ライフサイエンスコーパス: TAF

1 TAF + FTC NPs and TAF + FTC solution (each drug at 200 m

2 TAF accumulated inside genital epithelial cells as TFV-D

3 TAF has the potential advantages that dose adjustment is

4 TAF is formulated to deliver the active metabolite to ta

5 TAF was below assay sensitivity in all CSF specimens.

6 TAF(I)41 immunodepletion from nuclear extracts dramatica

7 TAF(I)41 resides at the rDNA promoter in the nucleolus a

8 TAF-I associates with chromatin in vitro and can substit

9 TAFs have also been recently found to enhance antisense

10 binding domain within a Selectivity Factor 1 TAF.

11 By 21 days PT, 100% TAF + FTC solution-treated and control-untreated mice we

12 ed >=1 dose of study drug (DTG/3TC, N = 369; TAF-based regimen, N = 372).

13 P-associated factors (TAFs) called TAF(I)48, TAF(I)63 and TAF(I)110.

14 entially all embryonic transcription, TAF-5, TAF-9, and TAF-10 were dispensable at multiple developme

15 icipants receiving DTG/3TC and 1 receiving a TAF-based regimen met confirmed virologic withdrawal cri

16 eaf1 strain depletes recruitment of TFIID (a TAF-dependent form of TBP) but not the TAF-independent f

17 or in maintaining virologic suppression vs a TAF-based regimen at week 48, with no virologic failure

18 /3TC was 0.3% (1/369) vs 0.5% (2/372) with a TAF-based regimen (adjusted treatment difference [95% co

19 ith DTG/3TC and 3 (0.8%) and 2 (0.5%) with a TAF-based regimen, respectively.

20 ciency virus (HIV)-1 who were treated with a TAF-containing regimen.

21 PrEP efficacy, thus establishing long-acting TAF + FTC NPs as a potential PrEP modality.

22 We show that long-acting TAF depots can be designed as block copolymers or as hom

23 ereas genetic downregulation of SMAD3 in ADC-TAFs and control fibroblasts increased TGFbeta1/SMAD2 ac

24 hat tumor fibrosis is actually higher in ADC-TAFs than SCC-TAFs in vitro and patient samples.

25 transcription factor SMAD3 compared with ADC-TAFs, which elicited a compensatory increase in TGFbeta1

26 core optical fibers) and the role Teflon AF (TAF) has played in their development.

27 (SubQ) administrated tenofovir alafenamide (TAF) and emtricitabine (FTC) loaded nanoparticles (NPs)

28 The TDF analogue tenofovir alafenamide (TAF) has demonstrated equal efficacy but with decreased

29 il fumarate (TDF) and tenofovir alafenamide (TAF) have also proved effective in the treatment of HBV

30 l fumarate (TDF) with tenofovir alafenamide (TAF) improves renal tubular markers in HIV-infected indi

31 ation and efficacy of tenofovir alafenamide (TAF) in the male genital tract (MGT) and the semen quali

32 Tenofovir alafenamide (TAF) is a novel prodrug of tenofovir that efficiently de

33 o evaluate TFV and/or Tenofovir alafenamide (TAF) release from FRT cells.

34 anscriptase inhibitor tenofovir alafenamide (TAF) was decreased for some of the HIV-1C PYxE variants

35 corporate an ARV drug tenofovir alafenamide (TAF) with degradable linkers that can be designed to con

36 revention trials, and Tenofovir alafenamide (TAF), an improved prodrug of TFV, interfere with wound h

37 il fumarate (TDF) and tenofovir alafenamide (TAF), drugs with excellent safety profiles used clinical

38 TG/3TC or remain on a tenofovir alafenamide (TAF)-based regimen.

39 Tenofovir alafenamide (TAF)-based regimens are being evaluated for pre-exposure

40 /emtricitabine (FTC), tenofovir alafenamide (TAF)/FTC, abacavir (ABC)/lamivudine (3TC), and others we

41 tins on tenofovir (TFV) and TFV-alafenamide (TAF) on HIV infection and intracellular TFV-diphosphate

42 ns of p(glycerol monomethacrylate)-b-p(Alkyl-TAF-methacrylate) and p(glycerol monomethacrylate)-b-p(B

43 d 11), whereas following differentiation all TAFs are expressed.

44 Since not all TAFs are required in terminally differentiated cells, we

45 s TAF homologs collaborate in an alternative TAF-containing protein complex to regulate a testis-spec

46 ated detectable TAF/FTC vaginal levels among TAF + FTC NP-treated hu-BLT mice correlating with prolon

47 factors (TAFs) called TAF(I)48, TAF(I)63 and TAF(I)110.

48 l embryonic transcription, TAF-5, TAF-9, and TAF-10 were dispensable at multiple developmental and ot

49 ced division of labor between activators and TAF coactivators, thus providing another strategy to acc

50 xil fumarate (TDF) who switched to E/C/F and TAF.

51 itness in the absence or presence of LPV and TAF.

52 TAF + FTC NPs and TAF + FTC solution (each drug at 200 mg/kg) were adminis

53 acyclovir and penciclovir, respectively, and TAF was also twice as potent as ganciclovir.

54 2, suggesting an interaction between SMC and TAF to coordinate their growth.

55 The calculated efficacy of FTC/TAF and TAF was 91% (95% confidence interval [CI], 34.9%-98.8%)

56 /min, eGFR decreased with the use of TDF and TAF (-1.7 mL/min).

57 ate that MPA selectively compromises TFV and TAF protection in blood and genital CD4+ T cells and sug

58 h p(Alkyl-TAFMA) exhibited sustained TFV and TAF release profiles in skin and blood over 60 days, and

59 The interaction matrix of Arabidopsis TAFs is largely consistent with the three-lobed topologi

60 lation targets, including SET (also known as TAF-I or PHAPII) and the retinoblastoma protein, RB.

61 In a cell-based assay, TAF was 35- and 24-fold and TDF was 10- and 7-fold more

62 ted coculture experiments between autologous TAF and TAT.

63 In patients with chronic hepatitis B, TAF appears to be as effective as TDF, with lower bone a

64 and p(glycerol monomethacrylate)-b-p(Benzyl-TAF-methacrylate) were first characterized in a mouse su

65 lar seminal TFV distribution differs between TAF and TDF.

66 ences were observed in semen quality between TAF and TDF.

67 The presence of both TAFs 14 and 15 in plants suggests ancient roles for thes

68 UPCR decreased after replacing TDF by TAF, independent of baseline eGFR.

69 d three TBP-associated factors (TAFs) called TAF(I)48, TAF(I)63 and TAF(I)110.

70 We identified the histone chaperone TAF-I (also known as INHAT [inhibitor of histone acetylt

71 a previously undescribed complex comprising TAFs 2, 6, 7, 11 and TBP.

72 In contrast, TAF had no inhibitory effect on wound closure or tight j

73 In contrast, TAF in MED12-LM proliferated in response to estradiol, w

74 Conversely, TAF-I cannot stimulate transcript elongation when added

75 binding to and sequestering in the cytoplasm TAF-4, a component critical for assembly of TFIID and th

76 o the efficacy of Wnt16 knockdown in damaged TAFs as a promising combinatory strategy to improve effi

77 suggested that while off-targeted NP damaged TAFs and inhibited tumor growth after an initial dose, c

78 d at investigating the effects of NP damaged TAFs on neighboring cells and alteration of stromal stru

79 omposition of hESC TAFs, either by depleting TAFs that are present or ectopically expressing TAFs tha

80 The alkylcarbamate linker design (TAF 51 wt%) showed excellent sustained release profiles

81 oof-of-concept study demonstrated detectable TAF/FTC vaginal levels among TAF + FTC NP-treated hu-BLT

82 displays significant homology to Drosophila TAF(II)110, whereas the other is a predicted zinc bindin

83 lexes, in unicellular genomes, however, each TAF is encoded by a single gene.

84 se data indicated that in addition to EBNA2, TAF family members and MEF2C are essential for ESE activ

85 Emtricitabine/TAF provided a level of protection against vaginal chall

86 s that are present or ectopically expressing TAFs that are absent, results in misregulated expression

87 Adults aged >=18 years began D/C/F/TAF <=14 days from diagnosis without screening/baseline

88 TDF (150/150/200/300 mg once daily) to E/C/F/TAF (150/150/200/10 mg once daily) at week 12.

89 /TDF 150/150/200/300 mg once daily) to E/C/F/TAF (150/150/200/10 mg once daily) at week 12.

90 gh proportion of participants starting D/C/F/TAF achieved HIV-1 RNA <50 copies/mL and very few discon

91 gh proportion of participants starting D/C/F/TAF achieved HIV-1 RNA <50 copies/mL and very few discon

92 Switch to E/C/F/TAF was associated with reductions in TFV concentrations

93 Switch to E/C/F/TAF was associated with reductions in TFV concentrations

94 D/C/F/TAF was well tolerated, no participants discontinued due

95 t/emtricitabine/tenofovir alafenamide (D/C/F/TAF) 800/150/200/10 mg is a phase 3 prospective study ev

96 t/emtricitabine/tenofovir alafenamide (D/C/F/TAF) 800/150/200/10 mg is a phase 3 prospective study ev

97 tenofovir disoproxil fumarate (TDF) to E/C/F/TAF.

98 rticipants switching from E/C/F/TDF to E/C/F/TAF.

99 Tenofovir alafenamide-emtricitabine (F/TAF) was recently approved as a noninferior and potentia

100 persons older than 55 years, the ICER for F/TAF remained more than $3 million per QALY and the maxim

101 0 000 per QALY, the maximum fair price for F/TAF was $8670 per year.

102 and the maximum permissible fair price for F/TAF was $8970 per year.

103 F/TDF alternative, the improved safety of F/TAF is worth no more than an additional $370 per person

104 ver a 5-year horizon, compared with F/TDF, F/TAF averted 2101 fractures and 25 cases of ESRD for the

105 Preexposure prophylaxis with F/TAF versus F/TDF.

106 , the TATA-binding protein-associated factor TAF(II)250 and cyclin D1).

107 ly related to the basal transcription factor TAF(II)250, which is essential for cyclin A transactivat

108 stration of the general transcription factor TAF-4 and is regulated by mechanisms that orchestrate th

109 binding protein (TBP)/TBP-associated factor (TAF) complex.

110 is a TATA-binding protein associated factor (TAF) conserved from yeast to humans and shared by two tr

111 TBP-associated factor (TAF) family proteins, including TAF8, TAF11, and TAF3, w

112 1, a TATA-binding protein Associated Factor (TAF) of the RNA polymerase II transcription initiation f

113 ro transcription, the TBP-associated factor (TAF) subunits recognize downstream promoter elements, ac

114 Of the 14 TBP-associated factor (TAF) subunits that compose TFIID, TAF1 is one of the lar

115 ATA-binding protein (TBP)-associated factor (TAF)-dependent ribosomal protein genes.

116 ATA-binding protein (TBP)-associated factor (TAF).

117 TATA box-binding protein-associated factor (TAF)1 from Drosophila cells and determined the consequen

118 TATA-binding protein and associated factors (TAF(II)s), some of which are also present in SPT-ADA-GCN

119 ral TATA binding protein-associated factors (TAFs) and interacts with E proteins (E2A and HEB).

120 ng protein (TBP) and TBP-associated factors (TAFs) and is the only component of the general RNA polym

121 rotein (TBP) and the TBP-associated factors (TAFs) are assembled into a functional TFIID complex with

122 tein (TBP) and three TBP-associated factors (TAFs) called TAF(I)48, TAF(I)63 and TAF(I)110.

123 (TFs) and transcription associated factors (TAFs) representing about 5% of the total annotated seque

124 TA-binding protein (TBP)-associated factors (TAFs) within the TFIID complex and counteracts negative

125 ox-binding protein (TBP)-associated factors (TAFs), evolutionarily conserved from yeast to humans, pl

126 , an assembly of TBP and associated factors (TAFs), is essential for preinitiation complex formation

127 protein (TBP) and 13 TBP-associated factors (TAFs)-assembles into a functional transcription factor i

128 ng protein (TBP) and TBP-associated factors (TAFs)-is a central component of the Pol II promoter reco

129 protein (TBP) and 13 TBP-associated factors (TAFs).

130 and approximately 14 TBP-associated factors (TAFs).

131 TBP) and a series of TBP-associated factors (TAFs).

132 tein (TBP) and 12-15 TBP-associated factors (TAFs).

133 a complex of TBP and TBP-associated factors [TAFs])-dependent ribosomal protein genes involved in rib

134 laxin increased tumor-associated fibroblast (TAF) interaction with collagen fibers by stimulating bet

135 d abundance of tumor-associated fibroblasts (TAF) and robustly reduced tumor formation.

136 stroma rich in tumor-associated fibroblasts (TAF) is drawing increased therapeutic attention.

137 subset of the tumor-associated fibroblasts (TAF) was found to express B7H1 (PD-L1) and B7DC (PD-L2)

138 ch were mostly tumor-associated fibroblasts (TAF).

139 o, and deplete tumor-associated fibroblasts (TAFs) for improved therapeutic outcomes.

140 (Combo NP) on tumor-associated fibroblasts (TAFs).

141 Water-filled TAF-clad fused-silica (FS) tubes show the lowest attenua

142 more society ought to be willing to pay for TAF over TDF, in exchange for its improved toxicity prof

143 ssible, however, the appropriate premium for TAF will likely merit a downward adjustment, using gener

144 -specific TAF4b component of TFIID (formerly TAF(II)105) is a transcriptional regulator enriched in t

145 calculated the total attributable fraction (TAF) as a weighted average of these AFs.

146 BIC/FTC/TAF led to rapid decay of HIV-1 RNA in genital and recta

147 roviral-naive individuals initiating BIC/FTC/TAF.

148 Infection in FTC/TAF but not TAF-treated macaques was delayed relative to

149 Animals received clinical doses of FTC/TAF (n = 6) or TAF (n = 9) orally 24 hours before and 2

150 The calculated efficacy of FTC/TAF and TAF was 91% (95% confidence interval [CI], 34.9%

151 sults support the clinical evaluation of FTC/TAF for PrEP in women.

152 ts support the clinical investigation of FTC/TAF for PrEP.

153 or up to 19 weeks and received saline or FTC/TAF 24 hours before and 2 hours after each virus inocula

154 Five of the 6 animals in the FTC/TAF and 4 of the 9 animals in the TAF alone group were p

155 Tenofovir alafenamide fumarate (TAF) co-formulated with elvitegravir (EVG, E), cobicista

156 Tenofovir alafenamide fumarate (TAF) co-formulated with elvitegravir (EVG; E), cobicista

157 Tenofovir alafenamide fumarate (TAF), a new prodrug of tenofovir and a potential success

158 ir (DTG) and tenofovir alafenamide fumarate (TAF).

159 ranscription of the ribosomal protein genes, TAF-dependent antisense transcription of GAL10 also requ

160 ntified in the carboxyl-terminus of human (h)TAF(I)48.

161 Altering the composition of hESC TAFs, either by depleting TAFs that are present or ectop

162 tive genes are bound by TBP and all six hESC TAFs.

163 Next, the homopolymer design with a high TAF drug wt% of 73% was characterized in the same model.

164 Relatively little is known about how TAF(II)s contribute to metazoan transcription in vivo, e

165 However, TAF + FTC NPs resulted in significant (p = .0002) protec

166 The interaction between human TBP and human TAF(I)48 was initially examined using the yeast two-hybr

167 py reconstruction of a fully assembled human TAF-less PIC.

168 ition a nucleosome is a major determinant in TAF(II) dependency of genes in vivo.

169 secretion of Wnt16 in a paracrine manner in TAFs.

170 h differential SMAD3 promoter methylation in TAFs and provide new mechanistic insights on the selecti

171 In this manner, TAFs kinetically repress basal transcription.

172 At week 24, median TAF plasma concentration was 11.05 ng/mL (2 hours post-d

173 At week 24, median TAF plasma concentration was 11.05 ng/mL (range, 2.84-14

174 Although higher eukaryotes contain multiple TAF variants that specify tissue- and developmental stag

175 Furthermore, TFV but not TAF increased elafin and MIP3a secretion following injur

176 Infection in FTC/TAF but not TAF-treated macaques was delayed relative to controls (P

177 dent, and we provide evidence that SAGA, not TAF(II)s within TFIID, are largely responsible for TBP r

178 To evaluate the ability of TAF to modulate tumor-associated T cell (TAT) activation

179 rodimer interface and extensive cofolding of TAF subunits.

180 gate whether TAF alone or the combination of TAF and emtricitabine (FTC) can prevent vaginal infectio

181 We investigated whether the combination of TAF and emtricitabine (FTC) could prevent simian/human i

182 ells, siRNA-mediated decreased expression of TAF(I)41 leads to loss of SL1 from the rDNA promoter in

183 esults suggest that the specific function of TAF(II)s is to direct the chromatin remodeling step thro

184 At elevated levels of TAF treatment to match TFV intracellular TFV-DP concentr

185 ed with TAF-I still requires the presence of TAF-I during the polymerization reaction.

186 A subset of TAF proteins is shared in transcription factor II D (TFI

187 TAF-clad FS tubes and is better than that of TAF tubes or externally mirrored FS tubes.

188 n macaques to determine the potential use of TAF for pre-exposure prophylaxis (PrEP) to prevent human

189 this study, we describe a novel function of TAFs in directing genomic occupancy of a transcriptional

190 ed the tumor-promoting fibrotic phenotype of TAFs selectively in ADC.

191 TFIID and SAGA share a common set of TAFs, regulate chromatin, and deliver TBP to promoters.

192 g intracellular TFV-DP, but had no effect on TAF inhibition of infection or TFV-DP.

193 essed before switching and after 12 weeks on TAF.

194 that are either independent or dependent on TAFs (TATA-box Binding Protein-Associated Factors).

195 pattern: most active genes are bound by only TAFs 3 and 5 along with TBP, whereas the remaining activ

196 eceived clinical doses of FTC/TAF (n = 6) or TAF (n = 9) orally 24 hours before and 2 hours after eac

197 n with P300/CBP-associated factor (P/CAF) or TAF(II)250 bromodomains or the P/CAF or GCN5 HAT domains

198 elial cells following preloading with TFV or TAF correlated directly with ARV protection of CD4+ T ce

199 and fibroblasts were pre-loaded with TFV or TAF, and secretions tested for their ability to inhibit

200 incubation of blood CD4+ T cells with TFV or TAF, Medroxyprogesterone acetate (MPA), but not Levonorg

201 oter recognition factor (Trf2) and an orphan TAF subunit (Taf7l) in mammalian testis-specific gene tr

202 nd c-Jun) and regulatory protein (CBP, p300, TAF(II)250, and polymerase II) binding at both the upstr

203 Paradoxically, TAF carried no mutations in MED12, suggesting an interac

204 se are the first reports of sustained parent TAF dosing observed in mouse and TFV-DP in mouse PBMC.

205 bined with either of two tenofovir prodrugs (TAF and TDF) showed noninferior efficacy to treatment wi

206 DTG plus either of two tenofovir prodrugs - TAF (TAF-based group) or tenofovir disoproxil fumarate (

207 the high concentration of collagen-producing TAF.

208 g infected and uninfected macaques receiving TAF PrEP (351 and 143 fmols/106 cells, respectively; P =

209 % CI, 15.2 to 26.7) among patients receiving TAF/FTC, 10.5 (CI, 5.6 to 17.9) among those receiving TD

210 ma was 85% depleted and 87% of the remaining TAFs were TUNEL-positive.

211 urthermore, the recruitment of Rap1 requires TAF(II)s, suggesting a role for TFIID in stabilizing act

212 he high concentration of estrogen-responsive TAF in MED12-LM explains the inconsistent discoveries be

213 ate increased 1,25-(OH)(2)D(3) responsivity, TAF(II)-17 expression, or nuclear number per osteoclast.

214 stigated functions of four shared TFIID/SAGA TAF(II)s in Caenorhabditis elegans.

215 ective epigenetic repression of SMAD3 in SCC-TAFs in the clinical failure of nintedanib in SCC and su

216 sights on the selective poor response of SCC-TAFs to nintedanib.

217 uced fibrosis and nintedanib response of SCC-TAFs was associated with increased promoter methylation

218 tly, forcing global DNA demethylation of SCC-TAFs with 5-AZA rescued TGFbeta1/SMAD3 activation, where

219 to cigarette smoke particles, may prime SCC-TAFs to stronger SMAD3 epigenetic repression, because ci

220 osis is actually higher in ADC-TAFs than SCC-TAFs in vitro and patient samples.

221 l transcription in P0 and P1 by sequestering TAF-4, an essential component of TFIID.

222 Additionally, Set/TAF-Ibeta and pp32 associate with histone deacetylases i

223 of the complex between cytochrome c and SET/TAF-Ibeta.

224 study reveals that the histone chaperone SET/TAF-Ibeta interacts with cytochrome c following DNA dama

225 nucleosome assembly protein 1 and human SET/TAF-1beta/INHAT histone chaperones, Vps75 shows several

226 found to competitively hinder binding of SET/TAF-Ibeta to core histones, thereby locking its histone-

227 drugs to silence the oncogenic effect of SET/TAF-Ibeta's histone chaperone activity.

228 sis of cytochrome c-mediated blocking of SET/TAF-Ibeta, which subsequently may facilitate the develop

229 mbryonic stem cells (hESCs) contain only six TAFs (TAFs 2, 3, 5, 6, 7 and 11), whereas following diff

230 ovide evidence for a novel component of SL1, TAF(I)41 (MGC5306), which functions in Pol I transcripti

231 Here we show that testis-specific TAF (TBP-associated factor) homologs required for termin

232 iption of most genes requires TFIID-specific TAF-1.

233 taxin-7 protein, a member of the STAGA [SPT3-TAF(II)31-GCN5L acetylase] and TFTC (GCN5 and TRRAP) chr

234 clear extracts, transcription induces stable TAF binding to downstream promoter DNA, promoting subseq

235 pe-selective expression of the TFIID subunit TAF(II)105 (renamed TAF4b) in the ovary is essential for

236 t, with genital CD4+ T cells, MPA suppressed TAF inhibition of HIV infection and lowered of TFV-DP co

237 se of the depot coincided with the sustained TAF release.

238 plus either of two tenofovir prodrugs - TAF (TAF-based group) or tenofovir disoproxil fumarate (TDF)

239 -cross-linking results demonstrate that TAF1/TAF(II)250 interacts with the DCE subelement DNA in a se

240 ic stem cells (hESCs) contain only six TAFs (TAFs 2, 3, 5, 6, 7 and 11), whereas following differenti

241 effect of Combo NP works by first targeting TAFs and is more effective as an anti-tumor therapy than

242 ve histone acetyltransferase domain and TBP, TAF, and promoter binding domains.

243 and total plasma concentrations of EVG, TDF, TAF, tenofovir (TFV), and HIV RNA levels were measured a

244 of the five Drosophila genes encoding testis TAF homologs collaborate in an alternative TAF-containin

245 Testis TAFs also promoted relocalization of Polycomb Repression

246 tin immunoprecipitation revealed that testis TAFs bind to target promoters, reduce Polycomb binding,

247 When added apically to epithelial cells, TFV/TAF was released basolaterally, in part through Multidru

248 epithelial cells and fibroblasts release TFV/TAF for use by CD4+ T cells and suggest that the tissue

249 We conclude that TAF in human NSCLC are functionally and phenotypically h

250 es after 48 weeks of therapy have shown that TAF may be a good alternative to TDF for treating chroni

251 These data suggest that TAF(I)41 is integral to transcriptionally active SL1 and

252 We found that TAFs sharply decrease the rate at which Pol II, TFIIB, a

253 The TAF increased stepwise with age.

254 The TAF-based regimen had less effect on bone density and re

255 The TAF-targeting capability of Combo NP was evaluated by do

256 or B7DC was able to completely abrogate the TAF-mediated suppression.

257 In contrast, VPN only activates the TAF-independent core promoter and this activity increase

258 stics provide multiple opportunities for the TAF to influence cellular interactions within the tumor

259 To investigate how the TAF (TATA-binding protein-associated factor) subunits of

260 in the FTC/TAF and 4 of the 9 animals in the TAF alone group were protected against infection (P = .0

261 (both lean and fat mass) was greatest in the TAF-based group and among female patients (mean increase

262 emale patients (mean increase, 6.4 kg in the TAF-based group, 3.2 kg in the TDF-based group, and 1.7

263 than 50 copies per milliliter was 84% in the TAF-based group, 85% in the TDF-based group, and 79% in

264 SL1 and imply a role for SL1, including the TAF(I)41 subunit, in Pol I recruitment and, therefore, p

265 ID (a TAF-dependent form of TBP) but not the TAF-independent form of TBP to the promoters of ribosoma

266 Different members of the TAF family of proteins work in differentiated cells, suc

267 The functions of the TAF subunits of mammalian TFIID in physiological process

268 Overall, the TAF was 0.66 (95% confidence interval [CI]: 0.55-0.78) i

269 tyltransferase) is involved in targeting the TAF-independent form of TBP to the promoters of ribosoma

270 Thus, the TAF represents the overall fraction (where 0.00 = not at

271 ts expression is strictly dependent upon the TAF(II) subunits of TFIID, which are required for the re

272 domain (activation domain 3 [AD3]) with the TAF homology (TAFH) domain of TAF4, (2) is critical for

273 etry, we define the interactions between the TAFs and uncover a central role for TAF8 in nucleating t

274 The essentiality of the TAFs has made it difficult to ascertain their roles in T

275 AF7), which functions not only as one of the TAFs, but also a coactivator for c-Jun.

276 es undergo a slow isomerization in which the TAFs reorganize their contacts with the promoter to allo

277 Thus, TAF-I is required to facilitate transcription at a step

278 Thus, TAFs are involved in both establishing an upper limit of

279 OMA-1/2 binding to TAF-4 is developmentally regulated, requiring phosphoryl

280 of air-surrounded FS tubes is second only to TAF-clad FS tubes and is better than that of TAF tubes o

281 2 facilitates the binding of OMA proteins to TAF-4 and simultaneously inactivates their function in r

282 In vivo, promoter responses to TAF mutations correlate with the level of downstream, ra

283 dian age 50 years), 2404 (68.5%) switched to TAF.

284 Switching to TAF was associated with increases in eGFR of 1.5 mL/min

285 Switching from TDF to TAF improves eGFR and proteinuria in patients with renal

286 ss HIV Cohort Study who switched from TDF to TAF-containing antiretroviral regimen or continued TDF,

287 for essentially all embryonic transcription, TAF-5, TAF-9, and TAF-10 were dispensable at multiple de

288 In five of eight tumors, TAF elicited a contact-dependent enhancement of TAT acti

289 In the three other tumors, TAF had a net suppressive effect upon TAT activation, an

290 Whereas TAF-4 was required for essentially all embryonic transcr

291 acetylated lysine 12 on histone H4, whereas TAF(II)250 and PCAF recognized H3 and other acetylated h

292 ficiency virus (SHIV) to investigate whether TAF alone or the combination of TAF and emtricitabine (F

293 We propose a new model in which TAFs function as reinitiation factors, accounting for th

294 With TAF, TFV C24 was 11.9-fold higher in SP than in BP.

295 he median TFV-dp concentration achieved with TAF in SMCs was 6% that of TFV-dp in PBMCs.

296 nt transcription of chromatin assembled with TAF-I still requires the presence of TAF-I during the po

297 ing regimens, especially in combination with TAF, than with the standard-care regimen.

298 eless, TFV-dp C24 in SMC was comparable with TAF and TDF.

299 atment of cells during latency for 24 h with TAF still inhibited EBV lytic DNA replication at 72 h af

300 PBMC ratio was also significantly lower with TAF.