ライフサイエンスコーパス: TCF

1 TCF transcription induces epithelial-mesenchymal transit

2 TCF usually activates transcription on cis-regulatory el

3 TCF-1 acted through both GATA-3-dependent and GATA-3-ind

4 TCF-1 has been recently shown to critically regulate mem

5 TCF-1 is highly expressed in the earliest thymic progeni

6 TCF-1 thus has dual roles, i.e., acting cooperatively wi

7 TCF-1 was intrinsically required for the differentiation

8 TCF/LEF factors are ancient context-dependent enhancer-b

9 t ILC2 development required T cell factor 1 (TCF-1, the product of the Tcf7 gene), a transcription fa

10 study, we demonstrate that T cell factor 1 (TCF-1; encoded by Tcf7), a transcription factor also imp

11 ression of CD27, CXCR3, and T cell factor-1 (TCF-1), each a marker that is individually correlated wi

12 l factor/lymphoid enhancer binding factor-1 (TCF/LEF) motifs, consistent with canonical Wnt target re

13 , including posterior pharynx defect (POP-1)/TCF, APC related/adenomatosis polyposis coli (APR-1)/APC

14 pha-catenin binds with beta-catenin to LEF-1/TCF DNA-binding proteins in Wnt3a signaling cells and re

15 a-catenin but displayed high levels of LEF-1/TCF genes along with elevated levels of beta-catenin (LE

16 with elevated levels of beta-catenin (LEF-1/TCF target genes) responsive genes.

17 aluated: 4-6 of 6 matched dUCB-TCF (n = 120; TCF = total body irradiation [TBI] 200 cGy + cyclophosph

18 through formation of the beta-catenin-TCF-3/TCF-4/LEF-1 complex on the NR4A1 promoter.

19 analysis suggested that the T cell factor-4 (TCF-4E) transcription factor is responsible for HCV core

20 IP-seq and Hi-C data, we identified over 700 TCF-dependent SRF direct target genes involved in signal

21 A TCF/LEF luciferase assay was used to study functional ca

22 adherin in MM cells, but does not activate a TCF reporter or up regulate expression of canonical Wnt

23 utant DDX3X potentiates transactivation of a TCF promoter and enhances cell viability in combination

24 11A) reduced the ability of Dvl3 to activate TCF/LEF (T-cell factor/lymphoid enhancer factor)-driven

25 ocytes increases proliferation and activates TCF transcriptional activity.

26 was stimulated by Wnt3A, thereby activating TCF-mediated transcription and driving malignant invasiv

27 t, in the absence of Wnt pathway activation, TCF activates ttx-3 expression via a Zic binding site by

28 LEF-1 and TCF-1 coordinated such differentiation by two general me

29 model where Notch signals induce TCF-1, and TCF-1 in turn imprints the T-cell fate by upregulating e

30 tivating transcription of c-Jun-, ATF2-, and TCF-controlled genes.

31 Cxcr5 expression and, together with Bcl6 and TCF-1, formed a transcriptional circuit that guided TFC

32 of the transcription factors SMAD (BMP) and TCF (Wnt).

33 Inhibitor of beta-catenin and TCF (ICAT) inhibits beta-catenin transcriptional activit

34 ing the interaction between beta-catenin and TCF-1.

35 tes the interaction between beta-catenin and TCF-1.

36 The interaction between beta-catenin and TCF-4 is linked to inhibition of HIV replication in mult

37 ired the transcription factors Bcl6, E2A and TCF-1 but was inhibited by the transcriptional regulator

38 e transcription factors RORalpha, GATA3, and TCF-1 and produce the type 2 cytokines IL-4, IL-5, IL-9,

39 le and cell proliferation/survival genes and TCF/LEF targets.

40 Two vertebrate TCFs (TCF-1/TCF7 and TCF-4/TCF7L2) use the C-clamp as an alternatively splice

41 bling beta-catenin nuclear translocation and TCF/LEF-dependent gene transactivation.

42 gnificant decrease in intracellular WNT1 and TCF-4 proteins revealing novel Wnt-regulatory mechanisms

43 Thus, c-Jun, ATF2, and TCFs are required to connect the intracellular signaling

44 bd1 functionally interact with the Armadillo-TCF complex and mediate the same context-dependent Wingl

45 and beta-catenin-dependent signals, such as TCF-mediated transcription.

46 t the expression of exogenous ZMIZ2 augments TCF (T cell factor) and beta-catenin-mediated transcript

47 Thus, competition between TCFs and MRTFs for SRF determines the balance between an

48 marine alkaloid neoamphimedine (neo), block TCF activity in vitro and in vivo.

49 Most induced changes were TCF dependent, but TCF-independent TSSs exhibited the same hierarchy, indic

50 display an opposite regulation (activated by TCF in the absence of Wnt), but the mechanism behind thi

51 f beta-catenin, target genes are silenced by TCF-mediated recruitment of TLE/Groucho proteins, but th

52 s in a manner that is downstream of beta-cat/TCF loading on promoters.

53 signaling pathway and its effector beta-cat/TCF serve a beneficial role in suppressing hepatic gluco

54 In the absence of nuclear beta-catenin, TCF proteins act as transcriptional repressors by bindin

55 nalling responses by modulating beta-catenin-TCF activity.

56 ession through formation of the beta-catenin-TCF-3/TCF-4/LEF-1 complex on the NR4A1 promoter.

57 val from TCF/Lef, thus allowing beta-catenin-TCF/Lef complex assembly and initiation of a Wnt-specifi

58 for uPAR (pU) suppressed WNT-7a-beta-catenin-TCF/LEF-mediated transactivation both in vitro and in vi

59 eatment led to increased WNT-7a-beta-catenin-TCF/LEF-mediated transactivation, thereby promoting canc

60 r, association of uPAR with the beta-catenin.TCF/LEF complex and various other TF involved during emb

61 n organization, and stimulating beta-catenin/TCF and activating protein 1 transcription.

62 tream transcriptional target of beta-catenin/TCF and has a key contributing role in the cancer phenot

63 ted it with the activity of the beta-catenin/TCF complex.

64 t transcriptional target of the beta-catenin/TCF complex; its expression was higher in human intestin

65 beta-Catenin/TCF complexes bind Wnt responsive DNA elements (WREs) to

66 ene (MYC) is a direct target of beta-catenin/TCF complexes.

67 sulted in reduced expression of beta-catenin/TCF downstream targets Survivin and myc.

68 ta-catenin gene, activating the beta-catenin/TCF pathway.

69 of both inducing and repressing beta-catenin/TCF signaling in vivo, depending on the time and site of

70 Wnt/beta-catenin/TCF signaling stimulates bone formation and suppresses a

71 1, which acts as a repressor of beta-catenin/TCF transcriptional activity.

72 le of the mediator complex with beta-catenin/TCF transcriptional complex, and by CDK8 interacting wit

73 d EBP50 stabilized conventional beta-catenin/TCF-1 complexes and connected beta-catenin to dnTCF-1 to

74 Knockdown of beta-catenin/TCF-4 also impacted tethering of other transcription fac

75 indicate that modulation of the beta-catenin/TCF-4 axis impacts the basal level of HIV transcription

76 e the mechanism by which active beta-catenin/TCF-4 leads to inhibition of HIV replication, we knocked

77 he molecular mechanism by which beta-catenin/TCF-4 repress HIV replication.

78 Active Wnt/beta-catenin/TCF-4 signaling plays a significant role in repression o

79 ity to repress transcription of beta-catenin/TCF-dependent genes, as well as activation of E2F1-depen

80 cadherin expression and induced beta-catenin/TCF-dependent transcription of uPAR and c-Myc.

81 To directly examine the role of beta-catenin/TCF-dependent transcription, we developed synthetic cell

82 ated by the tonic activation of beta-catenin/TCF-dependent transcription.

83 atenin-LC3 complex, attenuating beta-catenin/TCF-driven transcription and proliferation to favour ada

84 udies support the role of SATB2/beta-catenin/TCF-LEF pathway in transformation and carcinogenesis.

85 Finally, beta-catenin/TCF-LEF pathway mediated the biological effects of SATB2

86 te that loss of Osr1 results in beta-catenin/TCF-mediated ectopic activation of Wnt4 enhancer-driven

87 ponses, that is, suppresses the beta-catenin/TCF/LEF pathway and tumorigenesis, but enhances PI3K-Akt

88 Mechanistically, we show that beta-Catenin/TCF/LEF-1 binds to the promoter of miR-183-96-182 cluste

89 R-183-96-182 biogenesis through beta-Catenin/TCF/LEF-1 pathway in gastric cancer cells.

90 multiple pathways including the beta-Catenin/TCF/LEF-1 pathway.

91 miR-182 and miR-183 through the beta-Catenin/TCF/LEF-1 pathway.

92 iption on cis-regulatory elements containing TCF binding sites when the pathway is active and repress

93 7L1, a Wnt pathway repressor, buffers CTNNB1/TCF target gene expression to promote CRC growth.

94 We identified a group of CTNNB1/TCF target genes that are activated in the absence of TC

95 d the activity of the beta-catenin-dependent TCF/LEF promoter.

96 size a critical role for Wnt/HIPK2-dependent TCF phosphorylation and suggest that TCF switching is an

97 Neo inhibition of TopoIIalpha-dependent TCF transcription also correlates with significant antit

98 ffective at preventing TopoIIalpha-dependent TCF transcription.

99 ein kinase 2) in the regulation of different TCF proteins in Xenopus embryos in vivo.

100 Analysis of direct TCF-SRF target genes and chromatin modifiers confirmed t

101 the 3'-UTRs of arm and pangolin (Drosophila TCF) in vivo.

102 nd overall mortality were similar after dUCB-TCF (relative risk [RR] 0.72, P = .72; RR 0.93, P = .60)

103 not overall mortality) was lower after dUCB-TCF (RR 0.57, P = .04; RR 0.87 P = .41).

104 The probabilities of survival after dUCB-TCF, dUCB-other RIC, and 8 of 8 PBPC and 7 of 8 PBPC tra

105 after 8 of 8, 7 of 8 matched PBPCs, and dUCB-TCF, these data support use of dUCB-TCF transplantation

106 groups were evaluated: 4-6 of 6 matched dUCB-TCF (n = 120; TCF = total body irradiation [TBI] 200 cGy

107 and dUCB-TCF, these data support use of dUCB-TCF transplantation in adults with acute leukemia who ma

108 oning as a coactivator for the Wnt effector, TCF/LEF protein.

109 beta-catenin level in the cells and enhanced TCF/LEF1 luciferase reporter activity, which could be pa

110 h TCF proteins, Osr1, but not Six2, enhances TCF interaction with the Groucho family transcriptional

111 or E-twenty six/ternary complex factors (Ets/TCF), affected 65.4% of the tumors, with even distributi

112 We show that the transcription factor TCF-1 is required for the efficient generation of all kn

113 the long isoform of the transcription factor TCF-1.

114 TCF7L2 codes for the transcription factor TCF/LF, part of the Wnt canonical pathway, and is one of

115 h beta-catenin (beta-cat) and T-cell factor (TCF) and that the nuclear accumulation of alpha-cat depe

116 ctivation of the beta-catenin/T-cell factor (TCF) complex occurs in most colon tumors, and its action

117 ssociates with members of the T-cell factor (TCF) family of transcription factors.

118 mphoid-enhancing factor (LEF)/T-cell factor (TCF) family, only TCF4 showed more effective stimulation

119 llo: the outcome is to oppose T-cell factor (TCF) function and Wg/Wnt pathway signaling in both fly a

120 hway transcriptional effector T cell factor (TCF) in an estrogen receptor (ER) dependent way.

121 enzymes via the beta-catenin/T-cell factor (TCF) pathway in DCs.

122 anscriptional coactivator for T-cell factor (TCF) proteins, the downstream transcriptional regulators

123 n be assessed using different T-cell factor (TCF) reporter assays as a readout for Wnt/beta-catenin-d

124 nd activation of beta-catenin/T-cell factor (TCF) signaling.

125 with the transcription factor T cell factor (TCF) to transactivate gene expression.

126 Aberrant T-cell factor (TCF) transcription is implicated in the majority of colo

127 press beta-catenin levels and T-cell factor (TCF) transcriptional activity in colon tumor cells.

128 Foxm1 decreased T-cell factor (TCF) transcriptional activity induced by activated beta-

129 n in cell adhesion and as the T-cell factor (TCF) transcriptional coactivator in canonical Wnt (wingl

130 e transcriptional activity of T cell factor (TCF), which is required for EMT to proceed.

131 tion of transcription factors T cell factor (TCF)-1 and beta-catenin regulate the frequency of promye

132 T cell factor (TCF)-1 and lymphoid enhancer-binding factor (LEF)-1 tran

133 CNQ1 promoter by beta-catenin:T-cell factor (TCF)-4.

134 beta-catenin participation in T cell factor (TCF)-mediated transcription.

135 partners with members of the T cell factor (TCF)/LEF transcription factors to regulate gene expressi

136 gative mutant of the ternary complex factor (TCF) Elk-1 attenuated the upregulation of AP-1 following

137 ding T-cell factor/lymphoid enhancer factor (TCF/LEF) family proteins.

138 T cell factor/lymphoid enhancer factor (TCF/LEF) transcription factors are downstream effectors

139 and T-cell factor/lymphoid enhancing factor (TCF/LEF).

140 directional actions of transcription factor (TCF) molecules and other complexities of the Wnt pathway

141 KK1 promoter through a transcription factor (TCF) response element site.

142 athways by binding the transcription factors TCF and CHOP, disrupting their interaction with the comm

143 The transcription factors TCF-1 and LEF-1 are essential for early T cell developme

144 responsive enhancers through T cell factors (TCF) and kept silent by Groucho/TLE co-repressors.

145 The ERK-regulated ternary complex factors (TCFs) act with the transcription factor serum response f

146 yocardin family and ternary complex factors (TCFs), respectively.

147 The ternary complex factors (TCFs; Elk1, Net, and Sap-1) are growth factor-responsive

148 Transparent conducting films (TCFs) are a critical component in many personal electron

149 e synthesis of transparent conductive films (TCFs) by exploiting the coffee-ring effect deposition co

150 study reveals an atypical mode of action for TCF that may apply to other binary decisions mediated by

151 Whereas CD8+ effectors deficient for TCF-1 and LEF-1 retained the capacity to express IFN-gam

152 ngs demonstrate an essential requirement for TCF-1 in ILC2 differentiation and reveal a link among Tc

153 ad decreased survival, suggesting a role for TCF-1 in promoting survival in the nonlymphoid tissues.

154 The complete spectra of regulatory roles for TCF-1 and LEF-1 in CD8+ T cell responses are yet unknown

155 dification decreases affinity of Gro/TLE for TCF/Lef.

156 competition between beta-catenin and TLE for TCFs as part of an activation-repression switch.

157 with a temperature coefficient of frequency (TCF) -6 ppm/ degrees C, a permittivity 28.9, and Qf va

158 ng and temperature coefficient of frequency (TCF) of -67 ppm/K are obtained using this shear mode.

159 nin signaling by diverting beta-catenin from TCF- to FOXO-mediated transcription.

160 of Gro/TLE that facilitates its removal from TCF/Lef, thus allowing beta-catenin-TCF/Lef complex asse

161 tion of the thermodynamic coupling function (TCF) formalism and Markov state model analysis to a 50-m

162 Novel functional TCF/LEF1 binding sites in the promoter regions of fibron

163 Several reports now reveal how TCF-1 and GATA-3 are mobilized in early T cells and the

164 ChIP identified TCF DNA binding sites in the ZNF148 promoter through whi

165 ymocytes, we demonstrated that deficiency in TCF-1 and LEF-1 diminished the output of CD4(+) T cells

166 oteolytic processing causing the increase in TCF/LEF promoter activity.

167 milarly, WNT3a enhanced luciferase levels in TCF/LEF luciferase assays, which also were blocked by sF

168 we propose that TopoIIalpha participation in TCF transcription may convey a mechanism of MDR to conve

169 +) ILC3 showed a dose-dependent reduction in TCF-1 expression.

170 This switch in TCF promoter binding was regulated by an adhesion-mediat

171 Microarray studies confirmed this switch in TCF regulation of proliferative genes and uncovered nove

172 ion of p-beta-catenin (Tyr654) and increased TCF/LEF-mediated transcription.

173 rter mice and transfection of an independent TCF/Lef reporter construct, we describe the pattern of c

174 a suggest a model where Notch signals induce TCF-1, and TCF-1 in turn imprints the T-cell fate by upr

175 Inhibition of beta-catenin-induced TCF/LEF transcription in the nucleus of HBMECs prevented

176 tially augmented GSK3beta inhibition-induced TCF-reporter luciferase expression, suggesting dual regu

177 ed that ZMIZ2 can enhance Wnt ligand-induced TCF/beta-catenin-mediated transcription.

178 entiviral shRNAi knockdown of PTPRZ1 induced TCF-mediated transcription and substantially augmented G

179 The regulatory role of Zmiz2 in Wnt-induced TCF/beta-catenin-mediated transcription can be restored

180 progression, but how the C-clamp influences TCF binding and activity genome-wide is not known.

181 CH-mediated downregulation of WBP2 inhibited TCF/beta-catenin transcription, in vitro transformation,

182 Instead, TCF-1 physically interacted with Runx3 to cooperatively

183 nase complex to the nucleus, the site of its TCF substrate.

184 phase, the Ag-specific CD8+ T cells lacking TCF-1 and LEF-1 exhibited an effector phenotype and were

185 ymphoid enhancer factor 1/T cell factor (LEF/TCF) family of transcription factors are downstream effe

186 e now demonstrate that TGF-beta1 induces LEF/TCF TOPFLASH reporter activation and nuclear beta-cateni

187 interacts directly with region-specific LEF/TCF factors, and with KLF4 in differentiating, but not p

188 However, it does not stimulate LEF/TCF, c-Myc or CCND1, and it does not accelerate G1/S cel

189 LEF/TCFs direct the final step in Wnt/beta-catenin signallin

190 LEF/TCFs have a DNA sequence-specific high-mobility group (H

191 on and proliferation and reveal a novel MAPK/TCF transcriptional switch that controls this process.

192 We show that, in MEFs, TCF inactivation significantly inhibits over 60% of TPA-

193 ion of muscle-specifying genes by modulating TCF and beta-catenin levels.

194 We identified for the first time multiple TCF-4 binding sites at -336, -143, +66, and +186 relativ

195 ogenitors (EILPs) expressing high amounts of TCF-1.

196 CD8+ T cells in the peritoneal cavity of TCF-1-deficient mice had decreased survival, suggesting

197 pha (TopoIIalpha) as a required component of TCF transcription promoting EMT.

198 key event in Wnt signaling is conversion of TCF/Lef from a transcriptional repressor to an activator

199 and by combination with germline deletion of TCF-1, we found that loss of both factors completely abr

200 nd involving tissue-specific derepression of TCF by Lbx2.

201 on specifically represses the enhancement of TCF/beta-catenin-mediated transcription by ZMIZ2.

202 Forced expression of TCF-1 in bone marrow progenitors partially bypassed the

203 maintains a balance between the two forms of TCF-1 is unclear.

204 REs) and promoters of direct target genes of TCF transcription, including: MYC, vimentin, AXIN2 and L

205 program begins earlier with the induction of TCF-1 (Tcf7 gene product) and GATA-3.

206 es a new strategy for targeted inhibition of TCF transcription that may lead to effective therapies f

207 Specifically, knockdown of TCF-4 enhanced binding of C/EBPbeta, C/EBPdelta, and NF-

208 Furthermore, loss of TCF-1 and LEF-1 unexpectedly caused derepression of CD4

209 Loss of TCF-1 expression impaired the capacity of these ILC subs

210 ation of beta-catenin and subsequent loss of TCF/LEF (T cell factor1/lymphoid enhancer factor1) activ

211 that differences in repression potential of TCF/LEFs correlates with their affinities for TLE-Q, rat

212 The role of TCF-1 and LEF-1 in the CD4-versus-CD8 lineage 'choice' w

213 This study aimed to investigate the role of TCF/LEF transcription factors in human articular chondro

214 lts are reminiscent of the critical roles of TCF-1 in early T cell development.

215 Our results suggest that upregulation of TCF-1 expression denotes the earliest stage of ILC fate

216 The "E tail" isoforms of TCFs are alternatively spliced to include a second DNA b

217 Thus, C-clamp containing isoforms of TCFs are potent transcriptional regulators with an expan

218 tes that ChiLS confers context-dependence on TCF/LEF by integrating multiple inputs from lineage and

219 early locus 'poising' function dependent on TCF-1 and GATA-3, a stochastic-permissivity function dep

220 Moreover, enhancement of Zmiz2 on TCF/beta-catenin-mediated transcription was further demo

221 ich encode the transcription factor LEF-1 or TCF-1, respectively) resulted in T(FH) cell defects, whi

222 signaling components, beta-cat/armadillo or TCF/pangolin, had relatively milder effects on cardiac f

223 Furthermore, knockdown of beta-catenin or TCF-4 enhanced docking of Tat at the TAR region of the H

224 Knockdown of either beta-catenin or TCF-4 induced LTR activity by 2- to 3-fold under both th

225 of -143, in conjunction with beta-catenin or TCF-4 knockdown in cells stably expressing an LTR report

226 replication, we knocked down beta-catenin or TCF/LEF members in primary astrocytes and astrocytomas t

227 Our TCF approach reveals a complex landscape of thermodynami

228 As a result, TCF-deficient MEFs exhibit hypercontractile and pro-inva

229 ns with Notch signaling, and roles of Runx1, TCF-1, and Hes1, providing bases for a comprehensively u

230 Specific TCF/LEF1 binding sites within the promoter and intron 1

231 uring mammalian nephrogenesis by stabilizing TCF-Groucho transcriptional repressor complexes to antag

232 y, we first identify Socs1, Socs3, and Tcf7 (TCF-1) as gene targets that are negatively regulated by

233 act ILC or NK cell development, GATA3, TCF7 (TCF-1), AHR, SOX4, RUNX2, and ZEB1 transcript levels are

234 Two vertebrate TCFs (TCF-1/TCF7 and TCF-4/TCF7L2) use the C-clamp as an alter

235 We further demonstrated that TCF-1 directly repressed LEF-1 expression in early thymo

236 Therefore, our data demonstrated that TCF-1 enhances DP thymocyte survival through transcripti

237 Unexpectedly, we found that TCF-1-deficient (Tcf7(-/-)) mice developed aggressive T

238 We also found that TCF-4, beta-catenin, and the nuclear matrix binding prot

239 Collectively, these data indicate that TCF-4 and beta-catenin at -143 associate with SMAR1, whi

240 er, which is a new discovery indicating that TCF transcription may directly regulate N-cadherin expre

241 We also showed that TCF-1 and LEF-1 were dispensable for T cell lineage comm

242 Studies with TCF Elk-1 mutants showed that TCF-dependent ERK-induced histone modifications required

243 pendent TCF phosphorylation and suggest that TCF switching is an important mechanism of Wnt target ge

244 The TCF homolog POP-1 binds a site in the egl-18 promoter in

245 The TCF-1 and LEF-1 transcription factors are known to play

246 cellular signal-regulated kinase 1/2 and the TCF Elk-1, resulting in a reduced VSMC dedifferentiation

247 enes, including TRIB2, is coordinated by the TCF and FoxA transcription factors in liver cancer cells

248 These patterns are regulated in part by the TCF-LEF transcription factor POP-1.

249 Our results highlight the power of the TCF analysis to elucidate the molecular mechanism of com

250 Transcription factors of the TCF family are key mediators of the Wnt/beta-catenin pat

251 tor of this pathway, binds to members of the TCF/LEF family of transcription factors to modulate hund

252 tein binding by transcription factors of the TCF/LEF family were observed for the risk-increasing all

253 F3 (also known as TCF7L1) is a member of the TCF/LEF transcription factor family that is central in r

254 h binds the most proximal DKK1 promoter, the TCF response element.

255 ylated histone H4 tails, suggesting that the TCF/TLE tetramer complex promotes structural transitions

256 The TCFs act as general antagonists of MRTF-dependent SRF ta

257 These data demonstrate a key role for the TCFs in adhesion-induced transcription and proliferation

258 Further characterization of these TCF-1-induced cells revealed expression of many T-lineag

259 the Pygo chromatin reader and acting through TCF/LEF-responsive enhancers.

260 Thus, TCF-1 and LEF-1 adopted distinct genetic 'wiring' to pro

261 Thus, TCF-1 and LEF-1 cooperatively regulate generation of mem

262 ho proteins, but the molecular basis for TLE/TCF-dependent repression is unclear.

263 acting as a transcriptional co-activator to TCF, yet without affecting its stability.

264 Although all four sites could bind to TCF-4, the strongest association occurred at -143.

265 beta-catenin mutants incapable of binding to TCF/LEF increased BACE1 gene promoter activity.

266 Wnt-activated beta-catenin binds to TCF to overcome this repression, but how it achieves thi

267 Wnt pathway activation, XIAP is recruited to TCF/Lef where it monoubiquitylates Groucho (Gro)/TLE.

268 ment that apposes the BCL9/B9L C-terminus to TCF.

269 terfering with the binding of Groucho/TLE to TCF, thereby preventing formation of transcription repre

270 mediate repression, even though they bind to TCFs with the same affinity as tetramers.

271 1 that mediates tetramerization and binds to TCFs.

272 -induced beta-CATENIN nuclear translocation, TCF activation, and proliferation.

273 Normal colonic epithelia express a truncated TCF-1 form, called dnTCF-1, that lacks the critical beta

274 e importance of PTPRZ1 as a tonic brake upon TCF-dependent transcription.

275 Using TCF/Lef:H2B-GFP reporter mice and transfection of an ind

276 Here we express three vertebrate TCF proteins (human TCF4, mouse LEF1 and Xenopus TCF3) i

277 Ancient, non-vertebrate TCFs contain two DNA binding domains, a High Mobility Gr

278 Two vertebrate TCFs (TCF-1/TCF7 and TCF-4/TCF7L2) use the C-clamp as an

279 aling directly regulates FGF1 expression via TCF binding elements in the FGF1-1C promoter locus.

280 Most induced changes were TCF dependent, but TCF-independent TSSs exhibited the sa

281 Most importantly, when TCF-1 is forcibly expressed in bone marrow (BM) progenit

282 equence showed distinct subregions, in which TCF-1 sites and a conserved element were required for T-

283 Stabilized beta-catenin associates with TCF proteins and enters the nucleus to promote target ge

284 In the nucleus, beta-catenin associates with TCF/LEF sequence specific transcription factors to activ

285 iation of the co-activator beta-catenin with TCF/LEF transcription factors.

286 1 acts as a transcriptional coactivator with TCF/LEF transcription factors, promoting expression of a

287 ould form protein interaction complexes with TCF proteins, Osr1, but not Six2, enhances TCF interacti

288 Tat coprecipitated with TCF-4 (a transcription factor that partners with beta-ca

289 ound to genomic regions highly enriched with TCF/LEF binding motifs.

290 rogenesis model system, DOT1L interacts with TCF and Wnt signaling.

291 amily cofactors, MKL1 and MKL2, but not with TCF-family cofactor, ELK-1.

292 Studies with TCF Elk-1 mutants showed that TCF-dependent ERK-induced

293 Podocan and a Wnt-TCF pathway marker were differently expressed in human c

294 nditions, we concomitantly evaluated the Wnt-TCF (T-cell factor) pathway.

295 In addition, upregulation of the Wnt-TCF pathway was found in SMCs of podocan-deficient mice

296 ration and proliferation, inhibiting the Wnt-TCF pathway.

297 eration, which likely is mediated by the Wnt-TCF pathway.

298 homolog 2 (TRIB2) as a direct target of Wnt/TCF in liver cancer and demonstrate that transcription o

299 egulating the nuclear level of the sole worm TCF protein.

300 e showed previously that WRM-1 binds to worm TCF and functions as the substrate-binding subunit for L