binding of TFIID and TFIIA is stable, promoter binding by TFIIB is highly tra
31 ith TFIIA, increase recruitment of TFIID and TFIIA to the promoter, and promote isomerization of the
32 mation by enhancing the binding of TFIID and TFIIA, whereas Gal4-VP16 could enhance the recruitment o
35 ies generated with purified Rap1, TFIID, and TFIIA on RPG enhancer-promoter DNA indicate that Rap1-TF
38 contact or creating a second contact between TFIIA and TBP that was not visible in the crystal struct
40 that loss of functional interaction between TFIIA and TAF40 results in conditional growth phenotypes
41 further explore the functional link between TFIIA and TAF11, the toa2-I27K allele was utilized in a
42 ocate the TATA-binding protein (TBP) between TFIIA and TFIIB at the top of the cavity that most likel
46 , such as INO1, was dramatically impaired by TFIIA depletion, activation of other genes, such as CUP1
47 ween these structural states is modulated by TFIIA, as the presence of TFIIA and promoter DNA facilit
48 ly to promoter DNA in a manner stabilized by TFIIA, and these complexes can be analyzed by native gel
49 f these genetic defects can be suppressed by TFIIA overexpression, strongly suggesting a role for yFA
52 osteoblast cells showed that in intact cells TFIIA gamma is recruited to the region of the osteocalci
53 ding RNA polymerase II and protein complexes TFIIA, TFIIB, TFIID (or TBP), TFIIE, TFIIF, TFIIH and TF
55 tiation complexes (partial PICs), containing TFIIA, TFIID (and/or SAGA), TFIIB, TFIIE, and TFIIF.
56 midated, but V96F substitution of deamidated TFIIA amino acid residues 91-100 stimulated IL-2 release
57 report a requirement for Taspase 1-dependent TFIIA proteolytic processing in the mouse testis to enab
60 rly to the DQ2-gamma-I-gliadin epitope (i.e. TFIIA, FOXJ2 and IgD; mean BestFit quality score=40 vers
64 cements in only one of these regions enhance TFIIA-TBP-DNA complex formation in vitro, suggesting tha
65 s, we found that ICP4 was able to facilitate TFIIA stabilized binding of TBP to the TATA box of the e
67 cleavage of the general transcription factor TFIIA ensures proper coordination of rapid cell prolifer
74 y shows that a general transcription factor, TFIIA gamma, facilitates osteoblast-specific gene expres
77 similarities between Bdp1 and Pol II factors TFIIA and TFIIF, and unravels essential interactions wit
81 o identified essential points of contact for TFIIA and Rap1 within the Rap1 binding domain of the Taf
82 re, we demonstrate an essential function for TFIIA in TIC- and TAFII-dependent basal transcription fr
86 ate promoter because ICP4 can substitute for TFIIA's ability to stabilize the binding of TFIID to the
87 nase domain of TAF(II)250 was sufficient for TFIIA phosphorylation, and this activity was inhibited b
91 fied general transcription factor IIA gamma (TFIIA gamma) as a Runx2-interacting factor in a yeast tw
92 pase1) cleaves a ubiquitously expressed GTF (TFIIA) to enable tissue-specific (testis) transcription,
95 ant human (rh)TRF2 nor the native flag.hTRF2-TFIIA complex is able to replace TBP or TFIID in basal o
101 r factors such as SP1, TFIIB, polymerase II, TFIIA, or p65, can be acetylated by CBP/p300 HAT domain.
102 nd TBP, TRF2 binds transcription factor IIA (TFIIA) and TFIIB and appears to be part of a larger prot
103 some then recruits transcription factor IIA (TFIIA) and TFIID to the promoter to form the DA complex.
108 overexpression of transcription factor IIA (TFIIA), suggesting that histone acetylation by Gcn5 can
111 n mutation of serine residues 316 and 321 in TFIIA alphabeta reduced TFIIA phosphorylation significan
116 repression was observed in reactions lacking TFIIA and with recombinant TATA-binding protein in place
117 ChIP analyses determined that noncleaved TFIIA accumulates at the p16Ink4a and p19Arf promoters t
118 four serine residues reduced the ability of TFIIA to stimulate transcription in transient transfecti
123 -TFIIA-DNA complex formation and addition of TFIIA overcame TRP-mediated transcription repression.
124 a genetic screen, we isolated a new class of TFIIA mutants and identified three regions on TFIIA that
128 ed FRET (gelFRET) to determine the effect of TFIIA on the conformation of the DNA in TBP/TATA complex
129 ryotic core promoter involves the effects of TFIIA on the interaction between TATA-binding protein (T
134 To determine the relative importance of TFIIA in the regulation of different genes, we construct
137 n cleavage reagents positioned on the NTD of TFIIA and assembled in PICs identified the SAGA subunit
140 ities can be suppressed by overexpression of TFIIA, TBP, or Nhp6, suggesting that these genes facilit
144 es is modulated by TFIIA, as the presence of TFIIA and promoter DNA facilitates the formation of a re
147 g protein (TBP), blocking the recruitment of TFIIA and TFIIB, and thereby inhibiting preinitiation co
151 BP-DNA complexes, since relevant segments of TFIIA and NC2 were not present in truncated TFIIA and NC
154 l were not observed in crystal structures of TFIIA-TBP-DNA and NC2-TBP-DNA complexes, since relevant
155 dentified a mutation in the small subunit of TFIIA (toa2-I27K) that is defective for interaction with
156 Mutational analyses of the Toa2 subunit of TFIIA indicate that loss of functional interaction betwe
162 FIIA mutants and identified three regions on TFIIA that are likely to be involved in TBP recruitment
172 educed DNA binding activity, and recombinant TFIIA could be stimulated by in vitro phosphorylation wi
173 a system consisting of purified recombinant TFIIA, TFIIB, TFIIE, TFIIF, CREB, and Tax, along with hi
177 to the promoter in a step that also requires TFIIA and confirm that recruitment of the PIC by E2F is
178 ors and general cofactors, such as TAF(II)s, TFIIA, Mediator, and PC4, are not required for E2-mediat
185 ranscription modulation, since it stimulates TFIIA-TBP association, enhances high-level transcription
186 at phosphorylation of yeast TFIIA stimulates TFIIA.TBP.TATA complex formation and transcription activ
187 onstituted with the testis-specific subunit, TFIIA (tau+gamma), formed the TFIIA-TBP-TATA DNA (T-A) a
189 ding the molecular organization of the TAF11-TFIIA interaction and define a mechanistic role for this
191 factors such as TATA binding protein (TBP), TFIIA, and TFIIB, but not with occupancy by TBP-associat
193 s for the general transcription factors TBP, TFIIA and IIB determined by TIRF-PBM are similar to thos
194 es of the general transcription factors TBP, TFIIA, TFIIB and TFIIH and showed that these factors are
195 to study the stepwise assembly of human TBP, TFIIA, TFIIB, Pol II, TFIIF, TFIIE and TFIIH onto promot
196 tified extremely divergent orthologs of TBP, TFIIA, TFIIB, and TFIIH which, together with the small n
199 n the TOA2 subunit of TFIIA that disrupt TBP-TFIIA complex formation in vitro are also synthetically
201 sults suggesting importance of TBP H2 in TBP-TFIIA interactions and TBP-NC2 interactions, and provide
202 reincubation of TRP with TFIIA inhibited TBP-TFIIA-DNA complex formation and addition of TFIIA overca
203 e find that the ability to stabilize the TBP-TFIIA complex on the hsp70 and c-fos TATA elements, and
207 Instead, a highly stable, preloaded TBP/TFIIA "pioneer" complex primes the rapid initiation of H
208 litates assembly of a complex containing TBP:TFIIA:TFIIB, which lacks TAFs, and provides a mechanism
210 nterfere with different interactions (TFIIB, TFIIA, or the TATA box) and a TFIIB mutant defective for
211 pies promoters with TBP, but not with TFIIB, TFIIA, or Pol II when cells are grown in normal conditio
212 echanism for how interactions between TFIID, TFIIA, and Rap1 contribute to the high rate of transcrip
218 on factors rapidly bind promoter-bound TFIID-TFIIA, after which complexes undergo a slow isomerizatio
220 de interference with either TBP-DNA or TFIID-TFIIA-DNA contacts both upstream and downstream of the T
222 caused a conformational change in the TFIID-TFIIA-promoter complex as assessed by DNase I footprinti
224 nt of TFIIF and RNA polymerase II to a TFIID/TFIIA/TFIIB/promoter complex dictates the rate of preini
226 ning the activator GAL4-VP16, Med, and TFIID/TFIIA (DA) recruits pol II and the remaining GTFs to a m
227 pendent variations in retention of the TFIID:TFIIA complex after release of the polymerase could be a
229 Immunoprecipitation assays confirmed that TFIIA gamma interacts with Runx2 in osteoblasts and when
230 present a refined model for the effect that TFIIA has on DNA conformation that takes into account po
231 Using purified proteins, it was found that TFIIA and Spt8 do not stably bind to each other, but rat
232 reduced by a similar extent, indicating that TFIIA function is largely nonselective for activators.
233 rologous DNA binding domain, indicating that TFIIA is important for transcription even in the absence
234 us activators and promoters, indicating that TFIIA phosphorylation is required globally for optimal f
235 ing noncleavable TASP1 targets revealed that TFIIA is the principal TASP1 substrate that orchestrates
245 Taken together, these results suggest that TFIIA plays an important role in both activator-dependen
247 facilitates DNA binding by TBP in vivo, that TFIIA may be regulated by factors that target distinct r
252 reduced by mutations in TRP that disrupt the TFIIA binding surface but not by mutations that disrupt
254 cific subunit, TFIIA (tau+gamma), formed the TFIIA-TBP-TATA DNA (T-A) and TFIIA-TFIIB-TBP-TATA DNA (T
255 at TBP H2 can be crosslinked to TFIIA in the TFIIA-TBP-DNA complex and in higher order transcription-
259 e results indicate that the stability of the TFIIA-TBP complex depends strongly on the sequence of th
262 IIA phosphorylation had little effect on the TFIIA.TBP.TATA complex in electrophoretic mobility shift
263 and that this phosphorylation stabilizes the TFIIA-TBP-DNA complex and is required for high-level tra
264 orylation is important for strengthening the TFIIA.TBP contact or creating a second contact between T
266 ce of the core promoter element and that the TFIIA-TBP complex plays an important function in recogni
267 omoters indicate that the sensitivity to the TFIIA-TBP interaction can map either to the upstream or
270 have found that TBP H2 can be crosslinked to TFIIA in the TFIIA-TBP-DNA complex and in higher order t
271 r, TFIIA (tau+gamma) was reduced relative to TFIIA (alphabeta+gamma) for stimulating transcription wi
273 as human chorionic gonadotrophin, ubiquitin, TFIIA, guanine nucleotide-binding protein (beta-subunit)
278 the structure of human TFIID in complex with TFIIA and core promoter DNA, determined by single-partic
279 rase II machinery that works in concert with TFIIA (IIA) and TFIIB (IIB) to assemble initiation compl
280 hTAF(II)250) to specifically cooperate with TFIIA to relieve TAF(II)250-mediated repression of TBP b
282 because activation domains can interact with TFIIA, increase recruitment of TFIID and TFIIA to the pr
283 no acid substitution mutants interacted with TFIIA-TFIID and CBP indistinguishably from the wild type
285 TAF11 allele defective for interaction with TFIIA exhibit conditional growth phenotypes and defects
286 idues were required for Zta interaction with TFIIA-TFIID and the CREB-binding protein (CBP) and for s
287 s surface is important for interactions with TFIIA and Brf1, TBP interactions with these two factors
289 y RBP is the same domain that interacts with TFIIA, but is disparate from the domain that interacts w
294 a trilobed, horseshoe-shaped structure, with TFIIA and TFIIB bound on opposite lobes and flanking a c
297 f TOA1 and TOA2, the genes that encode yeast TFIIA, overcomes the activation defects caused by the TB
298 eviously unknown yet critical role for yeast TFIIA in the integration of activator-TFIID contacts wit
299 we have found that phosphorylation of yeast TFIIA stimulates TFIIA.TBP.TATA complex formation and tr
300 t here that Toa1, the large subunit of yeast TFIIA, is phosphorylated in vivo and that this phosphory
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