ライフサイエンスコーパス: USF

1 USF and c-Myc are basic helix-loop-helix transcription f

2 USF binding is lost from both rearranged and germline Db

3 USF bound to the rat and human promoter but not to the m

4 USF has a similar binding affinity as Max to MLP DNA (K

5 USF imaging in porcine heart tissue and mouse breast tum

6 USF is a family of transcription factors that are struct

7 USF proteins have a novel role in repressing the express

8 USF was subject to degradation by the Ca(2+)-dependent p

9 USF-1 can also potentiate the induction of the Ov gene b

10 Upstream stimulatory factor 1 (USF 1), is a transcription factor controlling expression

11 ption factors upstream stimulatory factor 1 (USF-1) and USF-2 are indispensable for the transcription

12 1 (IRF-1) and upstream stimulatory factor 1 (USF-1) in gamma interferon (IFN-gamma)-treated hepatocyt

13 expression of upstream stimulating factor 1 (USF-1), a transcription factor important for basal C4 ex

14 nstrated that upstream stimulating factor 1 (USF-1), a transcription factor previously shown to regul

15 tors RFX5 and upstream stimulation factor 1 (USF-1).

16 e E-Box binds upstream stimulating factor-1 (USF-1), a constitutively expressed transcription factor.

17 of action of upstream stimulatory factor-1 (USF-1), which involves its tethering to the Ov gene 5'-f

18 contrast, the interactions of c-jun, USF-1, USF-2 and Sp1 with this promoter are metal-independent.

19 dditionally, the binding of Sp1, Sp3, USF-1, USF-2, and c-Myc to the TERT promoter is elevated in cel

20 that TR can physically interact with USF-1, USF-2, and C/EBPalpha.

21 only the upstream stimulatory factors USF-1/USF-2 but also the CCAAT-binding factor CBF, also known

22 NA was markedly decreased by expression of a USF-specific dominant negative mutant, identifying IGF2R

23 Furthermore, A-USF-expressing transgenic mice exhibit a defect in the f

24 We further show that the expression of A-USF reduces the expression of several key erythroid cell

25 sion of a dominant-negative mutant of USF, A-USF, in transgenic mice reduces the expression of all be

26 Mutation of the E box abolished USF/c-Myc-mediated up-regulation of CXCR4 promoter activ

27 our previous work, we successfully achieved USF imaging with several types of USF contrast agents an

28 In addition, USF-1 overexpression is able to induce Ov gene promoter

29 We show that the additional USF consensus element within the 3R construct confers gr

30 ereas the -20A allele retains a low affinity USF binding site.

31 Here we demonstrate that although USF is required for the efficient association of RNA pol

32 he previously demonstrated stimulation by an USF expression vector.

33 ast cancer cells is lost upon mutation of an USF/c-myc transcription factor binding site located 172

34 mannose receptor promoter, but only PU.1 and USF contributed to activation.

35 boxes are preferentially bound by USF-1 and USF-2 and, moreover, are dispensable for cyclin D2 promo

36 oter constructs revealed that both USF-1 and USF-2 caused an approximately tenfold increase in report

37 There was also upregulation of USF-1 and USF-2 during the differentiation of Th17 cells from naiv

38 alysis with specific antibodies to USF-1 and USF-2 indicates that USF-1 is the primary isoform bindin

39 er and demonstrate the role of the USF-1 and USF-2 transcription factors in regulating the expression

40 ene is regulated by the binding of USF-1 and USF-2, and this process may be favored by cytokines prom

41 K562 and CD34(+) cells showed that USF-1 and USF-2, but not MITF, induce the HOXB4 promoter in respon

42 rs upstream stimulatory factor 1 (USF-1) and USF-2 are indispensable for the transcription of RORgamm

43 hat the transcription factors Sp1, PU.1, and USF bound to the mannose receptor promoter, but only PU.

44 Glucose up-regulates both AP1 and USF binding activities 2-fold in A7r5 cells and selectiv

45 ative GABA(B)R1 promoters by CREB, ATF4, and USF may dynamically regulate expression of their gene pr

46 , GATA-1/2, HNF-3 beta, c/EBP alpha/beta and USF have been localized in the promoter region of Npr1 g

47 conversely, Stra13 inhibits DNA-binding and USF-mediated transactivation.

48 e promoter and additional factors, C/EBP and USF, bound in the first intron.

49 shown that transcription factors TFII-I and USF interact with the beta-globin promoter in erythroid

50 The data suggest that TFII-I and USF regulate chromatin structure accessibility and recru

51 LPS increased NF-kappaB and USF binding to the ADH promoter.

52 We show that both Myc and USF bind to the exact same E box on the cad promoter, su

53 itation protocol for the analysis of Myc and USF binding to the cad promoter.

54 uld not definitively prove that both Myc and USF bound to the exact same site on the cad promoter, no

55 Thus, NFkappaB and USF regulate BRCA2 expression through the BRCA2 promoter

56 is conserved regarding CBF-binding sites and USF-binding sites implies an important role for these ub

57 l and functional interactions between Sp and USF proteins may lead to a better understanding of the b

58 In Sp- and USF-null Drosophila Mel-2 cells, both Sp1 and USF1 stimu

59 nfirmed by immunoprecipitations with Sp- and USF-specific antibodies.

60 Because gI is essential and Sp1 and USF contribute to VZV pathogenesis in skin and T cells i

61 ocyte extracts revealed that Xenopus Sp1 and USF or closely related factors are present together in a

62 Stra13 and USF also colocalize and functionally interact in mammali

63 gether, our data demonstrate that Stra13 and USF interact physically and functionally, and identify a

64 rate a direct interaction between Stra13 and USF that is dependent upon the C-terminal repression dom

65 te comparable levels of nuclear factor Y and USF-1 binding and similar levels of Sp1 and Sp3 proteins

66 nd found that Sp1/Sp3, nuclear factor Y, and USF-1 were involved in the regulation of basal promoter

67 ree major transcription factors involved are USF, SREBP-1c, and LXRalpha.

68 factor (USF) binds to a composite CREB/ATF4/USF regulatory element only in the absence of CREB bindi

69 hat a functional relationship exists between USF and a second J chain positive-regulating factor, B-M

70 ocalized the functional interactions between USF and Sp proteins to the DNA binding domain of USF.

71 Physical interactions between USF and Sp proteins were confirmed by immunoprecipitatio

72 These elements bind USF proteins in vitro by electrophoretic mobility shift

73 in an upstream E-box that specifically binds USF nuclear factors or a downstream Sp1 binding site sig

74 revealed significantly lower levels of both USF and c-Myc bound to the endogenous CDK4 promoter in b

75 xpression, demonstrating involvement of both USF and Myc in CDK4 transcriptional control.

76 riven stages of B cell development that both USF and B-MEF2 are able to bind to their respective prom

77 se IV promoter constructs revealed that both USF-1 and USF-2 caused an approximately tenfold increase

78 TRAP transcriptional activation via a 12-bp USF binding site in the TRAP promoter.

79 Importantly, the 18-bp USF enhancer driving a minimal promoter was sufficient f

80 w that the -332 and -65 E-boxes are bound by USF in both fasted and refed mice, while the -150 SRE is

81 hese two E boxes are preferentially bound by USF-1 and USF-2 and, moreover, are dispensable for cycli

82 nce transactivation of pMyc3E1bLuc-driven by USF-1 and c-Myc expression relative to identically trans

83 e Ov gene abrogates induction of the gene by USF-1.

84 erol-3-phosphate acyltransferase promoter by USF and SREBP-1c.

85 Thus, OPN gene transcription is regulated by USF and AP1 in aortic VSMCs, entrained to changes in cel

86 Under fasting conditions, USF-1 is deacetylated by HDAC9, causing promoter inactiv

87 g rat breast nuclear proteins to a consensus USF oligonucleotide.

88 ed E boxes almost identical to the consensus USF DNA-binding sequence.

89 ts revealed that the small, highly conserved USF-specific region (USR) was responsible for the inacti

90 By contrast, USF (but not AP1) binding activity is suppressed by 2-DG

91 We demonstrated the principle of time-domain USF imaging by using two USF contrast agents.

92 pled device (ICCD) camera-based, time-domain USF imaging system.

93 iption factors, including CREB, ATF2, C/EBP, USF, and NFAT.

94 Expression of either USF or AP1 activates the proximal OPN promoter in A7r5 V

95 rectional promoters overlapping an essential USF binding site but with distinct TATA elements.

96 rect neuronal-specific activity, we examined USF expression and used a series of adenoviral reporters

97 The cellular factor USF bound specifically to its consensus site within the

98 h the ubiquitously expressed cellular factor USF.

99 ubiquitously expressed transcription factor USF and the tissue-restricted activator NF-E2 in the rec

100 Transcription factor USF is a ubiquitously expressed member of the helix-loop

101 The transcription factor USF is required for the activation of FAS transcription,

102 nds upon the cellular transcriptional factor USF to support its virulence in human skin in vivo.

103 Upstream regulatory factor (USF) and sterol regulatory element binding protein (SREB

104 tion identified upstream stimulating factor (USF)-2 and micropthalmia transcription factor (MITF).

105 such proteins, upstream stimulatory factor (USF) 1 and 2, readily associate with two E-boxes in the

106 monstrated that upstream stimulatory factor (USF) 1 and USF2 bind to the CGRP neuroendocrine-specific

107 tor 1 (Sp1) and upstream stimulatory factor (USF) and an open reading frame 29 (ORF29)-responsive ele

108 Upstream stimulatory factor (USF) and CCAAT enhancer binding proteins (C/EBPs) bind t

109 ionship between upstream stimulatory factor (USF) and SREBP-1c, two transcription factors that we hav

110 cription factor upstream stimulatory factor (USF) and to contribute to efficient in vitro transcripti

111 ation-sensitive upstream stimulatory factor (USF) binds to a composite CREB/ATF4/USF regulatory eleme

112 tor 1 (NF1) and upstream stimulatory factor (USF) families bind to and regulate HGF gene transcriptio

113 otein levels of upstream stimulatory factor (USF) increase during differentiation of murine erythrole

114 binding of the upstream stimulatory factor (USF) to an E-box motif immediately upstream from the BSA

115 omoter, whereas upstream stimulatory factor (USF) was shown previously to bind to a more proximal sit

116 4, CAAT, GATA, upstream stimulatory factor (USF), estrogen receptor (ER), and sex-determining region

117 ires binding of upstream stimulatory factor (USF)-1 to a noncanonical E-box within the Dbeta2 12-reco

118 nding sites for upstream stimulatory factor (USF)-1/-2.

119 activity via an upstream stimulatory factor (USF)-activated cognate inhibited by LRP6.

120 tor 1 (Sp1) and upstream stimulatory factor (USF).

121 ssays show that upstream stimulatory factor (USF)1 and USF2 preferentially bind the -20C allele, wher

122 cription factor upstream stimulatory factor (USF)1 influences susceptibility to familial combined hyp

123 assays identify upstream stimulatory factor (USF; USF1:USF2) and activator protein-1 (AP1; c-Fos:c-Ju

124 ly distributed (upstream stimulatory factor [USF]) protein-DNA complexes.

125 on by the constitutive transcription factor, USF.

126 ds not only the upstream stimulatory factors USF-1/USF-2 but also the CCAAT-binding factor CBF, also

127 ctor, and the bHLH-ZIP transcription factors USF-1 (for upstream regulatory factor 1) and c-Myc were

128 we showed that upstream stimulatory factors (USF) 1 and 2 are implicated in the RANKL-induced TRAP tr

129 p sequence are upstream stimulatory factors (USF) 1 and 2.

130 ed the role of upstream stimulatory factors (USF) in the regulation of APEG-1 transcription via this

131 recruitment of upstream stimulatory factors (USF) transcription factors.

132 identified the upstream stimulatory factors (USFs) as a major E-box-binding protein complex in both R

133 Urethroscrotal fistula (USF) is an abnormal communication between the urethra an

134 loped an ultrasound-switchable fluorescence (USF) imaging technique whereby ultrasound was used to sw

135 Ultrasound-switchable fluorescence (USF) imaging, a new imaging technique, was recently prop

136 odality, ultrasound-switchable fluorescence (USF) imaging, for achieving this goal.

137 hnology, ultrasound-switchable fluorescence (USF), for high-resolution imaging in centimeter-deep tis

138 ne-rich tract (SRT), and binding domains for USF, TFIIB, and TATA box binding protein (TBP).

139 oter suggested two in vivo binding sites for USF-1 and -2.

140 However, USF-1 is not able to bind to the Chirp-III site independ

141 co-immunoprecipitation experiments identify USF-1 as a component of Chirp-III.

142 ncer cell lines, suggesting that a defect in USF function may contribute to down-regulation of IGF2R

143 en allows recruitment of P/CAF, resulting in USF-1 acetylation and FAS promoter activation.

144 In vivo ChIP assays verified increased USF binding to the apelin promoter in breast of lactatin

145 DNA-PK-deficient SCID mice, feeding-induced USF-1 phosphorylation/acetylation, DNA breaks, and FAS a

146 sorders in which the role of glucose-induced USF expression has already been established and autoimmu

147 Unexpectedly, there was more intense USF immunostaining in neurons than nonneuronal cells.

148 In contrast, the interactions of c-jun, USF-1, USF-2 and Sp1 with this promoter are metal-indepe

149 BP-1 and the leucine zipper from either MAX, USF, or MITF indicate that both the HLH and leucine zipp

150 binding of the three B-HLH-ZIP proteins MAX, USF, or MITF, even at 100 molar eq.

151 lating MT-I gene (e.g., MTF-1, Sp 1 and MLTF/USF) are active in P1798 cells.

152 the metal regulatory elements (MREs) or MLTF/USF are occupied in response to heavy metals.

153 on domains of both proteins and that mutated USF or SREBP lacking the N-terminal activation domain co

154 view summarizes the known activities of Myc, USF, TFII-I, and Tal11/SCL and discusses how they may fu

155 se 53 genes into ten families; PAS, HES, Myc/USF, Hand, Mesp, Shout, p48, NeuroD/Neurogenin, Atonal a

156 airy-Enhancer of Split, Hand, p48, Mesp, MYC/USF, and the bHLH-Per, Arnt, Sim (PAS) domain.

157 eriments demonstrated that dominant negative USF repressed APEG-1 promoter activity, and USF1, but no

158 In this study, we introduced a new USF imaging system: an intensified charge-coupled device

159 We synthesized and characterized unique NIR USF contrast agents.

160 s of the most successful near-infrared (NIR) USF contrast agents.

161 The bHLH-zip protein TFE3, but not USF, cooperated with the ETS domain proteins PU.1 and Et

162 ansactivation of SREBP-1 and SREBP-2 but not USF.

163 dney (BHK) cells with BETA2 and E47, but not USF.

164 consensus element that alters the ability of USF proteins to bind and thus alters the transcriptional

165 the results of USF imaging, the accuracy of USF imaging was proved.

166 we demonstrate that reducing the activity of USF decreased beta-globin gene expression, while diminis

167 gene, we noted that the binding activity of USF to the HGF promoter element increased while that of

168 iated with an increase in the association of USF and RNA po ly mer ase II with regulatory elements of

169 further reduces the application barriers of USF imaging.

170 s effect is mediated by increased binding of USF to the ADH promoter and not by NF-kappaB, which has

171 Mutation of the E-box prevented binding of USF, although stimulation of reporter gene expression by

172 an HOXB4 gene is regulated by the binding of USF-1 and USF-2, and this process may be favored by cyto

173 l GAS element is dependent on the binding of USF-1 to the adjacent E box.

174 supershift experiments indicated binding of USF-1/-2 to the rat (-114/-109 bp) and human (-84/-79 bp

175 Likewise, coexpression of USF proteins with Foxa2 yielded greater activation than

176 Furthermore, cotransfection of USF and SREBP-1c with an FAS promoter-luciferase reporte

177 ng cell culture, transient cotransfection of USF expression vectors with dipeptidyl peptidase IV prom

178 te that the basic helix-loop-helix domain of USF interacts directly with the basic helix-loop-helix a

179 and Sp proteins to the DNA binding domain of USF.

180 main of Stra13 and the DNA-binding domain of USF.

181 cellular targets that mediate the effects of USF on cellular proliferation and transformation remain

182 Co-expression of USF abrogates Stra13-mediated repression of target genes

183 Mutant forms of USF-1 and -2 lacking the DNA binding or transcriptional

184 We recently reported the importance of USF-1 phosphorylation and subsequent acetylation in insu

185 (USR) was responsible for the inactivity of USF in Saos-2 cells.

186 In vivo, knockdown of USF expression in the liver of transgenic mice expressin

187 inhibitor calpeptin increased the levels of USF and strongly induced expression of the adult alpha-

188 genotoxic dsDNA breaks lead to rapid loss of USF binding and gain of transcriptionally primed 5'Dbeta

189 of the USF proteins and the frequent loss of USF function in cancer cells suggest a role for these ub

190 monstrate that a partial or complete loss of USF function is a common event in breast cancer cell lin

191 etal IUGR state was characterized by loss of USF-1 binding at the proximal promoter of Pdx1, recruitm

192 al COX-2 expression is through modulation of USF transcriptional activity in the 5' upstream region o

193 ibiting p38-MAP kinase, a known modulator of USF activity.

194 expression of a dominant-negative mutant of USF, A-USF, in transgenic mice reduces the expression of

195 n of DNA-PK by PP1 causes phosphorylation of USF that in turn recruits P/CAF to be acetylated for tra

196 To investigate the binding properties of USF during VSMC differentiation, nuclear extracts were p

197 ckground temperature (TBG) on the quality of USF images.

198 Furthermore, a reduction of USF activity resulted in a significant decrease in acety

199 We have mapped the regions of USF and IE62 required for direct physical interaction.

200 the results of CT imaging and the results of USF imaging, the accuracy of USF imaging was proved.

201 cotransfection studies verified the role of USF in regulation of BRCA2 transcription.

202 To test the functional role of USF, we first demonstrated that small interfering RNAs d

203 stream targets, we investigated the roles of USF and c-Myc in expression of CDK4, a known direct targ

204 With a series of USF imaging experiments, we demonstrated the tradeoffs a

205 ction experiments, a second possible site of USF interaction with the dipeptidyl peptidase IV promote

206 The success of USF imaging highly relies on excellent contrast agents.

207 y achieved USF imaging with several types of USF contrast agents and imaging systems.

208 There was also upregulation of USF-1 and USF-2 during the differentiation of Th17 cells

209 n, and possible changes in the expression of USFs might be of interest for inflammatory conditions wi

210 l regulation of TS is dependent, in part, on USF proteins binding within the tandem repeats.

211 t-negative mutants specific to either Myc or USF family proteins inhibited reporter gene activity as

212 , with two base pair substitutions in Sp1 or USF sites, replicated like rOKA in vitro, but infectivit

213 cancer, was investigated here as a possible USF target in both nontumorigenic and tumorigenic breast

214 e evidence that the binding of BSAP prevents USF and B-MEF2 from interacting with the J chain promote

215 The bHLHZip protein USF (Upstream Stimulatory factor) was identified as a St

216 und by a heterodimer of the bHLH-Zip protein USF-1 and -2 and a cell-specific factor from thyroid C c

217 nscription factors are the b/HLH/z proteins: USF, Max, Myc, and Mad.

218 r to determine the occupancy of the putative USF and SREBP binding sites, we examined their protein-D

219 s show that USF is recruited to the putative USF binding site in the human apelin promoter in culture

220 ging strategies for achieving a high-quality USF image via this time-domain system.

221 Recombinants, rOKAgI-Sp1 and rOKAgI-USF, with two base pair substitutions in Sp1 or USF site

222 of these agents, combined with the sensitive USF imaging system developed in this study, enabled us t

223 The repaired protein, rOKAgI:rep-Sp1/USF, was as infectious as rOKA.

224 A double mutant, rOKAgI-Sp1/USF, did not replicate in skin but yielded low titers of

225 ion assays confirmed in vivo binding of Sp3, USF-1, and nuclear factor YA (NF-YA) to the CBS -1b prom

226 Additionally, the binding of Sp1, Sp3, USF-1, USF-2, and c-Myc to the TERT promoter is elevated

227 ion factors (TFs) SP1, NF-Y, ETS, CREB, TBP, USF, and NRF-1.

228 II (Pol II) with immobilized LCR templates, USF and NF-E2 together regulate the association of Pol I

229 ed binding of SREBP to the -150 SRE and that USF binding to the -65 E-box is also required for SREBP

230 ppresses HGF gene promoter activity and that USF has an activating function.

231 Our studies demonstrate that USF factors contribute to the regulation of APEG-1 expre

232 In summary, the data demonstrate that USF regulates globin gene expression indirectly by enhan

233 Previous work demonstrated that USF regulates genes during erythroid differentiation, in

234 on analysis of mouse liver demonstrates that USF binds constitutively to the mitochondrial glycerol 3

235 We provide evidence demonstrating that USF interacts with known regulatory DNA elements in the

236 We have determined that USF proteins bind to footprint IV.

237 We have found that USF can synergize with IE62 to a similar extent on model

238 of FAS transcription, and we show here that USF phosphorylation by DNA-PK, which is dephosphorylated

239 Collectively, our data indicate that USF binding to the hTERT promoter may be transcriptional

240 antibodies to USF-1 and USF-2 indicates that USF-1 is the primary isoform binding to the E-box in nuc

241 ty shift and supershift assays revealed that USF and NF1 have high binding affinity for this region a

242 Together, our findings show that USF exerts a stimulatory role in regulation of breast ap

243 ChIP experiments show that USF is recruited to the putative USF binding site in the

244 enesis and overexpression assays showed that USF up-regulates basal and inducible apelin transcriptio

245 omatin immunoprecipitation assay showed that USF, c-Myc, and Max proteins were associated with the FG

246 s in both K562 and CD34(+) cells showed that USF-1 and USF-2, but not MITF, induce the HOXB4 promoter

247 urthermore, we provide evidence showing that USF interacts with NF-E2 in erythroid cells.

248 These data suggest that USF/c-Myc and YY1 may play an important role in the HIV-

249 on, we demonstrate, for the first time, that USF and SREBP-1 interact in vitro and in vivo.

250 atory factors 1 and 2 (USF1/2) and show that USFs are required for the activation of CaRE2-dependent

251 The USF binding site was disrupted in the recombinant virus,

252 In HeLa cells, the USF proteins are transcriptionally active and their over

253 ox-binding factor that was distinct from the USF and Myc/Mad families.

254 extract) regulators appear to influence the USF-E-box interaction and affect P4Halpha(I) expression.

255 cell lines, and the ubiquitous nature of the USF cast doubts about its role.

256 USF1, but not USF2, of the USF family stimulated HGF gene promoter activity.

257 The antiproliferative activities of the USF proteins and the frequent loss of USF function in ca

258 localization, or DNA-binding activity of the USF proteins in HeLa and Saos-2 cells.

259 However, overexpression of the USF proteins in myocytes depresses CPT-1beta activity an

260 in which the transcriptional activity of the USF proteins, and consequently their antiproliferative a

261 Mutagenesis of the USF sites shows that the transcriptional regulation of T

262 maT promoter and demonstrate the role of the USF-1 and USF-2 transcription factors in regulating the

263 Importantly, mutation of the USF-binding site partially blocks RANKL-induced TRAP tra

264 tic role of hSET1 and NURF in regulating the USF-bound barrier insulator to prevent erythroid genes f

265 ous CGRP RNA and preferentially targeted the USF binding site at the 18-bp enhancer in the neuronal-l

266 The results showed that the USF contrast agent adopted in this study was very stable

267 ed proximal to the TATA with homology to the USF binding site was identified as a potential regulator

268 his site were identified as belonging to the USF family of transcription factors.

269 ion of erythroid progenitor cells, while the USF proteins and Tal1 regulate genes that specify the di

270 n the second repeat of 3R alleles within the USF consensus element that alters the ability of USF pro

271 These results suggest a new function for the USFs in the regulation of activity-dependent transcripti

272 ind that the transcriptional activity of the USFs is regulated by Ca(2+)-activated signaling pathways

273 d signaling pathways in neurons and that the USFs bind to the promoters of a number of neuronal activ

274 Thus, USFs are important for the molecular mechanisms of Th17

275 ershift analysis with specific antibodies to USF-1 and USF-2 indicates that USF-1 is the primary isof

276 the conserved USR domain and, in contrast to USF, is not ubiquitous.

277 feeding induces the recruitment of DNA-PK to USF-1 and its phosphorylation, which then allows recruit

278 Two USF family E-box consensus elements are found within the

279 iple of time-domain USF imaging by using two USF contrast agents.

280 gin to address the paradox of how ubiquitous USF proteins might direct neuronal-specific activity, we

281 Unlike USF proteins, USF1/2 mRNA levels are unaffected by O(2)

282 ransferase pulldown experiments with various USF and sterol regulatory element-binding protein (SREBP

283 In vivo and ex vivo USF imaging of the mouse spleen via intravenous injectio

284 However, in vivo USF imaging has not been achieved so far because of the

285 udy, for the first time, we achieved in vivo USF imaging successfully in mice with high resolution.

286 perature of 37 degrees C) for future in vivo USF imaging.

287 IGF2R promoter-driven expression was USF-independent in both MCF-7 and MDA-MB-231 breast canc

288 two different breast cancer cell lines where USF is transcriptionally inactive and c-Myc is overexpre

289 ts confirmed that these proteins, along with USF-1, bind to the HOXB4 promoter in vitro.

290 DNA break/repair components associated with USF induce transient DNA breaks during FAS activation.

291 d allows a direct interaction of BAF60c with USF-1 that is phosphorylated by DNA-PK and acetylated by

292 orter gene expression by cotransfection with USF was reduced by only 50%.

293 hen assayed by transient cotransfection with USF-dependent reporter genes.

294 ermined that TR can physically interact with USF-1, USF-2, and C/EBPalpha.

295 TOR complex to allow direct interaction with USF-1 for recruitment to lipogenic promoter regions.

296 moter nor a direct physical interaction with USF.

297 TFIIIA gene have been identified as Xenopus USF (Xl-USF) and B3 (homolog of Vg1 RBP/VERA).

298 Xl-USF binds to element 1 of the TFIIIA gene which is immed

299 gene have been identified as Xenopus USF (Xl-USF) and B3 (homolog of Vg1 RBP/VERA).

300 helix-loop-helix leucine zipper (B-HLH-ZIP) [USF (upstream stimulating factor) and Mitf] proteins.