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

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

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

12 vided by SRY and lymphoid enhancer factor 1 (LEF-1): whereas the SRY tail remains in the minor groove

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

33 the Wnt pathway including Wnt-1, Wnt-2b and LEF-1.

34 es for two members of this family, TCF 7 and LEF 1, produce full-length forms that mediate Wnt signal

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 bute to its invariance among SOX-related and LEF-1-related transcription factors.

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

43 3A-stimulated beta-catenin stabilization and LEF/TCF reporter activity.

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

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

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

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

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

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

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

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

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

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

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

55 ls of beta-catenin and activate beta-catenin/LEF/TCF-dependent transcriptional activity.

56 binding and transactivation of beta-catenin:LEF-1 complexes on chromatin templates in vitro.

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

58 We show here that CK2 enhances beta-catenin:LEF-1 transactivation in vivo and in vitro and that beta

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

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

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

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

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

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

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

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

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

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

80 cer-binding factor 1/T cell-specific factor (LEF/TCF) family of transcription factors on the c-myc pr

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 of the photosynthetic linear electron flux (LEF).

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

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

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

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

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

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

92 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

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

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

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

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

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

98 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

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

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

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

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

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

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

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

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

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

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

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

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

111 Promoter 1 produces full-length LEF-1 protein, which recruits beta-catenin to Wnt target

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

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

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

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

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

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

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

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

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

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

122 -catenin is a transcriptional coactivator of LEF-1/TCF DNA-binding proteins in the Wnt/Wg signaling p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

137 Here, we demonstrate the essential nature of LEF-4 by RNA interference and bacmid knockout technology

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

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

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

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

142 cate that the hAR gene is a direct target of LEF-1/TCF transcriptional regulation in PCa cells but al

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 transcription factors on the c-myc promoter LEF/TCF-binding elements (TBE1 and TBE2).

155 hoid enhancer factor/T cell factor proteins (LEF/TCFs) mediate Wnt signals in the nucleus by recruiti

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

175 ion/nuclear translocation, and abrogates TCF/LEF-specific transcriptional co-activation by beta-caten

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

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

178 A promotes the transcriptional activity (TCF/LEF transactivation) of beta-catenin; (iii) mutation of

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

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

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

182 sphorylation, nuclear translocation, and TCF/LEF transcriptional activation is effectively blocked by

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

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

185 beta-catenin as a coactivator for AR and TCF/LEF.

186 We propose that the balance between TCF/LEF and coactivator(s), achieved by elevating coactivato

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

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

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

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

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

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

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

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

195 3-96-182 biogenesis through beta-Catenin/TCF/LEF-1 pathway in gastric cancer cells.

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

197 182 and miR-183 through the beta-Catenin/TCF/LEF-1 pathway.

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

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

200 Msx2-CM stimulated Wnt-dependent TCF/LEF transcription, and Msx2-transduced cells exhibited i

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

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

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

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

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

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

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

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

209 T-cell factor/lymphoid enhancer factor (TCF/LEF) family of transcriptional activator proteins and fo

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

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

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

213 T-cell factor/lymphoid enhancer factor (TCF/LEF) transcription factors to regulate genes important f

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

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

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

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

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

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

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

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

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

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

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

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

226 nucleus leading to beta-catenin-mediated TCF/LEF-transcriptional co-activation.

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

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

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

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

231 -catenin, a transcriptional activator of TCF/LEF genes.

232 Activation of TCF/LEF signalling decreases factor withdrawal-induced apopt

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

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

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

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

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

238 (the canonical pathway) and/or reducing TCF/LEF levels (worm endoderm), determines Wnt signal streng

239 tion in the nucleus, where it stimulates TCF/LEF-dependent gene transcription.

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

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

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

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

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

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

246 Canonical Wnt signaling converts the TCF/LEF transcription factor from repressor to activator by

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

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

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

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

251 yclin-D1, and c-Myc) in conjunction with TCF/LEF (TCF).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

267 The LEF/TCF family exhibits extensive patterns of alternativ

268 the minor groove distal to the HMG box, the LEF-1 tail binds back across the center of the bent DNA

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

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

271 The size of the LEF/TCF family is small: approximately four members in v

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