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 a key transcription factor in progenitor exhaus

6 TCF-1 mediated a T-bet-to-Eomes transcription factor tra

7 TCF-1 mediated the bifurcation between divergent fates,

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

9 TCF-1 used a pre-existing regulatory landscape establish

10 TCF-1 was dispensable for the generation of specified EI

11 TCF-1 was intrinsically required for the differentiation

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

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

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

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

16 T cell factor-1 (TCF-1), encoded by Tcf7, is a transcription factor and h

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

18 dogenous pop-1, support the model that POP-1(TCF) induces differentiation at a high nuclear level, wh

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

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

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

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

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

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

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

26 tudy suggests dual roles for beta-catenin: a TCF/LEF-independent nuclear function that coordinates an

27 (scRNA-seq) and lineage tracing identified a TCF-1(+)Ly108(+)PD-1(+) CD8 T cell population that seeds

28 11A) reduced the ability of Dvl3 to activate TCF/LEF (T-cell factor/lymphoid enhancer factor)-driven

29 ocytes increases proliferation and activates TCF transcriptional activity.

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

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

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

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

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

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

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

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

38 t genes transcription in a beta-catenin- and TCF/LEF-dependent manner.

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

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

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

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

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

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

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

46 expression of transcription factors such as TCF-1.

47 sion of beta-catenin-dependent genes such as TCF/LEF1 and ZIC3 TFs, transporters, and junctional prot

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

49 Screening 23dd in a cell-based TCF/LEF reporter gene assay restored the activation of W

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

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

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

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

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

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

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

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

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

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

60 her, our data indicate that the beta-catenin-TCF/LEF complex directly regulates G-CSF receptor levels

61 beta-Catenin-TCF/LEF complexes may function primarily in feedback reg

62 tended previous findings that a beta-catenin-TCF/LEF interaction is not required for differentiation,

63 Disruption of the beta-catenin-TCF/LEF interaction resulted in the accumulation of imma

64 F4) that specifically abrogates beta-catenin-TCF/LEF interaction.

65 etic and chemical inhibition of beta-catenin-TCF/LEF signaling in human CD34+ cells reduced granulocy

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

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

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

69 bitors against the MDM2/p53 and beta-catenin/TCF interactions resulted in the generation of potent pr

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

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

72 1, which acts as a repressor of beta-catenin/TCF transcriptional activity.

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

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

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

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

77 ZH2 expression is essential for beta-CATENIN/TCF-4/LEF-1 transcription.

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

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

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

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

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

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

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

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

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

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

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

89 ion and the development of TOX(+) and CD39(-)TCF-1(+) cells.

90 a expression via an evolutionarily-conserved TCF/LEF site within the WNT3A promoter.

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

92 In contrast, TCF(RNAi) does not rescue the Ck1alpha(RNAi) -induced WC

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 This was associated with decreased TCF/LEF activity, a readout of canonical WNT activity, a

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

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

98 ffective at preventing TopoIIalpha-dependent TCF transcription.

99 ne-3-cyano-4,5,5-trimethyl-2,5-dihydrofuran (TCF).

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

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

105 e a Wnt-like transcriptional response, i.e., TCF/LEF dependent.

106 o identify PD-1 as a protector of this early TCF-1 subset.

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

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

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

110 we demonstrate that the transcription factor TCF-1 (Tcf7) regulates CD8(+) T cell fate decisions in d

111 owever, the role of the transcription factor TCF-1 in early fate decisions and initial generation of

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

113 duced expression of the transcription factor TCF-1, and inhibited the dysfunctional phenotype, culmin

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

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

116 ell factor/lymphoid enhancer-binding factor (TCF/LEF) transcription factors and subsequent transcript

117 ell factor/lymphoid enhancer-binding factor (TCF/LEF), causing subsequent repression of target gene t

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

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

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

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

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

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

124 T-cell factor (TCF) transcription is a major driving force in CRC, and

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

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

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

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

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

130 r of Split (TLE) to block Wnt/T-cell factor (TCF)-mediated transcription, and dual inhibition of TEAD

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

132 ion, increase in beta-catenin/T-cell factor (TCF)-mediated transcriptional activation, and target gen

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

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

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

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

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

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

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

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

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

142 tive expression of the transcription factors TCF-1 and T-bet, and by discrete levels of CD27 expressi

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

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

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

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

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

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

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

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

151 highlight recent reports showing promise for TCF-1 as a novel biomarker to identify recently characte

152 (TOP2A) as a DNA-binding factor required for TCF-transcription.

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

154 shing these lineages and the requirement for TCF-1 throughout lineage differentiation and maintenance

155 These data define a role for TCF-1 in early-fate-bifurcation-driving Tex precursor ce

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

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

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

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

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

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

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

163 h HMGA2 and EZH2 displaced Groucho/TLE1 from TCF-4 and served as gatekeepers for K49 acetylation on b

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

165 In contrast, genes without functional TCF sites at the promoter may be predominantly regulated

166 nique signature implicating activity of HMG (TCF) and RHD (NF-kappaB) transcription factor family mem

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

168 and RORgammat Overall, our study reveals how TCF-1 exerts central control of T cell differentiation i

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

170 d explant transfection assays, we identified TCF/LEF-binding sequences within two distal enhancers of

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

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

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

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

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

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

177 nt ligands, including WNT7B, which increases TCF/LEF-dependent transcription without activating Wnt c

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

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

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

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

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

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

184 (BMP/TGF-beta-directed SMADs or WNT-induced TCFs) and affecting target gene expression.

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

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

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

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

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

190 ersistent CM proliferation required both LEF/TCF activity and AKT phosphorylation but was independent

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

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

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

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

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

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

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

198 ated N-terminus that interacted with nuclear TCF-4 resulting in luciferase reporter activity and cycl

199 Ablation of TCF-1 resulted in enhanced Tc17 cell development and exp

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

201 ipitation assays confirmed direct binding of TCF/LEF factors to the promoter and putative enhancer re

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

217 view, we discuss the multifunctional role of TCF-1 in establishing these lineages and the requirement

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

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

220 their quantity, notably among the subset of TCF-1(+) self-renewing T cells.

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

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

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

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

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

226 c to proliferative cell division by opposing TCF-related transcriptional repression.

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

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

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

230 Our TCF approach reveals a complex landscape of thermodynami

231 development within T cell factor 1-positive (TCF-1(+)) early innate lymphoid progenitors (EILPs), whi

232 OP2A ATP-competitive inhibitors that prevent TCF-transcription and modulate or reverse EMT in mCRC.

233 the dorsal midline, the DNA-binding protein TCF binds and actively represses gene activity only when

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

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

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

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

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

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

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

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

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

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

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

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

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 ts, including transcription factors from the TCF/LEF family.

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

254 ly, USP21 deubiquitinates and stabilizes the TCF/LEF transcription factor TCF7, which promotes cancer

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 n or in the solid state, brighter than their TCF analogues.

258 ex precursor cells, and PD-1 stabilized this TCF-1(+) Tex precursor cell pool.

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

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

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

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

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

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

270 1 that mediates tetramerization and binds to TCFs.

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

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

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

274 nto T(H)1-like cells, but instead upregulate TCF-1 expression and acquire stemness-associated feature

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

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

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

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

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

280 provide insight into the mechanisms by which TCF-1 promotes developmental progression of ILC precurso

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

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

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

284 1 acts as a transcriptional coactivator with TCF/LEF transcription factors, promoting expression of a

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

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

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

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

289 ssion of MAF and RORgammat, in parallel with TCF-1-driven modulation of chromatin state.

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

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

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

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

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

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

296 the shaping of opposing poles of BMP and Wnt/TCF activity and the anterior-posterior patterning of ne

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

298 /TAZ-Groucho/TLE interaction to suppress Wnt/TCF-mediated transcription, thereby resulting in intesti

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