ライフサイエンスコーパス: LEF1

1 LEF1 also directly augments expression of the effector f

2 LEF1 alterations were detected in 63 cases (13%), includ

3 LEF1 and TOPGAL expression ceased during catagen and tel

4 LEF1 competed with TCF4 for binding to NF-kappaB p65.

5 LEF1 expression is highest in fetal and bone marrow B-1

6 LEF1 inactivation was associated with a younger age at t

7 LEF1 is a cell-type-specific transcription factor and me

8 LEF1 is a member of the lymphoid enhancer factor (LEF)/T

9 LEF1 is a nuclear effector of the Wnt/LRP5/beta-catenin

10 LEF1 is highly expressed in androgen-independent prostat

11 LEF1 protein abundance is selectively modulated by lymph

12 LEF1 works as a key hub of Wnt signaling to build rachis

13 LEF1-altered cases were associated with increased centra

14 LEF1-mediated MMP13 gene expression is repressed by SIRT

15 soderm), lymphoid enhancer-binding factor 1 (LEF1) and mesoderm posterior BHLH transcription factor 1

16 cts with lymphoid enhancer-binding factor 1 (LEF1) and potentiates Wnt signaling in T-ALL cells with

17 factors lymphoid enhancer binding factor 1 (LEF1) and transcription factor 7 (TCF7) (T cell factor-1

18 L with lymphocyte enhancer-binding factor 1 (LEF1) as a signature gene.

19 scription factor lymphoid enhancer factor 1 (LEF1) in the postselection expansion of iNKT cells throu

20 n factor lymphoid enhancer-binding factor 1 (LEF1) is aberrantly expressed across all subtypes and st

21 eta3 stimulates lymphoid-enhancing factor 1 (LEF1) mRNA synthesis in MEE cells.

22 for the lymphoid enhancer-binding factor 1 (LEF1) transcription factor, reducing LEF1 responsiveness

23 protein lymphoid enhancer-binding factor 1 (LEF1) was found adjacent to the proximal Runx2-binding s

24 ssion of lymphoid enhancer-binding factor 1 (LEF1), a downstream effector in the canonical Wnt signal

25 RT1) and lymphoid enhancer binding factor 1 (LEF1), both reported to have contrasting effects on cart

26 ing with lymphoid enhancer binding factor 1 (LEF1).

27 activated by the lymphoid enhancer factor 1 (LEF1)/beta-catenin complex, a transducer of wnt signalin

28 enin and lymphoid enhancer-binding factor 1 (LEF1)/T cell factor regulates proliferation in stem cell

29 on activation of lymphoid enhancer factor 1 (LEF1)/T-cell factor (TCF) target genes underlie the onco

30 lymphoid-enhancing factor 1/T cell factor 1 (LEF1/TCF1), the ultimate executor of the Wnt pathway, im

31 scription of the lymphoid enhancer factor-1 (LEF1) gene is aberrantly activated in sporadic colon can

32 get gene lymphoid enhancer binding factor-1 (LEF1) in chronic lymphocytic leukemia (CLL).

33 Lymphoid enhancer-binding factor-1 (LEF1) is a key transcription factor of Wnt signaling.

34 paper is the first to show that the Smad2,4/LEF1 complex replaces beta-catenin/LEF1 during activatio

35 ), 11p15.5 (C11orf21, P=2.15x10(-10)), 4q25 (LEF1, P=4.24x10(-10)), 2q33.1 (CASP10 or CASP8 (CASP10/C

36 reporter gene is hyperinduced vegetally in a LEF1/TCF3-binding-site-dependent manner.

37 pression conditions the promoter region of a LEF1 target gene is hypoacetylated.

38 d H4 acetylation patterns, derepression of a LEF1.beta-catenin model system, and transcription of HDA

39 lude that the biological outcome of aberrant LEF1 activation in colon cancer is directed by different

40 We recently showed that aberrant LEF1 expression induces acute myeloid leukemia (AML) in

41 p-regulate synthesis of LEF1 and to activate LEF1 transcription during induction of palatal EMT.

42 Although all LEF1 isoforms bind to a core set of proliferation- and a

43 Moreover, although LEF1 and TCF4 synergize with beta-catenin and plakoglobi

44 ription, including: MYC, vimentin, AXIN2 and LEF1.

45 ptionally active complex of beta-catenin and LEF1.

46 anscriptional activation by beta-catenin and LEF1/TCF, but Fli-I disrupted the synergy of FLAP1 with

47 ey regulatory mechanism for beta-catenin and LEF1/TCF-mediated transcription and thus for Wnt signali

48 anscriptional activation by beta-catenin and LEF1/TCF.

49 hanceosome consisting of Runx1, CBFbeta, and LEF1.

50 expressed in the developing hippocampus, and LEF1-deficient embryos lack dentate gyrus granule cells

51 The WNT/TCF target genes HOXB9 and LEF1 are identified as mediators of chemotactic invasion

52 The expression of LEF1 and LEF1-regulated genes in primary BL suggests that LEF1 is

53 between the DNA-binding domains of Runx2 and LEF1 was identified and found crucial for LEF1-mediated

54 scription factors, including CEBPA, SPI1 and LEF1, are uniquely inaccessible in these leukemias.

55 tooth development at the late bud stage and LEF1 is required for a relay of a Wnt signaling to a cas

56 show that the transcription factors TCF1 and LEF1 are critical regulators of B-1a cells.

57 ecific genes, Rorc and Blk, whereas TCF1 and LEF1 countered the SOX proteins and induced genes of alt

58 ptive transfer of B-1 cells lacking TCF1 and LEF1 fails to suppress brain inflammation.

59 In the absence of TCF1 and LEF1, B-1 cells proliferate excessively and acquire an e

60 ranscription factors, SOX4, SOX13, TCF1, and LEF1, and not by conventional TCR signaling.

61 mmune cells, including CD28, CCR7, TCF7, and LEF1.

62 A novel interaction between the VDR and LEF1 (lymphoid enhancer-binding factor-1) that is indepe

63 y abrogated interactions between the VDR and LEF1 but also impaired the ability of the VDR to enhance

64 ates a novel interaction between the VDR and LEF1 that is mediated by the DNA-binding domain of the V

65 that controls proliferation by antagonizing LEF1/beta-catenin-mediated transcription.

66 As LEF1/TCF3 family transcription factors have previously b

67 d the expression of Wnt target genes such as LEF1, cyclin D1, and fibronectin, depressed LRP6 levels,

68 s; and HMG box transcription factors such as LEF1, TCF1, and Sox4.

69 In transcription assays, LEF1 repressed Runx2-induced activation of the mouse ost

70 e main LEF1 promoter activity and attenuates LEF1 mRNA transcription.

71 y in the human hair matrix (increased AXIN2, LEF1) by upregulating WNT6 and WNT10B, and inhibiting SF

72 strate a direct physical interaction between LEF1/beta-catenin complex and the Dkk4 promoter using Ch

73 To further explore the link between LEF1 expression and the Wnt pathway, we studied two resp

74 -ALL and identified monoallelic or biallelic LEF1 microdeletions in 11% (5 of 47) of these primary sa

75 sion has been overridden, beta-catenin binds LEF1 and the beta-catenin-LEF1 complex is competent to a

76 The mutations impaired both LEF1 binding to beta-catenin and transcriptional activat

77 ls compromised transcriptional activation by LEF1/TCF, beta-catenin and the p160 coactivator GRIP1.

78 to beta-catenin, implying that repression by LEF1 is mediated by promoter-targeted HDAC.

79 We show here that repression by LEF1 requires histone deacetylase (HDAC) activity.

80 cells by down-regulating Wnt (beta-catenin, LEF1) and TGF-beta (Smad2/3, collagen type I, alpha-SMA)

81 beta-catenin binds LEF1 and the beta-catenin-LEF1 complex is competent to activate the expression of

82 th stimulate transcription of a beta-catenin-LEF1-dependent reporter gene.

83 e Smad2,4/LEF1 complex replaces beta-catenin/LEF1 during activation of EMT in vivo by TGFbeta3.

84 ns in AER formation through the beta-catenin/LEF1 pathway.

85 leads to the activation of the beta-catenin/LEF1-dependent pathway.

86 l enhanceosome consisting of RUNX1, CBFbeta, LEF1, and Aly.

87 l key transcription factors, including CDX2, LEF1 and members of HOX clusters.

88 Concordantly, LEF1 expression is significantly upregulated in ERG-high

89 , gel shift, and luciferase assays confirmed LEF1 occupancy and regulation of the AR promoter.

90 otein can interact, in vitro, with consensus LEF1/TCF3-binding sites found within the Xtwn promoter.

91 and found that transcript levels of CTNNB1, LEF1, FZD8, WNT3A, and SFRP4 were negatively correlated

92 In addition, decreasing LEF1 expression in control neurons using shLEF1 caused h

93 Most importantly, our data defined LEF1 as a direct target of ERG and that LEF1 inhibition

94 t regulation and restores the IRES-dependent LEF1 expression.

95 detected in TCF3 (also known as E2A), EBF1, LEF1, IKZF1 (IKAROS) and IKZF3 (AIOLOS).

96 y submucosal glands, indicating that ectopic LEF1 expression alone is insufficient to induce submucos

97 es with activated NOTCH and AKT and elevated LEF1 levels were sensitive to inhibition of beta-catenin

98 n these cells, the association of endogenous LEF1 and beta-catenin was induced by stimulation with th

99 on assays detected YY1 binding to endogenous LEF1 P2.

100 constitutively active beta-catenin enhanced LEF1-dependent repression of Runx2.

101 nase (MMP) 13, partially because of enhanced LEF1 transcriptional activity.

102 tokine involved in OA pathogenesis, enhanced LEF1 protein levels and gene expression, resulting in in

103 eta-catenin deacetylation, thereby enhancing LEF1-beta-catenin complex formation and long-range chrom

104 Our findings establish LEF1 as an oncogenic transcription factor in CLL whose b

105 In this study, we examined LEF1 expression in androgen-independent cancer as well a

106 iants with biological insights (for example, LEF1).

107 antly expressed TCF4 and to a lesser extent, LEF1 and TCF3 mRNA.

108 The HMG-box transcription factor LEF1 controls many developmentally regulated genes, incl

109 rough repression of the transcription factor LEF1, a known modulator of MMP13 gene expression.

110 tion of the proinvasive transcription factor LEF1.

111 maintains WNT effector, transcription factor LEF1.

112 yte enhancer binding factor 1/T cell factor (LEF1/TCF) proteins with the assistance of multiple coreg

113 any member of the lymphoid enhancer factor (LEF1) and T-cell factor (TCF1, TCF3, TCF4) family of tra

114 Tc1), and lymphoid enhancer-binding factor1 (LEF1) proteins.

115 Lymphoid-enhancing factor/T-cell factors (LEF1/TCF) are a high-mobility group of transcriptional f

116 n enhanced affinity of S37A beta-catenin for LEF1 and TCF4, as observed here by immunoprecipitation a

117 nd LEF1 was identified and found crucial for LEF1-mediated repression of Runx2.

118 n promoter was surprisingly not required for LEF1 repression.

119 y supports a functionally important role for LEF1 and its target genes in BLs.

120 uncovered a dual, context-dependent role for LEF1 that is determined by its protein levels.

121 First, HDAC1 is dissociated from LEF1 and its enzymatic activity is attenuated.

122 mmitment of proliferative progeny by fueling LEF1- and MITF-dependent differentiation.

123 Further, LEF1 associates in vivo with HDAC1, and transcription of

124 Furthermore, LEF1 expression positively correlated with expression of

125 ded with upregulation of hair-related genes, LEF1 and WNT10B, and downregulation of a marker of sebac

126 On circulating lymphocytes, three genes, LEF1, FASLG, and MMP9, could efficiently stratify patien

127 ed TCR-translocated oncogene partners: GNAG, LEF1, NKX2-4, and IL2RB.

128 High LEF1 expression (LEF1high) associated with significantly

129 ectal carcinomas, most of which express high LEF1 levels.

130 eloid leukemia (AML) in mice, and found high LEF1 expression in a subset of cytogenetically normal AM

131 In summary, we provide evidence that high LEF1 expression is a novel favorable prognostic marker i

132 TCF1 and its homologue LEF1 are historically known as effector transcription fa

133 ated virus was used to overexpress the human LEF1 gene in a human bronchial xenograft model of regene

134 Thus, we identified LEF1 as a potential marker for androgen-independent dise

135 n of SIRT1 during IL-1beta challenge impeded LEF1 levels and MMP13 gene expression.

136 ty in NR neurons was connected to changes in LEF1 and in the Wnt/B-catenin pathway.

137 utic strategy to enhance chemosensitivity in LEF1-deleted T-ALL cases.

138 LNCaP) cells revealed 100-fold increases in LEF1 expression in LNCaP-AI cells.

139 this study, we assessed the role of SIRT1 in LEF1-mediated MMP13 gene expression in human OA chondroc

140 ith survival of patients with MDS, including LEF1, CDH1, WT1, and MN1.

141 artilage from Sirt1(-/-) presented increased LEF1 and MMP13 protein levels, similar to human OA carti

142 ng T cells preferentially express inhibitory LEF1 and TCF7 (TCF-1) isoforms and that T cell activatio

143 e activation of a promoter for a full-length LEF1 isoform that binds beta-catenin, but not a second,

144 stinct transcriptional programs; full-length LEF1 promotes a quiescence gene signature and limits leu

145 es can activate the promoter for full-length LEF1, indicating that in cancer high levels of these com

146 and/or progenitor cell markers ALDH1, LGR5, LEF1, CD133 and CK6B.

147 Low LEF1 protein, characteristic of indolent disease, suppor

148 thelial-mesenchymal phenotype presenting low LEF1 expression, the NAT is synthesized and remains unpr

149 , this unspliced NAT down-regulates the main LEF1 promoter activity and attenuates LEF1 mRNA transcri

150 We show that the TCF family members LEF1, TCF4, and TCF3 are phosphorylated in embryonic ect

151 PBepsilon, RUNX1/AML1, Notch family members, LEF1, and Cdc42 as additional nodes in this pathway.

152 ivo with HDAC1, and transcription of a model LEF1-dependent target gene is modulated by the ratio of

153 ed nuclear export, human TCF4, but not mouse LEF1 or Xenopus TCF3, can repress endoderm genes in MS,

154 e vertebrate TCF proteins (human TCF4, mouse LEF1 and Xenopus TCF3) in C. elegans embryos and compare

155 expressed the highest levels of Lef1 mRNAs, LEF1 concentrated in the precursor cells to the hair sha

156 Mutant LEF1 not only inhibited expression of beta-catenin targe

157 f a previously undescribed dominant-negative LEF1 isoform resulting from focal deletions of the exons

158 y either overexpression of dominant-negative LEF1 or overexpression of a secreted Wnt inhibitor Dickk

159 ominant-negative Smad4 and dominant-negative LEF1 showing that TGFbeta3 uses Smads both to up-regulat

160 down of LEF1 in BL cell lines identified new LEF1 target genes; these LEF1 targets are enriched with

161 ammatory pathways and were enriched for NF1, LEF1, and other transcription factors.

162 t signaling in prostate cancer and nominates LEF1 as a critical mediator of ERG-induced tumorigenesis

163 helial cells, and neither NAT transcript nor LEF1 mRNA are expressed, in cell lines with an intermedi

164 er B cells were devoid of detectable nuclear LEF1 expression, as were mantle cell lymphoma (0 of 5),

165 Herein, we report the expression of nucleic LEF1 in 15 of 18 patients with BL and the identification

166 -Smad2 and Smad4 are present in the nucleus, LEF1 is activated without beta-catenin.

167 l are uniquely potent in their activation of LEF1 and CDX1.

168 her, these findings imply that activation of LEF1-dependent genes by beta-catenin involves a two-step

169 Aberrant activations of LEF1/TCF-mediated transcription have been implicated in

170 potentiates the transcriptional activity of LEF1 and acetylates histone H3 lysine 56 in the promoter

171 c1 and decreases transcriptional activity of LEF1 proteins.

172 rbored nonsynonymous sequence alterations of LEF1, 2 of which produced premature stop codons.

173 hese data establish the mechanistic basis of LEF1 splicing regulation and demonstrate that LEF1 alter

174 of antisense transcription in the control of LEF1 transcription factor expression.

175 ed a comprehensive mechanistic dissection of LEF1 function in CLL using extensive functional analyses

176 t phosphorylation caused the dissociation of LEF1, TCF4, and TCF3 from a target promoter in vivo.

177 letion of the beta-catenin-binding domain of LEF1 in HNF-1beta-deficient cells abolishes the increase

178 Therefore, we propose that downregulation of LEF1 may account for Li resistance in NR neurons.

179 the epidermal and mesenchymal expression of LEF1 and (&bgr;)-catenin, suggesting that these changes

180 The expression of LEF1 and LEF1-regulated genes in primary BL suggests tha

181 everal cell lines revealed the expression of LEF1 mRNA and a constitutive association of the LEF-1 pr

182 ics, including Wnt-upregulated expression of LEF1, APCDD1, and ZIC3.

183 with a significant decrease in expression of LEF1.

184 Expression of the spliced form of LEF1 NAT in trans prevents the action of unspliced NAT b

185 8 patients with BL and the identification of LEF1 target genes.

186 Although the implication of LEF1 in colon cancer is well documented, its clinical re

187 Here we demonstrate that inclusion of LEF1 exon 6 is increased during thymic development and i

188 ressed, resulting from variable inclusion of LEF1 exon 6; however, the expression pattern of these is

189 om a promoter present in the first intron of LEF1 gene and undergoes splicing in mesenchymal cells.

190 At least two distinct isoforms of LEF1 are expressed, resulting from variable inclusion of

191 ssion profiling after transient knockdown of LEF1 in BL cell lines identified new LEF1 target genes;

192 Knockdown of LEF1, a downstream target of Wnt signaling, abrogated Ha

193 ion analysis indicated that higher levels of LEF1-AS1 correlated with reduced mortality risk (age-adj

194 eased expression and nuclear localization of LEF1 are also observed in cystic kidneys from Hnf1b muta

195 , however, what is the cellular mechanism of LEF1 signaling in regulating tooth morphogenesis.

196 in cell death and reduced phosphorylation of LEF1 as well as HDAC1 among NLK-deleted SP CD8(+) cells.

197 tor in vitro leads to the down-regulation of LEF1 and TCF7 (TCF-1) expression in human naive CD8 T ce

198 We validated the prognostic relevance of LEF1 expression by quantitative PCR, thereby providing a

199 ized to functionally investigate the role of LEF1 in initiating and supporting gland development in t

200 ghts into the prevalence and significance of LEF1 alterations in a comprehensive cohort of 474 pediat

201 tivation occurred transiently in a subset of LEF1-positive cells of pluripotent ectoderm and underlyi

202 uses Smads both to up-regulate synthesis of LEF1 and to activate LEF1 transcription during induction

203 in a manner mimicking the C-terminal tail of LEF1.

204 The NH(2) terminus of LEF1 is frequently mutated in human sebaceous tumors.

205 assays as well as in vitro transfections of LEF1 and beta-catenin show that Dkk4 is a potential down

206 Overexpression of TCF4, but not of TCF3 or LEF1, induced MMP-1, -3, and -13 expression and generic

207 tated LEF/TCF binding elements or by TCF4 or LEF1 mutants.

208 xpression of mammalian beta-cat with TCF4 or LEF1 results in nuclear accumulation of these proteins a

209 ires expression of both beta-cat and TCF4 or LEF1, and is not supported by mutated LEF/TCF binding el

210 mediated transcriptional activation by other LEF1/TCF proteins, the entire hippocampus including the

211 gyrus granule cells, and together with other LEF1/TCF proteins, the development of the hippocampus.

212 ut inhibits transcription by phosphorylating LEF1, a transcriptional activator.

213 logic c-MET up-expression, infra-physiologic LEF1 down-expression and YAP1 signature enrichment as dr

214 uding early T-cell precursor, HOXA-positive, LEF1-inactivated, and TAL1-positive subtypes, which have

215 First, we demonstrate that purified LEF1 protein can interact, in vitro, with consensus LEF1

216 ctor 1 (LEF1) transcription factor, reducing LEF1 responsiveness and enhancer activity in cultured hu

217 ein and mRNA expression, ultimately reducing LEF1 transcriptional activity, as judged by luciferase a

218 a-catenin oligonucleotides that up-regulated LEF1 is not activated by beta-catenin in palate EMT.

219 t the loss of function in placode regulators LEF1 and TBX3 in mESCs results in impaired skin and MEMO

220 ession, but we observed that SIRT1 repressed LEF1 protein and mRNA expression, ultimately reducing LE

221 Our data reveal LEF1 as a central regulator of iNKT cell number and Th2-

222 04 patients, age and the long non-coding RNA LEF1-AS1 were identified as predictive features, yieldin

223 y up-regulated, whereas in BDs, PAX5, Runx2, LEF1, TLE1, and CCND2 were significantly down-regulated.

224 double-nucleotide substitutions in the same LEF1 allele, irrespective of DNA mismatch repair status.

225 Mechanistically, DBC1 stabilizes LEF1-beta-catenin interaction by inhibiting SIRT1-mediat

226 We therefore studied LEF1 expression in 210 adults with CN-AML treated on Ger

227 ranscriptional corepressor CtBP and suppress LEF1/beta-catenin-mediated transcription.

228 nversely, overexpression of HIPK2 suppresses LEF1/beta-catenin-mediated transcriptional activation of

229 of the Wnt receptor FZD2 and the Wnt target LEF1 and decreased expression of Wnt antagonists DKK2 an

230 of beta-catenin-dependent genes such as TCF/LEF1 and ZIC3 TFs, transporters, and junctional proteins

231 criptional activity of complex B-catenin/TCF/LEF1, and reduced excitability in NR neurons.

232 -catenin level in the cells and enhanced TCF/LEF1 luciferase reporter activity, which could be partia

233 Novel functional TCF/LEF1 binding sites in the promoter regions of fibronecti

234 or to activator, analogous to control of TCF/LEF1.

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

236 atenin that forms a nuclear complex with TCF/LEF1, activating the Wnt/B-catenin transcription program

237 ollowed by a decrease in beta-catenin, TCF1, LEF1, Cyclin D1, c-myc, Wnt7a, and PSD95 protein levels

238 oteins (Dkk-1, GSK3beta, beta-catenin, TCF1, LEF1, Cyclin D1, c-myc, Wnt7a, Wnt1, and PSD95) were mea

239 TCF1-LEF1 double deficient mice have reduced B-1a cells and d

240 Our findings define a TCF1-LEF1-driven transcriptional program that integrates stem

241 For both NK and T lineages, a TCF1-LEF1-MYC axis dominated the regulatory landscape of long

242 and WNT enhanceosome members including TCF4, LEF1 and BCL9 were also decreased after GSK3-alpha/beta

243 In contrast, in high CHIR, TCF7/LEF1/B-catenin complexes replaced TCF7L1/TCF7L2 binding

244 ined LEF1 as a direct target of ERG and that LEF1 inhibition fully abolished ERG-induced Wnt signalin

245 EF1 splicing regulation and demonstrate that LEF1 alternative splicing is a contributing determinant

246 In summary, these studies demonstrate that LEF1 expression is required, but in and of itself is ins

247 in a ferret xenograft model demonstrate that LEF1 is functionally required for submucosal gland forma

248 aken together, our findings demonstrate that LEF1/TCF3 is necessary but not sufficient for TOPGAL act

249 We report here that LEF1 is a new type of target gene ectopically activated

250 To test the hypothesis that LEF1 signaling regulates the fate of the dental epitheli

251 Thus, these results indicate that LEF1 gene expression is attenuated by an antisense non-c

252 We propose that LEF1 NH(2)-terminal mutations play a dual role in skin c

253 vitro and in vivo experiments revealed that LEF1-driven proliferation is mediated by these short, al

254 In this study, we show that LEF1 and TCF7 (TCF-1) are not only expressed in thymocyt

255 Previous reports showed that LEF1 binds to the MMP13 promoter and transactivates its

256 We showed that LEF1 overexpression in LNCaP cells resulted in increased

257 Our findings suggest that LEF1 inactivation is an important step in the molecular

258 Our studies suggest that LEF1 is a critical survival factor for the dental epithe

259 Our results suggest that LEF1 may be a useful target for the discovery of new dru

260 ansient transfection assays, suggesting that LEF1 is a target of the Wnt pathway in colon cancer.

261 yme in the Lef1 null mutant, suggesting that LEF1 may not affect the cell cycle progression of the mu

262 -regulated genes in primary BL suggests that LEF1 is not only aberrantly expressed but also transcrip

263 The LEF1 gene is aberrantly transcribed in colon cancers bec

264 ty of the osteocalcin promoter; however, the LEF1 recognition site in the osteocalcin promoter was su

265 utant promoter constructs, we identified the LEF1 site in the cyclin D1 promoter as essential for the

266 Mutations in the LEF1-binding site increased the basal activity of the os

267 In a second model, the LEF1 gene was ectopically overexpressed under the direct

268 have shown previously that promoter 1 of the LEF1 gene is activated by T cell factor (TCF)-beta-caten

269 Lef1 and other genes of the LEF1/TCF family of transcription factors are nuclear med

270 the ability of beta-catenin to regulate the LEF1 promoter, and they severely impair the ability of T

271 Surprisingly we found that the LEF1 promoter is selectively activated by specific isofo

272 ptional activator that functions through the LEF1 site and is insensitive to beta-catenin.

273 and in particular, transcription through the LEF1 site as critical for endostatin action in vitro and

274 promoter and facilitates PRC2 binding to the LEF1 promoter and trimethylation of lysine 27 in histone

275 Alternative promoters within the LEF1 locus produce polypeptides of opposing biological a

276 ines identified new LEF1 target genes; these LEF1 targets are enriched with genes associated with can

277 of detectable TOPGAL expression, even though LEF1 was still expressed.

278 f human HSPCs could be partly driven through LEF1 regulation.

279 a distinct WNT/TCF signaling program through LEF1 and HOXB9 enhances the competence of lung adenocarc

280 Thus, LEF1 regulates the generation of dentate gyrus granule c

281 Unspliced LEF1 NAT interacts with LEF1 promoter and facilitates PR

282 f beta -catenin, but was also dependent upon LEF1/TCF3 in skin.

283 N-deficient MRC-5 cells failed to upregulate LEF1 in response to GSK3-alpha/beta inhibition.

284 also acts downstream of GSK-3B, upregulated LEF1 and Wnt/B-catenin gene targets, increased transcrip

285 Quantitative PCR validated LEF1-AS1's adaptability to be measured in hospital setti

286 nhanced growth and invasion ability, whereas LEF1 knockdown in LNCaP-AI cells decreased AR expression

287 Whether LEF1 expression associates with clinical and molecular p

288 To determine whether LEF1 expression was sufficient for the induction of airw

289 conferred by beta-catenin's association with LEF1 and BCL9-2/B9L, which accumulate during Wnt stimula

290 ression of MYC and MYC targets in cases with LEF1 inactivation, as well as differentiation arrest at

291 Coexpression of beta-catenin with LEF1 and HDAC1 results in the formation of a beta-cateni

292 onses were still competent to cooperate with LEF1 to activate the c-myc promoter.

293 quires the targeting of its interaction with LEF1 and/or BCL9/B9L, as exemplified by carnosate.

294 Unspliced LEF1 NAT interacts with LEF1 promoter and facilitates PRC2 binding to the LEF1 p

295 Tumour cell lines stably transfected with LEF1(DN) or APC2, or transiently transfected with short-

296 Wnt/LEF1 pathway might provide novel targets for therapeutic

297 Here, we report that ERG activates Wnt/LEF1 signaling cascade through multiple mechanisms.

298 rthermore, functional assays showed that Wnt/LEF1 activation phenocopied that of ERG in inducing cell

299 oblasts induced stromal HA synthesis via Wnt/LEF1 and altered the chemokine profile of stromal fibrob

300 and NFASC and upregulated CTGF, BMP4, YAP1, LEF1, and HLA-DRB1 genes were found to be associated wit