ライフサイエンスコーパス: Oct-1

1 quisitely dependent on physiologic levels of Oct-1.

2 the multidomain transcription factor, human Oct-1.

3 tion factors, one of which was identified as Oct-1.

4 eral cellular DNA binding proteins including Oct-1.

5 or basal transcription, and are activated by Oct-1.

6 t interacts with the POU homeodomain protein Oct-1.

7 a coactivator with the transcription factor Oct-1.

8 ites for NF-kappaB (p50-p50 and p50-p65) and OCT-1.

9 n but did not affect the activity of SP-1 or OCT-1.

10 ion factor that specifically associates with Oct-1.

11 epends on recognition of the core element by Oct-1.

12 vity of the regulator of iNOS transcription, Oct-1.

13 that UV could mediate PDRG upregulation via Oct-1.

14 LIX did not activate Oct-1.

15 by p38 kinase inhibitor is mediated through Oct-1.

16 a binding site for the transcription factor Oct-1.

17 We identified 57 studies published between Oct 1, 1980, and June 21, 2007.

18 haemoglobin, or lithium measurements between Oct 1, 1982, and March 31, 2014, compared with controls

19 s for Disease Control and Prevention between Oct 1, 1994, and Mar 31, 2005.

20 ld Mulago Hospital (Kampala, Uganda) between Oct 1, 1995, and Dec 31, 2008.

21 ll-specific coactivator OCA-B, together with Oct-1/2, binds to octamer sites in promoters and enhance

22 nuclear factor-1beta (HNF-1beta) is a Pit-1, Oct-1/2, Unc-86 (POU) homeodomain-containing transcripti

23 nuclear factor-1beta (HNF-1beta) is a Pit-1, Oct-1/2, UNC-86 (POU)/homeodomain-containing transcripti

24 Between Oct 1, 2001, and Jan 20, 2009, 228,966 men were invited

25 Between Oct 1, 2003 and June 30, 2011, consecutive children and

26 Between Oct 1, 2003, and June 30, 2011, we enrolled eligible pat

27 Between Oct 1, 2003, and Sept 30, 2012, 2 010 398 cohort partici

28 Between June 1, 2002, and Oct 1, 2004, 44,986 and 48,984 patients registered with

29 02, to Sept 30, 2004) versus after (phase 2: Oct 1, 2004, to March 31, 2007) study of the effect of e

30 02, to Sept 30, 2004) versus after (phase 2: Oct 1, 2004, to March 31, 2007) study of the effect on p

31 entry to the UK in a pilot programme between Oct 1, 2005, and Dec 31, 2013.

32 Between Oct 1, 2005, and Nov 3, 2008, 112 patients were register

33 and postherpetic neuralgia occurring between Oct 1, 2005, and Sept 30, 2016, obtaining data from 164

34 From Oct 1, 2005, to July 31, 2016, 173 patients (median age

35 From Oct 1, 2006, to March 1, 2015, we enrolled 25 patients w

36 ys to 19 years with AIS from Jan 1, 2003, to Oct 1, 2007, were collected with standardised case-repor

37 Between Oct 1, 2008, and Dec 31, 2011, we recruited 30 patients.

38 Between Oct 1, 2008, and March 15, 2010, GATS used nationally re

39 Between Oct 1, 2008, and Oct 31, 2012, we enrolled and followed

40 antimicrobial stewardship programme between Oct 1, 2009, and Sept 30, 2014.

41 From Oct 1, 2009, to July 31, 2013, outpatient clinics repres

42 Between Jan 1, 2005 and Oct 1, 2010, 503 of 542 eligible women were randomly all

43 randomised, placebo-controlled trial between Oct 1, 2010, and Dec 20, 2013, at 21 primary care sites

44 infection, or colonisation published before Oct 1, 2011.

45 ce Research Datalink had a livebirth between Oct 1, 2012 and Sept 3, 2013; the average vaccine covera

46 Between Oct 1, 2012, and Dec 19, 2013, we recruited 26,503 parti

47 Between Oct 1, 2012, and June 20, 2014, we randomly assigned 155

48 d on 82 confirmed cases in infants born from Oct 1, 2012, and younger than 3 months at onset was 91%

49 From Oct 1, 2012, to June 30, 2013, 6680 neonates were enroll

50 Between Oct 1, 2013, and Dec 31, 2015, we recruited 5781 pregnan

51 ere born to pregnant women recruited between Oct 1, 2013, and Feb 10, 2015, and were therefore eligib

52 During the intervention period (Oct 1, 2013, to June 30, 2014), empirical antibiotic the

53 study took place between March 15, 2010, and Oct 1, 2013.

54 Between June 30, 2013, and Oct 1, 2014, 134 patients were screened and 70 were enro

55 Between April 5, 2007, and Oct 1, 2014, 16 046 dried blood spot samples were sent f

56 We did a field evaluation study between Oct 1, 2014, and April 30, 2016, at the urban Rahima Moo

57 .71 years, IQR 2.46-6.35) were enrolled from Oct 1, 2014, to Dec 2, 2015.

58 ients from UCSF and between Nov 1, 2012, and Oct 1, 2014, we recruited 387 patients from SARP.

59 dual antiplatelet therapy, published before Oct 1, 2014.

60 hildren's hospital between Nov 11, 2011, and Oct 1, 2014.

61 topsy-confirmed alpha synucleinopathy (as of Oct 1, 2015) who were previously included in other studi

62 an 15, 2015, and April 30, 2015, and between Oct 1, 2015, and April 30, 2016, we enrolled 720 patient

63 or electronic databases from inception until Oct 1, 2015, for studies reporting risks of maternal dea

64 r studies published between Jan 1, 2005, and Oct 1, 2015.

65 The study was done between May 12, 2012, and Oct 1, 2015.

66 remaining nine intervention clusters between Oct 1, 2016 and March 31, 2016.

67 ubiquitously expressed transcription factor Oct-1, a member of the POU domain factors, is involved i

68 ound that SUMOylation regulates CSCs through Oct-1, a transcription factor for aldehyde dehydrogenase

69 Oct-1, a ubiquitous POU homeodomain transcription factor

70 nic fibroblasts, and reintroduction of human Oct-1 abolishes these differences.

71 Oct-1 activates transcription in part by helping recruit

72 A-induced activation of AP-1, NF-kappaB, and Oct-1 activities was severely diminished in BCBL1 cells

73 These results suggest that Oct-1 acts as a positive regulator of EBV lytic gene exp

74 Osteoblast-like cell lines 2T3 and Oct-1 also show increased expression of E11 with differe

75 The transcription factors Oct-1 and -2 inhibit and enhance, respectively, the expr

76 o form a complex with the POU domain protein Oct-1 and a VP16-responsive DNA sequence.

77 Site-directed mutations of both OCT-1 and CAAT motifs abrogate induction of the GADD45 p

78 Both OCT-1 and CAAT motifs are able to confer BRCA1 inducibil

79 Oct-1 and NF-YA proteins or mutations in the OCT-1 and CAAT motifs disrupt BRCA1 binding to the GADD4

80 the GADD45 promoter is mediated through the OCT-1 and CAAT motifs located at the GADD45 promoter reg

81 Site-directed mutations of both OCT-1 and CAAT motifs substantially abrogate the inducti

82 Oct-1 and NF-YA, which directly bind to the OCT-1 and CAAT motifs, are established by biotin-strepta

83 Oct-1 and CTCF bind their cognate sites cooperatively, a

84 a interchromosomal associations organized by Oct-1 and CTCF.

85 The binding of Rta to both Oct-1 and DNA contributes to the transactivation of the

86 ctivator VP16 acting with cellular cofactors Oct-1 and HCF-1.

87 protein 16 eliminate Rta's interactions with Oct-1 and K-bZIP promoter DNA but not RBP-Jk.

88 tive formation of a complex between Sox2 and Oct-1 and mediate Sox2/Oct-1-dependent transactivation o

89 increased dramatically when binding of both OCT-1 and NF-kappaB was abolished.

90 novel observation that transcription factors Oct-1 and NF-YA participate in the cellular response to

91 5 promoter because either immunodepletion of Oct-1 and NF-YA proteins or mutations in the OCT-1 and C

92 of BRCA1 protein with transcription factors Oct-1 and NF-YA, which directly bind to the OCT-1 and CA

93 Gene-targeting studies showed that Oct-1 and Oct-2 are largely dispensable for B-cell devel

94 Oct-1 and Oct-2 are members of the POU homeodomain famil

95 In MDA-MB-231 cells, both Oct-1 and Oct-2 bind the iNOS promoter, forming a higher

96 As Ig promoter-binding factors, Oct-1 and Oct-2 each work together with a B lymphocyte-s

97 The POU domain transcription factors Oct-1 and Oct-2 interact with the octamer element, a mot

98 Oct-1 and Oct-2 were recruited to the enhancer upon macr

99 nsient- and stable-transfection assays bound Oct-1 and Oct-2, both of which are expressed constitutiv

100 Both Oct-1 and Pit-1 bind the B29 3' enhancer in in vitro ele

101 type but not the mutant K-bZIP promoter, and Oct-1 and Rta proteins bind to each other directly in vi

102 Oct-1 and SNAPc bind cooperatively to DNA when their res

103 gion that recruits the transcription factors Oct-1 and Staf (ZNF143).

104 Both Oct-1 and the related but tissue-restricted Oct-2 protei

105 ted that BRCA1 binds to transcription factor OCT-1 and up-regulates the transcription of MAD2.

106 l factor-1 (HCF-1) functions in concert with Oct-1 and VP16 to assemble the herpes simplex virus (HSV

107 Between Oct 3, and March 30, 2012, and Oct 1, and March 29, 2013, we randomly assigned 308 infa

108 y, in resting human IgM+IgD+ B cells, HoxC4, Oct-1, and Ku70/Ku86 can be readily identified as bound

109 cription factors, the serum response factor, Oct-1, and myocyte enhancer factor-2, whereas the other

110 complex binding pattern formed by NF-kappaB, Oct-1, and Oct-2 (but not by Pax5).

111 es suggested a putative role for C/EBP-beta, OCT-1, and OCT-3 transcription factor binding sites in t

112 In this report, we used Oct-1 antisense transformants to determine that Oct-1 re

113 New DNA binding data for OCT-1 are presented.

114 a number of other proximal elements, but not OCT-1, are critical for basal as well as xanthotoxin- an

115 atter two, HCF-1 and octamer binding protein Oct-1, are transcriptional factors regulated in a cell c

116 de-3-phosphate dehydrogenase, and binding to Oct-1, as well as OCA-S function, is stimulated by NAD(+

117 Moreover, Pbx1 and Oct-1, as well as Prep1 and Oct-1, form functional compl

118 The presence of VP16 and Oct-1 at IE promoters did not depend on the activation d

119 Sequestration of Oct-1 at the nuclear periphery by lamin B1 may be a mech

120 The DRI OCT-1 Atlantis 3D SS OCT (Topcon Medical Systems, Oaklan

121 Furthermore, we show that cotransfected Oct-1 augments BRLF1 binding to a variety of lytic EBV p

122 ll nuclear extract had about 50% increase in Oct-1 binding activity suggesting that the increased U6

123 NOS promoter was identified as high-affinity Oct-1 binding by electrophoretic mobility shift assay in

124 of these experiments reveal that COUP-TF and Oct-1 binding does not play a functional role in Ad pack

125 ereas disrupting the predicted TATA boxes or Oct-1 binding elements had no effect.

126 Mutation of this OCT-1 binding motif resulted in a similar effect as the

127 orrelation between the p38 kinase levels and Oct-1 binding on U6 promoter, suggesting that U6 promote

128 iption in fibroblasts, while mutation of the Oct-1 binding site increased ORF63 reporter transcriptio

129 RHS6 and the IL-17 promoter both bear Oct-1 binding sites.

130 this loss of inducibility is attributable to Oct-1 binding to the HLA-DRA promoter.

131 Ethanol exposure significantly inhibited OCT-1 binding to the Slc7a11 promoter region, although i

132 e Slc7a11 promoter and that ethanol inhibits OCT-1 binding to the Slc7a11 promoter, thereby increasin

133 nt is stimulated by a peptide containing the Oct-1-binding domain of SNAP190.

134 is of PDRG promoter revealed the presence of Oct-1-binding element and a putative head-to-tail-type p

135 latory region, each in close proximity to an Oct-1-binding site.

136 In MCF-7 cells Oct-1 binds the iNOS promoter, recruits RNA PolII and tr

137 ity shift assay and chromatin IP reveal that Oct-1 binds to the putative octamer-binding sequences of

138 a third cellular protein, octamer-1 protein (Oct-1), binds to minimal packaging domains.

139 and microinjection studies demonstrate that Oct-1 blocks tumor necrosis factor alpha-stimulated E-se

140 The cellular protein Oct-1, but not Oct-2, binds to the K-bZIP element in a s

141 novel way, represses, whereas replacement of OCT-1 by p50-p65 induces CRP transcription in cooperatio

142 NA binding proteins, such as CSL/RBP-Jkappa, Oct-1, C/EBPalpha, and c-Jun.

143 n factors, including Sp1, AP2, CCAAT, Est-1, Oct-1, CNBP, and NFkB, but lacks a TATA box.

144 functionally characterized a multicomponent Oct-1 coactivator, OCA-S which is essential for S phase-

145 rategy has previously been shown to maintain Oct-1:cofactor interactions that are highly binding-site

146 a GT1-7 cDNA library to search for specific Oct-1 cofactors.

147 t transcription factors (TFs), NF-kappaB and OCT-1, comprises three steps: (i) optimized selection of

148 e, the enhanceosome contains c-Jun/c-Fos and OCT-1 constitutively.

149 trate that the cellular transcription factor Oct-1 cooperates with the EBV immediate-early protein BR

150 es are expressed after high moi infection of Oct-1-deficient cells, the assembly of viral replication

151 Oct-1-deficient embryos died during gestation, frequentl

152 of RAG-1(-/-) animals was reconstituted with Oct-1-deficient fetal liver hematopoietic cells.

153 fied a second group of genes dysregulated in Oct-1-deficient fibroblasts following irradiation, inclu

154 Consistent with this finding, Oct-1-deficient fibroblasts were hypersensitive to gamma

155 Here, HSV infection of Oct-1-deficient mouse embryonic fibroblast cells demonst

156 used to evaluate gene expression changes in Oct-1-deficient mouse fibroblasts.

157 To address the role of Oct-1 in vivo, an Oct-1-deficient mouse strain was generated by gene targe

158 endent gene expression is more pronounced in Oct-1-deficient than in wild-type murine embryonic fibro

159 We show that several Oct-1-dependent genes, including a subset involved in ox

160 plex between Sox2 and Oct-1 and mediate Sox2/Oct-1-dependent transactivation of the Pax6 lens ectoder

161 SUMO does not modify Oct-1 directly, but regulates the expression of TRIM21 t

162 ese embryos displayed a dramatic decrease in Oct-1 DNA binding activity and a lack of octamer-depende

163 These findings suggest a critical role for Oct-1 during development and a stringent gene dosage eff

164 the transcription start site, containing an Oct-1 element, was crucial for the PPARgamma ligand-medi

165 ity of a reporter plasmid driven by multiple Oct-1 elements.

166 yl 3-methylbutanoate, 3-methylbutyl acetate, oct-1-en-3-one, ethyl hexanoate, (Z)-hex-3-enyl acetate,

167 In this report, we identify Oct-1, encoded by the Pou2f1 gene, as a co-factor for So

168 yclic compound incorporating a bicyclo[4.2.0]oct-1-ene core, a portion of which is found in a number

169 is work identifies a far-upstream functional Oct-1 enhancer motif at -10.2 kb in the hiNOS promoter t

170 The coexpression of Oct-1 enhances Rta-mediated transactivation of the wild

171 We show that cotransfected Oct-1 enhances the ability of BRLF1 to activate lytic ge

172 The p38 component of OCA-S binds directly to Oct-1, exhibits potent transactivation potential, is sel

173 inally, we show that knockdown of endogenous Oct-1 expression reduces the level of constitutive lytic

174 Exogenous Oct-1 expression showed a concentration-dependent activa

175 quently lytic reactivation by competing with Oct-1 for the octamer motif in the ORF50 promoter.

176 reover, Pbx1 and Oct-1, as well as Prep1 and Oct-1, form functional complexes that enhance GnRH gene

177 Results from this study suggest that OCT-1 functions as a repressor on the Slc7a11 promoter a

178 s generated by alternative splicing from the Oct-1 gene and its transcript exhibits a frameshift foll

179 Finally, the cytokine interleukin-6 induces Oct-1 gene expression, providing a biologically relevant

180 Deletion of either of these sites or Oct-1 gene impairs the association.

181 te and equilibrium dissociation constant for Oct-1 > or = 5-fold and approximately 20-fold, respectiv

182 rus late in infection, and that the modified Oct-1 has a reduced affinity for its cognate DNA site.

183 Oct-1 has previously been shown to colocalize partly wit

184 and cells depleted of Oct-2 and its homolog Oct-1 have a reduced capacity to differentiate into neur

185 Multiple alternatively spliced isoforms of Oct-1 have been identified in human and mouse cells.

186 All of these factors (GR, c-Jun, OCT-1) have transcription activation domains, but STAT3

187 l signaling networks and signals through the Oct-1-HMGCL-acetoacetate axis to selectively promote BRA

188 We show here that the HoxC4 and Oct-1 homeodomain proteins together with the Ku70/Ku86 h

189 Nuclear OCT-1 immunoreactivity was seen in normal B cells, in ma

190 paired, revealing a second critical role for Oct-1 in HSV replication.

191 However, the role of Oct-1 in regulating hiNOS gene expression has not been r

192 We demonstrate that the expression of Oct-1 in the brain is regulated by Notch signaling and t

193 To study the role of Oct-1 in these processes, the lymphoid compartment of RA

194 attenuated for the ability to interact with Oct-1 in vitro is also resistant to Oct-1-mediated trans

195 To address the role of Oct-1 in vivo, an Oct-1-deficient mouse strain was gener

196 for octamer-binding transcription factor 1 (OCT-1) in the deleted fragment.

197 Overexpression of Oct-1 increased cytokine-induced hiNOS protein expressio

198 r HSF-1, NF-1, and octamer binding proteins (Oct-1) increased ORF62 reporter transcription in skin.

199 1-defective EBV mutant (BRLF1-stop) and that Oct-1 increases BRLF1-mediated activation of lytic EBV p

200 Indeed, UV as well as exogenous Oct-1 independently increased PDRG promoter activity, su

201 Our data suggest that the Rta/Oct-1 interaction is essential for optimal KSHV reactiva

202 merization interface are also used for OBF-1/Oct-1 interactions on the PORE.

203 We find that Oct-1 interacts directly with BRLF1 in vitro and that a

204 Biochemically, Oct-1 interacts with p65, suggesting that Oct-1 is invol

205 t with the Oct-1 POU domain through the same Oct-1 interface, a single nucleotide within the U1 octam

206 Together, Oct-1 is a downstream effector of Notch signaling during

207 inding activity of transcriptional repressor OCT-1 is a mechanism by which ethanol up-regulates Slc71

208 Oct-1 is a member of the POU family of transcription fac

209 Oct-1 is a sequence-specific DNA binding transcription f

210 embryonic fibroblast cells demonstrates that Oct-1 is critical for IE gene expression at low multipli

211 y, Oct-1 interacts with p65, suggesting that Oct-1 is involved in the regulation of NF-kappaB transac

212 Here we report that Oct-1 is posttranscriptionally modified late in infectio

213 Oct-1 is present in both cell lines but MDA-MB-231 also

214 uced, NF-kappaB-dependent gene expression by Oct-1 is promoter-specific.

215 ain is regulated by Notch signaling and that Oct-1 is sufficient and necessary for radial glia format

216 DNA sequence but fulfil distinct functions: Oct-1 is ubiquitous and regulates a variety of genes whi

217 The POU-domain transcription factor Oct-1 is widely expressed in adult tissues and has been

218 Oct-1Z is another ubiquitously expressed Oct-1 isoform, its transcript being detected in all mous

219 dy, we have cloned and sequenced a new mouse Oct-1 isoform, named mOct-1Z.

220 he C-terminus from the previously identified Oct-1 isoforms A, B, and C.

221 e suggested that the structural variation of Oct-1 isoforms may be important in conferring target and

222 CD40 signaling dissociates the HoxC4.Oct-1.Ku complex from the Igamma and Iepsilon promoter S

223 Dissociation of HoxC4.Oct-1.Ku from DNA is hampered by CD153 engagement, a CD4

224 Thus, these findings outline a HoxC4.Oct-1.Ku-dependent mechanism of selective regulation of

225 scence resonance energy transfer, we confirm Oct-1-lamin B1 association at the nuclear periphery and

226 MGCL through an octamer transcription factor Oct-1, leading to increased intracellular levels of HMGC

227 rest in VSMCs, at least in part, by inducing Oct-1-mediated transcription of GADD45.

228 act with Oct-1 in vitro is also resistant to Oct-1-mediated transcriptional enhancement in 293 BRLF1-

229 These results indicate that Oct-1 modulates the activity of genes important for the

230 h complete vitreomacular traction release on OCT 1 month following treatment.

231 Mutation of Oct-1 motif at -10.2 kb in the hiNOS promoter decreased

232 Furthermore, the Oct-1 motif at -10.2 kb of the hiNOS promoter conferred

233 could still effectively bind to a consensus Oct-1 motif oligonucleotide and, like Oct-1B, activated

234 1 promoter region, although it did not alter OCT-1 mRNA and protein levels.

235 In addition, we demonstrate that an Oct-1 mutant defective in DNA binding (the S335D mutant)

236 We found constitutive binding of Oct-1, NFAT species, YY1, NF-kappaB-p52, Pax5, E2A, and

237 on, as well as for iNOS promoter activation, Oct-1 nuclear binding capacity, and Oct-1 protein conten

238 n immunoprecipitation assay, indicating that Oct-1 occupies the endogenous HLA-DRA promoter when the

239 Decreased expression of Oct-1, Oct-2, or Bob-1 by RNA interference resulted in a

240 LANA-1 promoter in 293 cells, and YY1, Sp1, Oct-1, Oct-6, C/EBP, and c-Jun transcription factors see

241 driven transcription as induced by HoxC4 and Oct-1/Oct-2 suggests an important role of these homeodom

242 HoxC4, Oct-1/Oct-2, and Oca-B recruitment is negligible in pro-

243 These two sites recruit HoxC4 and Oct-1/Oct-2, which act synergistically with the Oca-B co

244 lement to the aryl hydrocarbon receptor) and OCT-1 (octamer-1 binding site) element known to be utili

245 from Sp1 on the C allele to SP1, GATA-1, and OCT-1 on the G allele.

246 CF-1 and the POU domain transcription factor Oct-1, on TAATGARAT-containing sequences found in the pr

247 w that BRD7 is present, along with BRCA1 and Oct-1, on the ESR1 promoter (the gene which encodes ERal

248 This octamer element can be bound by either Oct-1 or Oct-2 but requires the expression of Oct-2 to a

249 -specific differences in the requirement for Oct-1 or RBP-Jk in Rta-mediated transactivation of the K

250 istant homology to the transcription factors Oct-1, Pit-1, and POU-M1.

251 ents are found to be actually reached by the Oct-1 POU domain and lambda repressor.

252 singly, binding of a transcriptionally inert Oct-1 POU domain near a core promoter enables an enhance

253 ugh SNAP190 and OCA-B both interact with the Oct-1 POU domain through the same Oct-1 interface, a sin

254 The U1 octamer only weakly recruits the Oct-1 POU domain, although recruitment is stimulated by

255 Structural analysis of the Oct-1 POU domain/U1 octamer/SNAP190 peptide complex reve

256 90 makes extensive protein contacts with the Oct-1 POU-specific domain and with the DNA phosphate bac

257 Oct-1 (POU2f1) and Oct-2 (POU2f2) are members of the POU

258 Moreover, we have identified Oct-1 (POU2f1), a POU transcription factor, as a downstr

259 DNA-protein binding analyses indicated that Oct-1 prevents HLA-DRA promoter activation by mediating

260 Oct-1 protein belongs to the Pit-Oct-Unc domain transcri

261 ivation, Oct-1 nuclear binding capacity, and Oct-1 protein content by transient transfection, electro

262 PPARgamma activation induced Oct-1 protein expression and DNA binding and stimulated

263 Thus, the Oct-1 protein is dispensable for B cell development and

264 Recruitment of Oct-1 protein to the octamer sequence of U6 promoter is

265 ive binding of YY1, NF-kappaB-p52, Pax5, and Oct-1 proteins to CD21 sequences in B cells but no speci

266 onding direct transfers of the HoxD9 and the Oct-1 proteins, although the affinities of the three pro

267 components of previously characterized OPT (Oct-1, PTF, transcription) domains.

268 ations between TALE homeodomain proteins and Oct-1 regulate neuron-specific expression of the GnRH ge

269 ally important binding sites for GATA-1- and Oct-1-related proteins.

270 OCT-1 reportedly functions as either a transcriptional e

271 A DNA-binding mutant of Oct-1 represses NF-kappaB-dependent reporter gene expres

272 ort that the POU domain transcription factor Oct-1 represses the expression of E-selectin and vascula

273 -1 antisense transformants to determine that Oct-1 represses the interferon-gamma response of the end

274 ction with OBF-1 is precluded since the same Oct-1 residues that form the MORE dimerization interface

275 endogenous genes thought to be regulated by Oct-1 showed no change in expression.

276 R-146a promoter and identified a role for an Oct-1 site in conferring basal and induced expression.

277 Mutational analysis of the Oct-1 sites abolished RTA-mediated transcriptional activ

278 r activity was also significantly reduced by Oct-1 small interfering RNA targeting.

279 Oct-1, Sox2, and Pax6 are co-expressed during lens and n

280 1 ubiquitination and, consequently, reducing Oct-1 stability.

281 A version of Oct-1 that encompasses the amino-terminal activation reg

282 lex contains the cellular POU domain protein Oct-1, the viral transactivator VP16, and the cellular c

283 follow-up examination to have resolved on SD OCT 1 to 4 months later.

284 F1, and SM promoters) and that BRLF1 tethers Oct-1 to lytic EBV promoters.

285 ne expression can be selectively reverted by Oct-1 to quiescent levels.

286 is mediated by its recruitment of BRCA1 and Oct-1 to the ESR1 promoter.

287 BRD7 prevented the recruitment of BRCA1 and Oct-1 to the ESR1 promoter; however, it had no effect on

288 The binding of Oct-1 to the ORF50 promoter has been shown to significan

289 EMSA lead us to conclude that the binding of OCT-1 to the promoter, facilitated by p50-p50 in a novel

290 n in mammalian cells is codependent upon the Oct-1 transcription factor and its cognate, OCA-S coacti

291 e 3'-untranslated region disrupts a putative Oct-1 transcription factor binding site, when inserted 3

292 e promoter sequence revealed the presence of Oct-1 transcription factor binding sites within the -116

293 ential binding sites for the AP-1, AP-2, and OCT-1 transcription factors and the absence of TATA and

294 ent with the hypothesis that modification of Oct-1 transcriptional factor could account at least in p

295 rn of CLP-1 is similar to that of LCR-F1 and Oct-1, two widely expressed transcription factors that a

296 lates the expression of TRIM21 that enhances Oct-1 ubiquitination and, consequently, reducing Oct-1 s

297 Of note, endogenous Oct-1 was preferentially recruited to the IL13-1512C ris

298 Oct-1 was previously determined to be critical but not e

299 genes by activating the transcription factor Oct-1, while p53 has been reported to suppress transcrip

300 cule bis((4-(4-pyridyl)ethynyl)bicyclo[2.2.2]oct-1-yl)buta-1,3-diyne, 1, contains two 1,4-bis(ethynyl