ライフサイエンスコーパス: Oct-1

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

2 quisitely dependent on physiologic levels of Oct-1.

3 the multidomain transcription factor, human Oct-1.

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

5 eral cellular DNA binding proteins including Oct-1.

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

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

8 a coactivator with the transcription factor Oct-1.

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

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

11 ion factor that specifically associates with Oct-1.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

28 02, to Sept 30, 2004) versus after (phase 2: Oct 1, 2004, to March 31, 2007) study of the effect of e

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

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

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

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

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

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

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

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

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

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

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

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

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

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

43 cipants recruited between April 4, 2006, and Oct 1, 2010, of which 5391 participants had COPD with a

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 11 993 PWID

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

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

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

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

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

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

53 334 participants were enrolled between Oct 1, 2013, and March 8, 2018, when the study was close

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

55 done in 30 communities across Botswana from Oct 1, 2013, to June 30, 2018.

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

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

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

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

60 Between Oct 1, 2014, and Dec 31, 2018, of 2819 children recruite

61 .71 years, IQR 2.46-6.35) were enrolled from Oct 1, 2014, to Dec 2, 2015.

62 ealth-care facilities throughout Bukoba from Oct 1, 2014, to March 31, 2017, when national ART-eligib

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

64 m CD4 counts of less than 350 cells per muL (Oct 1, 2014-Dec 31, 2015) and 500 or less cells per muL

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

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

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

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

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

70 the smoke-free private vehicle regulation on Oct 1, 2015.

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

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

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

74 Between Nov 12, 2012, and Oct 1, 2016, 334 patients were recruited (166 in the cis

75 Between Oct 1, 2016, and April 30, 2019, 20 facilities were rand

76 Between Sept 1, 2014, and Oct 1, 2016, we randomly assigned 226 patients; 112 to V

77 2016) to any CD4 cell count (test and treat, Oct 1, 2016-March 31, 2017).

78 Between Oct 1, 2017, and Aug 9, 2018, we analysed 7.8 million si

79 Between April 15, 2014, and Oct 1, 2017, we enrolled 323 women, of whom 234 had peri

80 At data cutoff (Oct 1, 2018), after a median follow-up of 11.0 months (I

81 Between July 7, 2014, and Oct 1, 2018, 81 eligible patients were enrolled and rand

82 eved spontaneous HBsAg loss, published up to Oct 1, 2018.

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

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

85 Oct-1, a ubiquitous POU homeodomain transcription factor

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

87 Oct-1 activates transcription in part by helping recruit

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

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

90 Between Oct 1 and Nov 12, 2018, 1152 mother-child dyads were enr

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

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

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

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

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

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

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

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

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

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

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

102 5 promoter because either immunodepletion of Oct-1 and NF-YA proteins or mutations in the OCT-1 and C

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

182 Moreover, POU2F1/Oct-1 expression was induced during KSHV reactivation, a

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

207 1-defective EBV mutant (BRLF1-stop) and that Oct-1 increases BRLF1-mediated activation of lytic EBV p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

241 1 promoter region, although it did not alter OCT-1 mRNA and protein levels.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

272 OCT-1 reportedly functions as either a transcriptional e

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

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

275 -1 antisense transformants to determine that Oct-1 represses the interferon-gamma response of the end

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

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

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

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

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

281 1 ubiquitination and, consequently, reducing Oct-1 stability.

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

294 ined using a Topcon swept-source system (DRI OCT-1 Triton, Topcon, Tokyo, Japan).

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