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 is a family of transcription factors that are struct

6 USF overexpression can prevent c-Myc-dependent cellular

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

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

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

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

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

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

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

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

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

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

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

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 ardation experiments indicate that USF-1 and USF-2 also bind to this element, which contains an imper

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

63 Stra13 and USF also colocalize and functionally interact in mammali

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

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

66 Both TFE3 and USF enhanced Ets-1 DNA binding in vitro by relieving the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

88 In the non-tumorigenic MCF-10A cells, USF in general, and USF2 in particular, exhibited strong

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

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

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

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

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

94 In contrast, USF overexpression had essentially no effect on the prol

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

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

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

98 the involvement of endogenous and exogenous USF in the activation of the BRCA2 promoter.

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

100 h the ubiquitously expressed cellular factor USF.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

118 4, CAAT, GATA, upstream stimulatory factor (USF), estrogen receptor (ER), and sex-determining region

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

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

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

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

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

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

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

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

127 on by the constitutive transcription factor, USF.

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

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

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

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

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

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

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

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

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

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 herefore context dependent, and evidence for USF DNA-binding activity in particular cells is insuffic

140 a conformational change that is required for USF activity at promoters lacking an initiator.

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

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

143 other myeloid promoters, we have identified USF as the ubiquitous factor, and demonstrated that the

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

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

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

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

148 particular cells is insufficient to indicate USF function in transcriptional activation and growth co

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

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

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

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

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

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

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

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

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

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

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

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

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

162 We synthesized and characterized unique NIR USF contrast agents.

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

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

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

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

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

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

169 ue confirmed the transcriptional activity of USF in normal human mammary epithelial cells.

170 The activity of USF is therefore context dependent, and evidence for USF

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

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

173 further reduces the application barriers of USF imaging.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

204 4, acted as a dominant-negative regulator of USF-mediated activation of the class I promoter.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

222 ind that cad promoter constructs that retain USF binding but lose Myc binding in vivo no longer displ

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

242 Gel retardation experiments indicate that USF-1 and USF-2 also bind to this element, which contain

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

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

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

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

247 In this study, we show that USF/c-Myc up-regulates, while YY1 down-regulates the pro

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

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

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

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

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

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

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

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

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

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

258 Mutations in the USF binding motif significantly decrease J chain promote

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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 moter nor a direct physical interaction with USF.

296 Co-transfection studies with USF proteins and the varicella zoster IE62 protein provi

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.