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Lymphoid enhancer-binding factor 1

Lymphoid Enhancer-Binding Factor 1, LEF-1
This gene encodes a transcription factor belonging to a family of proteins that share homology with the high mobility group protein-1. The protein encoded by this gene can bind to a functionally important site in the T-cell receptor-alpha enhancer, thereby conferring maximal enhancer activity. This transcription factor is involved in the Wnt signaling pathway, and it may function in hair cell differentiation and follicle morphogenesis. Mutations in this gene have been found in somatic sebaceous tumors. This gene has also been linked to other cancers, including androgen-independent prostate cancer. Alternative splicing results in multiple transcript variants. [provided by RefSeq, Oct 2009] (from NCBI)
Top mentioned proteins: TCF, CAN, V1a, PCNA, TCF4
Papers on Lymphoid Enhancer-Binding Factor 1
Regulation of the TMEPAI promoter by TCF7L2: the C-terminal tail of TCF7L2 is essential to activate the TMEPAI gene.
Itoh et al., Machida, Japan. In J Biochem, Jan 2016
We previously found that TCF7L2 could activate the TMEPAI gene efficiently, whereas LEF1 could not nearly augment its transcription.
Esophageal squamous cell carcinoma cells modulate chemokine expression and hyaluronan synthesis in fibroblasts.
Fischer et al., Düsseldorf, Germany. In J Biol Chem, Jan 2016
Knockdown of LEF1, a downstream target of Wnt signaling, abrogated Has2 and Has2os2 induction.
A novel cell-penetrating peptide suppresses breast tumorigenesis by inhibiting β-catenin/LEF-1 signaling.
Tsai et al., Kao-hsiung, Taiwan. In Sci Rep, Dec 2015
The inhibition of β-catenin/LEF-1 signaling is an emerging strategy in cancer therapy.
WNT-associated gene expression in human mesenchymal stromal cells under hypoxic stress.
Buravkova et al., Moscow, Russia. In Dokl Biochem Biophys, Nov 2015
FZD1, FZD3, SFRP1, and SFRP4 genes were up-regulated after short-term hypoxic stress (0.1% O2), whereas the expression of LEF-1 and RUVBL1 genes was significantly inhibited (down-regulated).
Non-genomic and Immune Evolution of Melanoma Acquiring MAPKi Resistance.
Lo et al., Los Angeles, United States. In Cell, Oct 2015
We identified in the tumor cell compartment supra-physiologic c-MET up-expression, infra-physiologic LEF1 down-expression and YAP1 signature enrichment as drivers of acquired resistance.
LEF-1 and TCF-1 orchestrate T(FH) differentiation by regulating differentiation circuits upstream of the transcriptional repressor Bcl6.
Crotty et al., Los Angeles, United States. In Nat Immunol, Sep 2015
Here we report that selective loss of Lef1 or Tcf7 (which encode the transcription factor LEF-1 or TCF-1, respectively) resulted in T(FH) cell defects, while deletion of both Lef1 and Tcf7 severely impaired the differentiation of T(FH) cells and the formation of GCs.
Novel mechanisms for the vitamin D receptor (VDR) in the skin and in skin cancer.
Jiang et al., San Francisco, United States. In J Steroid Biochem Mol Biol, Apr 2015
Whereas, VDR binding to β-catenin may block its activation of TCF/LEF1 sites, β-catenin binding to VDR may enhance its activation of VDREs.
MicroRNA-10a Influences Osteoblast Differentiation and Angiogenesis by Regulating β-Catenin Expression.
He et al., In Cell Physiol Biochem, 2014
Cell viability were analyzed by MTT and the protein expression of β-catenin, LEF1, cyclinD1, MMP2, and VEGF were detected by Western blotting; VEGF and VE-cadherin release were assessed by ELISA, and the migration of MUVECs, as well as tube formation were also detected.
Targeting the β-catenin nuclear transport pathway in cancer.
Henderson et al., Sydney, Australia. In Semin Cancer Biol, 2014
In response to a wnt stimulus or specific gene mutations, β-catenin is stabilized and translocates to the nucleus where it binds TCF/LEF-1 transcription factors to transactivate genes that drive tumor formation.
A molecular basis for classic blond hair color in Europeans.
Kingsley et al., Stanford, United States. In Nat Genet, 2014
This enhancer contains a common SNP (rs12821256) that alters a binding site for the lymphoid enhancer-binding factor 1 (LEF1) transcription factor, reducing LEF1 responsiveness and enhancer activity in cultured human keratinocytes.
TCF-1 and LEF-1 act upstream of Th-POK to promote the CD4(+) T cell fate and interact with Runx3 to silence Cd4 in CD8(+) T cells.
Xue et al., Iowa City, United States. In Nat Immunol, 2014
The transcription factors TCF-1 and LEF-1 are essential for early T cell development, but their roles beyond the CD4(+)CD8(+) double-positive (DP) stage are unknown.
Through the glass darkly: intraepithelial neoplasia, top-down differentiation, and the road to ovarian cancer.
Xian et al., Boston, United States. In J Pathol, 2013
Both direct and indirect ('surrogate') precursors suggest that the benign tube undergoes important biological changes after menopause, acquiring abnormalities in gene expression that are often shared with malignancy, including PAX2, ALDH1, LEF1, RCN1, RUNX2, beta-catenin, EZH2, and others.
[In situ analyses of molecular mechanisms of colorectal carcinogenesis].
Kriegl, München, Germany. In Pathologe, 2013
Clearly more homogeneous is the expression of TCF4 and LEF1 which are the main binding partners of β-catenin and γ-catenin and are likewise important prognostic markers.
Identification of gene expression-based prognostic markers in the hematopoietic stem cells of patients with myelodysplastic syndromes.
Boultwood et al., Bournemouth, United Kingdom. In J Clin Oncol, 2013
RESULTS: We identified several genes, the expression of which was significantly associated with survival of patients with MDS, including LEF1, CDH1, WT1, and MN1.
Physiological role of β-catenin/TCF signaling in neurons of the adult brain.
Wisniewska, Warsaw, Poland. In Neurochem Res, 2013
Wnt/β-catenin pathway, the effectors of which are transcription factors of the LEF1/TCF family, is primarily associated with development.
MiR-218 reverses high invasiveness of glioblastoma cells by targeting the oncogenic transcription factor LEF1.
Jiang et al., Beijing, China. In Oncol Rep, 2012
miR-218 is involved in the invasive behavior of glioblastoma cells by targeting LEF1 and blocking the invasive axis.
LEF-1 regulates proliferation and MMP-7 transcription in breast cancer cells.
Hass et al., Hannover, Germany. In Genes Cells, 2012
our results indicate a pivotal role of LEF-1 in the regulation of proliferation and MMP-7 transcription in breast cancer cells.
Hepatocyte growth factor activates Wnt pathway by transcriptional activation of LEF1 to facilitate tumor invasion.
Jeng et al., Taipei, Taiwan. In Carcinogenesis, 2012
findings suggest that transcriptional activation of LEF1 is a mechanism of cross talk between HGF/c-Met and Wnt/beta-catenin pathways and is essential for HGF-induced tumor invasion
NLK positively regulates Wnt/β-catenin signalling by phosphorylating LEF1 in neural progenitor cells.
Ishitani et al., Fukuoka, Japan. In Embo J, 2012
Nlk2 is essential for the phosphorylation and activation of Lef1 transcriptional activity in neural progenitor cells.
Aberrant beta-catenin and LEF1 expression may predict the clinical outcome for patients with oropharyngeal cancer.
Papagerakis et al., Ann Arbor, United States. In Int J Immunopathol Pharmacol, 2012
results suggest that assessing intracellular beta-catenin and LEF1 expression might help in patient risk stratification and outcome prediction
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