ライフサイエンスコーパス: LEF

1 LEF offers an alternative with comparable efficacy to MT

2 LEF-1 and TCF-1 coordinated such differentiation by two

3 LEF-1 was aberrantly upregulated in premalignant Tcf7(-/

4 LEF-7 suppresses DDR-induced accumulation of phosphoryla

5 LEF-7 was necessary and sufficient to block gamma-H2AX a

6 LEF-LG patients were dichotomized into </=mild MR (n=52)

7 LEF/TCFs direct the final step in Wnt/beta-catenin signa

8 LEF/TCFs have a DNA sequence-specific high-mobility grou

9 LEFs and OEEFs are shown to be equivalent and to obey th

10 Lymphoid enhancer factor 1 (LEF-1) mediates Wnt signaling via recruitment of beta-ca

11 catenin, lymphoid enhancer-binding factor 1 (LEF-1), cyclin D1, N-Myc, and INSM1 levels, ultimately l

12 n factor lymphoid enhancer-binding factor 1 (LEF-1), which plays a definitive role in granulocyte col

13 protein, lymphoid enhancer-binding factor 1 (LEF-1).

14 Lymphoid enhancer-binding factor-1 (LEF-1) is one of the regulators of the Wnt signaling pat

15 n factor lymphoid enhancer-binding factor-1 (LEF-1).

16 -catenin/lymphoid enhancer-binding factor-1 (LEF-1).

17 CREB, as well as factors, such as ATF, AP-2, LEF-1, GATA and PAX-6, that had not yet been recognized

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

19 pression is essential for beta-CATENIN/TCF-4/LEF-1 transcription.

20 port that VentX, a human Xom homologue, is a LEF/TCF-associated inhibitor of canonical Wnt/beta-caten

21 Thus, TCF-1 and LEF-1 adopted distinct genetic 'wiring' to promote the C

22 The transcription factors TCF-1 and LEF-1 are essential for early T cell development, but th

23 provide insight into the role of Nkx3-1 and LEF-1 as potential regulators of the hormone response in

24 We find that Nkx3-1 and LEF-1 bind to several ER cis-regulatory elements in vivo

25 We show that Nkx3-1 and LEF-1 can inhibit ER binding to chromatin, suggesting co

26 Thus, TCF-1 and LEF-1 cooperatively regulate generation of memory precur

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

28 e Ag-specific CD8+ T cells lacking TCF-1 and LEF-1 exhibited an effector phenotype and were severely

29 te spectra of regulatory roles for TCF-1 and LEF-1 in CD8+ T cell responses are yet unknown.

30 The role of TCF-1 and LEF-1 in the CD4-versus-CD8 lineage 'choice' was mediate

31 ereas CD8+ effectors deficient for TCF-1 and LEF-1 retained the capacity to express IFN-gamma, granzy

32 The TCF-1 and LEF-1 transcription factors are known to play critical r

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

34 We also showed that TCF-1 and LEF-1 were dispensable for T cell lineage commitment but

35 ector complexes composed of beta-catenin and LEF/TCF transcription factor.

36 Wnt, Gpr177 is activated by beta-catenin and LEF/TCF-dependent transcription.

37 d by restoration of LEF-1 protein levels and LEF-1 messenger RNA autoregulation.

38 ve novel tripeptides, IVF, LLF, LNF, LSW and LEF, with predicted IC50 values lower than 10 muM were s

39 entify the statistical enrichment of Nkx and LEF motifs.

40 of antibody recognizing the anthrax RBD and LEF domains, as well as the full-length PA protein in mi

41 ned to inhibit the binding between Smad4 and LEF/TCF reduced c-myc expression and the growth rate of

42 3A-stimulated beta-catenin stabilization and LEF/TCF reporter activity.

43 cription factors (SNAIL1, SNAIL2, TWIST, and LEF-1).

44 signaling further increases Ser5P-RNAPII at LEF-1 sites and ME gene promoters, indicating that elong

45 y, persistent CM proliferation required both LEF/TCF activity and AKT phosphorylation but was indepen

46 ling and cell proliferation as determined by LEF luciferase reporter assay and colonic organoid proli

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

48 Finally, we determined that beta-catenin-LEF-1 complexes can promote EMT without upstream signali

49 ng through direct inhibition of beta-catenin/LEF chromatin binding.

50 HNF-1beta and beta-catenin/LEF compete for binding to this element, and thereby HNF

51 quently stimulates formation of beta-catenin/LEF-1 complexes that induce EMT.

52 d expression of fibronectin via beta-catenin/LEF-1 signaling in a phosphatase and tensin homologue (P

53 in orchestrating PTEN-mediated beta-catenin/LEF-1 signaling in EC migration, cell-cell adhesion, and

54 -catenin restored LPP3-mediated beta-catenin/LEF-1 signaling.

55 he ability of LPP3 to stimulate beta-catenin/LEF-1 signaling.

56 hoid enhancer binding factor 1 (beta-catenin/LEF-1) to induce EC migration and formation of branching

57 ily that promotes canonical Wnt/beta-catenin/LEF-1-mediated transcription, displays exonic mutations

58 we show here that Wnt3a-induced beta-catenin:LEF-1 enhancers recruit cohesin to direct enhancer-promo

59 s on LEF, and particularly those on combined LEF+MTX, should be monitored closely for hepatotoxicity.

60 le imputation for estimating the conditional LEF and the variance of the estimator in the right-censo

61 rized functional activity (disruption of DNA-LEF-1 binding) at the intended target and site (inhibiti

62 the lethal and edema factor binding domain (LEF or domain 1') were engineered into functional chimer

63 ancer, where overactive Wnt signaling drives LEF/TCFs to transform cells.

64 munoprecipitation showed that the endogenous LEF-1 is situated at the CD1D promoter and interacts wit

65 Recent studies have re-examined LEF as an alternative to MTX and demonstrated comparable

66 Late expression factor LEF-4, which is an essential gene, is a component of the

67 nsensus sequence of the transcription factor LEF-1 followed by assessment of the candidate compounds

68 Tcf7 (which encode the transcription factor LEF-1 or TCF-1, respectively) resulted in T(FH) cell def

69 ctor (TCF)/lymphoid enhancer-binding factor (LEF) binding sites in the LBH locus and rapid beta-caten

70 ta-catenin/lymphoid enhancer binding factor (LEF) site overlapping with an HNF-1beta half-site.

71 TCF)-1 and lymphoid enhancer-binding factor (LEF)-1 transcription factors have redundant roles in pro

72 he lymphoid enhancer factor 1/T cell factor (LEF/TCF) family of transcription factors are downstream

73 the lymphoid enhancer factor/T-cell factor (LEF/TCF) family.

74 ssion requires binding of LEF/T-cell factor (LEF/TCF) transcription factors to Wnt response elements

75 ell factor (TCF) x lymphoid enhancer factor (LEF) factors contain HMG domains and bind to related con

76 interact with TCF/lymphoid enhancer factor (LEF) family members via their respective high-mobility-g

77 -cell factor (TCF)-lymphoid enhancer factor (LEF) family transcription factor complex.

78 -cell factor (TCF)/lymphoid enhancer factor (LEF) transcription factors.

79 on of beta-catenin-lymphoid enhancer factor (LEF)-1 complexes that initiate EMT.

80 ur members of the lymphoid-enhancing factor (LEF)/T-cell factor (TCF) family, only TCF4 showed more e

81 tion, encode a conserved replication factor, LEF-7, that manipulates the DDR via a novel mechanism.

82 ated, at least in part, by two T-cell factor/LEF-binding sites within the proximal promoter.

83 ing the T cell-specific transcription factor/LEF (TCF/LEF) dual luciferase reporter assay, we demonst

84 When such loop-extruding factors (LEF) bind to chromosomes, they progressively bridge site

85 by use of (designed) local-electric fields (LEFs), i.e., by embedding charges or dipoles into molecu

86 of the photosynthetic linear electron flux (LEF).

87 pre-operative risk score accounted only for LEF and lower LVEF.

88 B-cell lymphocytosis, suggesting a role for LEF-1 early in CLL leukemogenesis.

89 omes of patients with low ejection fraction (LEF), paradoxical low flow (PLF), and normal flow (NF) a

90 he conditional lifetime expectancy function (LEF) is the expected lifetime of a subject given surviva

91 Three functional LEF-1/TCF binding sites lie within the promoter of the h

92 nt with low-ejection fraction, low-gradient (LEF-LG) severe aortic stenosis and concomitant relevant

93 alve area was lower in low flow/LVEF groups (LEF: 0.71 +/- 0.20 cm(2) and PLF: 0.65 +/- 0.23 cm(2) vs

94 Among these patients, 206 (18%) had LEF as defined by LVEF of <50%; 319 (28%) had PLF as def

95 However, LEF-LG patients assigned to medical therapy have a disma

96 We also identified LEF-1 expression in CD19(+)/CD5(+) cells obtained from p

97 In this study, we have identified LEF-1 as a regulator of the expression of the gene encod

98 Importantly, LEF-1 knockdown decreased CLL B-cell survival.

99 e 30-day mortality was higher (p < 0.001) in LEF and PLF groups than in the NF group (6.3% and 6.3% v

100 after AVR, overall survival was 72 +/- 4% in LEF group, 81 +/- 2% in PLF group, and 85 +/- 2% in NF g

101 As in LEF-1, partial truncation of the distal SRY tail reduces

102 The decline in LEF is paralleled by a gradual increase in cyclic electr

103 g independent predictor of late mortality in LEF-LG patients undergoing TAVI.

104 g to LEF-1 ubiquitination and a reduction in LEF-1 protein levels.

105 rowth factor (TGF)-beta3 signaling increases LEF-1 gene expression causing formation of beta-catenin-

106 We now demonstrate that TGF-beta1 induces LEF/TCF TOPFLASH reporter activation and nuclear beta-ca

107 desired phenotypic cellular change (inhibit LEF-1-driven cell transformation) provided two lead comp

108 itutively active STAT5a (caSTAT5a) inhibited LEF-1-dependent autoregulation of the LEF-1 gene promote

109 including c-Myc and Cyclin D1 by inhibiting LEF transcriptional activity in GC cells.

110 target and site (inhibition of intracellular LEF-1-mediated gene transcription) resulting in a desire

111 ic mice expressing LacZ driven by the 2.5-kb LEF-1 promoter demonstrated expression in the tooth epit

112 omparing methotrexate (MTX) and leflunomide (LEF) monotherapy, in combination with biologic therapies

113 Full-length LEF-1, TCF-1E, and TCF-1E with a mutated C-clamp all bin

114 Full-length LEF-10 or its candidate prion-forming domain (cPrD) can

115 Our finding links LEF-1 to CD1D and suggests a role of Wnt signaling in th

116 emonstrated added benefit of combination MTX+LEF over either alone.

117 in intron 2 (P2) produces dominant negative LEF-1 isoforms (dnLEF-1), but P2 is silent because it is

118 Decreased expression of Bmi-1, Notch1, LEF-1, Mcl-1, and GATA2 was also observed in Cited2-/- L

119 morphogenetic protein 4 pathway, as a novel LEF/TCF-associated transcriptional modulator.

120 significant differences in the abilities of LEF/TCF family members to regulate Wnt target genes.

121 Addition of LEF to MTX in rheumatoid arthritis patients who have fai

122 ation of gene expression requires binding of LEF/T-cell factor (LEF/TCF) transcription factors to Wnt

123 is associated with corresponding changes of LEF/TCF target oncogenes such as cyclin D1, suggesting a

124 (beta-cat), a transcriptional coactivator of LEF-1/TCF HMG proteins in the Wnt/Wg signaling pathway.

125 ty of infection can induce the conversion of LEF-10 into an aggregated state in virus-infected cells,

126 a enhanced ubiquitination and degradation of LEF-1 protein by hyperactivated STAT5.

127 Deletion of LEF-7 from the baculovirus genome allowed gamma-H2AX acc

128 Forced expression of LEF-1 enhanced T(FH) differentiation.

129 The normal expression of LEF-1 in monocytes and lymphocytes, whose differentiatio

130 we identified aberrant protein expression of LEF-1 specifically in CLL but not in normal mature B-cel

131 ective expression of the activating forms of LEF/TCFs and a bias against suppressing, truncated forms

132 utive activation and prosurvival function of LEF-1 and the Wnt pathway in CLL and uncovered a possibl

133 e importance of the mRNA capping function of LEF-4.

134 enous CD1D transcripts, whereas knockdown of LEF-1 using LEF-1-specific small interfering RNA increas

135 Knockdown of LEF-1 using small interfering RNA potentiates an acetyla

136 of beta-catenin but displayed high levels of LEF-1/TCF genes along with elevated levels of beta-caten

137 gether, our data define a novel mechanism of LEF-1 downregulation in CN patients via enhanced ubiquit

138 However, the exact mechanism of LEF-1 downregulation is unclear.

139 The effect of MR on clinical outcomes of LEF-LG patients undergoing TAVI is unknown.

140 Overexpression of LEF-1 in K562 or Jurkat cells suppresses CD1D promoter a

141 ffect that was accompanied by restoration of LEF-1 protein levels and LEF-1 messenger RNA autoregulat

142 Silencing of LEF-4 in wild-type virus-infected cells suppressed expre

143 because its activity is redundant to that of LEF-4.

144 We demonstrate that collective action of LEFs leads to formation of a dynamic array of consecutiv

145 When the number of LEFs are used that match experimentally based estimates,

146 determined by the microscopic properties of LEFs and their abundance.

147 Safety data on LEF compared to MTX are less conclusive.

148 All patients on LEF, and particularly those on combined LEF+MTX, should

149 vestigated the effects of activated STAT5 on LEF-1 expression and functions in hematopoietic progenit

150 PITX2 transcriptional activation of the p21, LEF-1, and Pitx2c promoters.

151 gamma-catenin and its DNA-binding partner LEF-1 indirectly increase levels of H2AX by suppressing

152 catenin was bound to the Arm-binding partner LEF-1, and its activity was stimulated by phosphorylatio

153 ated by EpICD and its transcription partner, LEF-1.

154 AM580 significantly reduced LEF-1 association at the CD1d promoter region, induced C

155 r demonstrated that TCF-1 directly repressed LEF-1 expression in early thymocytes and that conditiona

156 omote thymocyte maturation while restraining LEF-1 expression to prevent malignant transformation of

157 enin interacts directly with region-specific LEF/TCF factors, and with KLF4 in differentiating, but n

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

159 We conditionally targeted LEF-1, and by combination with germline deletion of TCF-

160 element near a consensus T-cell factor (TCF)/LEF binding site.

161 ners with members of the T cell factor (TCF)/LEF transcription factors to regulate gene expression.

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

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

164 se patterns are regulated in part by the TCF-LEF transcription factor POP-1.

165 TCF/LEF activation in the central retina does not correlate

166 TCF/LEF activation was analyzed in the TOPgal (TCF optimal p

167 TCF/LEF factors are ancient context-dependent enhancer-bindi

168 ctor/lymphoid enhancer binding factor-1 (TCF/LEF) motifs, consistent with canonical Wnt target regula

169 HLH-1 and FOZI-1, 2) differential POP-1 (TCF/LEF) transcriptional activity along the anterior-posteri

170 A TCF/LEF luciferase assay was used to study functional canoni

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

172 brain at E9.5, demonstrated in vivo by a TCF/LEF-reporter transgene.

173 e study was to characterize more fully a TCF/LEF-responsive retinal progenitor population in the mous

174 reduced the ability of Dvl3 to activate TCF/LEF (T-cell factor/lymphoid enhancer factor)-driven tran

175 mice showed that hepatocytes with active TCF/LEF transcription are confined to the pericentral zone a

176 on of Sox proteins with beta-catenin and TCF/LEF proteins regulates the stability of beta-catenin and

177 ed reduction of beta-catenin protein and TCF/LEF reporter activity, and restored cell growth, suggest

178 nd cell proliferation/survival genes and TCF/LEF targets.

179 g beta-catenin nuclear translocation and TCF/LEF-dependent gene transactivation.

180 nes transcription in a beta-catenin- and TCF/LEF-dependent manner.

181 ulates the stability of beta-catenin and TCF/LEF.

182 Screening 23dd in a cell-based TCF/LEF reporter gene assay restored the activation of Wnt s

183 Upon Wnt signaling, beta-catenin binds TCF/LEF transcription factors.

184 scriptional activation was quantified by TCF/LEF luciferase reporter assays.

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

186 beta-Catenin-TCF/LEF complexes may function primarily in feedback regulat

187 ed previous findings that a beta-catenin-TCF/LEF interaction is not required for differentiation, and

188 Disruption of the beta-catenin-TCF/LEF interaction resulted in the accumulation of immature

189 that specifically abrogates beta-catenin-TCF/LEF interaction.

190 and chemical inhibition of beta-catenin-TCF/LEF signaling in human CD34+ cells reduced granulocytic

191 ought to be mediated by the beta-catenin-TCF/LEF-dependent canonical pathway.

192 uPAR (pU) suppressed WNT-7a-beta-catenin-TCF/LEF-mediated transactivation both in vitro and in vivo.

193 ent led to increased WNT-7a-beta-catenin-TCF/LEF-mediated transactivation, thereby promoting cancer s

194 ssociation of uPAR with the beta-catenin.TCF/LEF complex and various other TF involved during embryon

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

196 chanistically, we show that beta-Catenin/TCF/LEF-1 binds to the promoter of miR-183-96-182 cluster ge

197 3-96-182 biogenesis through beta-Catenin/TCF/LEF-1 pathway in gastric cancer cells.

198 182 and miR-183 through the beta-Catenin/TCF/LEF-1 pathway.

199 iple pathways including the beta-Catenin/TCF/LEF-1 pathway.

200 beta-catenin and decreased beta-catenin/TCF/LEF-mediated transcription.

201 pression via an evolutionarily-conserved TCF/LEF site within the WNT3A promoter.

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

203 e activity of the beta-catenin-dependent TCF/LEF promoter.

204 alization of beta-catenin and downstream TCF/LEF-mediated transcription, which are normally observed

205 specific protein complexes at the DPAGT1 TCF/LEF binding region that were competed off with antibodie

206 Interestingly, the DPAGT1 TCF/LEF sequence also interacted with gamma-catenin, a close

207 In addition, the DPAGT1 TCF/LEF sequence drove the expression of the luciferase repo

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

209 g as a coactivator for the Wnt effector, TCF/LEF protein.

210 beta-catenin, and also greatly enhanced TCF/LEF-regulated reporter gene activity in a beta-catenin-d

211 factor/lymphoid enhancer-binding factor (TCF/LEF) consensus sequence.

212 factor/lymphoid enhancer binding factor (TCF/LEF) family are a class of intrinsic regulators that are

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

214 T cell factor/lymphoid enhancer factor (TCF/LEF) reporter activity, and inhibited the expression of

215 factor/lymphoid enhancer-binding factor (TCF/LEF) transcription factors and subsequent transcription

216 T cell factor/lymphoid enhancer factor (TCF/LEF) transcription factors are downstream effectors of W

217 /T-cell factor/lymphoid enhancer factor (TCF/LEF) transcriptional activation was quantified by TCF/LE

218 T-cell factor/lymphoid enhancer factor (TCF/LEF) transcriptional activator.

219 factor/lymphoid enhancer-binding factor (TCF/LEF), causing subsequent repression of target gene trans

220 T cell factor/lymphoid enhancer factor (TCF/LEF)-reporter mice (TOPGal mice) and liver-specific beta

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

222 fication of a potential binding site for TCF/LEF factors, obligate binding partners for beta-catenin,

223 plant transfection assays, we identified TCF/LEF-binding sequences within two distal enhancers of the

224 rly, WNT3a enhanced luciferase levels in TCF/LEF luciferase assays, which also were blocked by sFRP1.

225 lytic processing causing the increase in TCF/LEF promoter activity.

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

227 igands, including WNT7B, which increases TCF/LEF-dependent transcription without activating Wnt corec

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

229 ockout cells, we show that FGF19 induces TCF/LEF reporter activity in parental (WT/Delta45) and in WT

230 small interfering RNA (siRNA) inhibited TCF/LEF-mediated gene transcription.

231 cell-specific transcription factor/LEF (TCF/LEF) dual luciferase reporter assay, we demonstrated con

232 re we demonstrate that beta-catenin, not TCF/LEF, is required for muscle differentiation.

233 n of beta-catenin and subsequent loss of TCF/LEF (T cell factor1/lymphoid enhancer factor1) activity.

234 Furthermore, removal of TCF/LEF binding sites in a CD24-luciferase reporter resulted

235 though it reduced both the expression of TCF/LEF factors and their induction by Wnt.

236 ation assays confirmed direct binding of TCF/LEF factors to the promoter and putative enhancer region

237 s study aimed to investigate the role of TCF/LEF transcription factors in human articular chondrocyte

238 ause of its function as a coactivator of Tcf/LEF-family transcription factors.

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

240 ication, we knocked down beta-catenin or TCF/LEF members in primary astrocytes and astrocytomas trans

241 in binds near to and activates potential TCF/LEF sites in the Mitf and Otx2 enhancers.

242 confidence scores are two members of the TCF/LEF family of DNA-binding proteins that control the tran

243 of this pathway, binds to members of the TCF/LEF family of transcription factors to modulate hundreds

244 examined the pituitary expression of the TCF/LEF family of transcription factors, which mediate WNT s

245 binding by transcription factors of the TCF/LEF family were observed for the risk-increasing allele

246 including transcription factors from the TCF/LEF family.

247 en and studies focused on members of the TCF/LEF gene family refine our understanding of how aberrant

248 also known as TCF7L1) is a member of the TCF/LEF transcription factor family that is central in regul

249 USP21 deubiquitinates and stabilizes the TCF/LEF transcription factor TCF7, which promotes cancer cel

250 The TCF/LEF-beta-catenin complex then recruits a variety of tran

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

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

253 Endogenous GAC63 was recruited to TCF/LEF-responsive enhancer elements when beta-catenin level

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

255 he nucleus, beta-catenin associates with TCF/LEF sequence specific transcription factors to activate

256 ts as a transcriptional coactivator with TCF/LEF transcription factors, promoting expression of a bro

257 on of the co-activator beta-catenin with TCF/LEF transcription factors.

258 t differences in repression potential of TCF/LEFs correlates with their affinities for TLE-Q, rather

259 Activation of TCF/LEFs is a hallmark of the Wnt/beta-catenin pathway; howe

260 t an important role of beta-catenin and TCF4/LEF binding-sites for activating (alpha)-promoter, while

261 We concluded that LEF-7 expedites virus replication most likely by selecti

262 Site-directed mutagenesis demonstrated that LEF-7's N-terminal F-box is necessary for gamma-H2AX rep

263 We determined that LEF-7 is a nuclear F-box protein that interacts with hos

264 Moreover, we find that LEF-1 and other hESC enhancers recruit RNAPII complexes

265 We found that LEF-1 binds specifically to the CD1D promoter.

266 of histone H3/H4, supporting the notion that LEF-1 acts as a transcriptional repressor for the CD1D g

267 Here we report that LEF-10, a baculovirus-encoded protein, behaves as a prio

268 associated protein 1 (SKP1), suggesting that LEF-7 acts as a substrate recognition component of SKP1/

269 The LEF-1 tail relieves electrostatic repulsion that would o

270 ibited LEF-1-dependent autoregulation of the LEF-1 gene promoter by binding to the LEF-1 protein, rec

271 n synergistically enhanced activation of the LEF-1 promoter in combination with PITX2 and Lef-1 isofo

272 PITX2 isoforms regulate the LEF-1 promoter, and beta-catenin synergistically enhance

273 of the LEF-1 gene promoter by binding to the LEF-1 protein, recruiting Nemo-like kinase and the E3 ub

274 location and subsequent interaction with the LEF/TCF was required for the EMT process.

275 >/=moderate MR assigned to medical therapy, LEF-LG patients with >/=moderate MR undergoing TAVI had

276 e luciferase expression confirmed that these LEF-1/TCF binding elements are able to confer robust upr

277 Thus, LEF-7 is essential for efficient baculovirus replication

278 hat alpha-catenin binds with beta-catenin to LEF-1/TCF DNA-binding proteins in Wnt3a signaling cells

279 3 ubiquitin-ligase NARF to LEF-1, leading to LEF-1 ubiquitination and a reduction in LEF-1 protein le

280 am of G-CSF receptor signaling that leads to LEF-1 downregulation.

281 e kinase and the E3 ubiquitin-ligase NARF to LEF-1, leading to LEF-1 ubiquitination and a reduction i

282 ranscripts, whereas knockdown of LEF-1 using LEF-1-specific small interfering RNA increases CD1D tran

283 ect on the PITX2 synergistic activation with LEF-1 and beta-catenin co-factors.

284 As compared with LEF-LG patients with >/=moderate MR assigned to medical

285 rval, 1.31-8.15]; P=0.011), as compared with LEF-LG patients with </=mild MR.

286 ndent function for Smad4 in cooperating with LEF/TCF to activate c-myc expression.

287 dual roles, i.e., acting cooperatively with LEF-1 to promote thymocyte maturation while restraining

288 Patients with LEF had the worst survival outcome, whereas patients wit

289 Patients with LEF or PLF AS have a higher operative risk, but pre-oper

290 s undergoing TAVI, 113 (18.7%) patients with LEF-LG severe aortic stenosis (mean gradient </=40 mm Hg

291 t be withheld from symptomatic patients with LEF-LG severe aortic stenosis even in the presence of mo

292 ies have shown greater withdrawal rates with LEF, the incidence of infection and elevated transaminas

293 promoter identified multiple consensus TCF x LEF elements, one of which was also a consensus binding

294 TCF x LEF factors are normally repressive but when bound to DN

295 wed that in hypertrophic chondrocytes, TCF x LEF x beta-catenin complexes occupy the consensus TCF x

296 catenin complexes occupy the consensus TCF x LEF x Sox9 site and activate Ccn2 expression.

297 ose that differential occupancy of the TCF x LEF x Sox9 site by Sox9 versus beta-catenin restricts hi

298 ng luciferase reporter constructs, the TCF x LEF x Sox9 site was found to be involved in stage-specif

299 expression by binding to the consensus TCF x LEF x Sox9 site.

300 At 1 year, LEF-LG patients with >/=moderate MR had an adjusted 3-fo