Human LEF1 blocking peptide

Name: Human LEF1 blocking peptide
SKU: CDBP1740
Rating: 5 (1 reviews)

Synthetic Human LEF1 blocking peptide for Apuri, BL, ELISA

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COA

SDS

Datasheet

Product Overview

Blocking/Immunizing peptide for anti-LEF1 antibody

Target

LEF1

Nature

Synthetic

Tag/Conjugate

Unconjugated

Application Notes

For in vitro research use only. Not intended for any diagnostic or therapeutic purpose. Not for human or animal consumption.

Format

Lyophilized powder

Preservative

None

Storage

Shipped at ambient temperature, store at -20°C.

Gene ID

51176

UniProt ID

Q9UJU2

Antigen Description

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]

Function

C2H2 zinc finger domain binding; DNA binding; DNA binding, bending; armadillo repeat domain binding; beta-catenin binding; beta-catenin binding; chromatin binding; cysteine-type endopeptidase inhibitor activity involved in apoptotic process; enhancer bind

Synonyms

LEF1; lymphoid enhancer-binding factor 1; TCF1ALPHA; TCF7L3; TCF10; TCF1-alpha; T cell-specific transcription factor 1-alpha; LEF-1; FLJ46390; DKFZp586H0919;

Citations

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Customer Reviews

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Transforming growth factor-beta 1 enhances proliferative and metastatic potential by up-regulating lymphoid enhancer-binding factor 1/integrin alpha M beta 2 in human renal cell carcinoma

MOLECULAR AND CELLULAR BIOCHEMISTRY

Authors: Liu, Yuting; Shang, Donghao

Abstract

Renal cell carcinoma (RCC) is a kind of malignant tumor with high recurrence, and it is urgent to find molecular markers for diagnosis and prognosis of RCC. Our study investigated the expression and function of integrin alpha M beta 2 in RCC cells, aiming to understand the role of integrin alpha M beta 2 in RCC and develop new therapeutic target for RCC. Overexpression and knockdown of lymphoid enhancer-binding factor 1 (LEF1) were performed using vector containing full-length cDNA and via siRNA technology, respectively. The expressions of mRNA and protein were detected by RT-PCR and Western blot, respectively. Proliferation of RCC cell was analyzed using WST-1 assay, and metastasis of RCC cell was evaluated using the transwell system. Our results demonstrated that LEF1 and integrin alpha M beta 2 were up-regulated in RCC cells via TGF-beta 1-dependent mechanism, and LEF1 together with beta-catenin directly increased integrin alpha M beta 2 level. On the other hand, TGF-beta 1-induced proliferation, migration and invasion were suppressed by function-blocking antibody against integrin alpha M beta 2 in RCC cells. In addition, integrin alpha M beta 2 is crucial for LEF1 mediated cell invasion by regulating MMP-2, MMP-9 and calpain-2 secretion in RCC cells. LEF1/integrin alpha M beta 2 expression was regulated by TGF-beta 1, and LEF1/integrin alpha M beta 2 was involved in TGF-beta 1's improvement effects on the proliferation and metastasis of RCC. Blocking integrin alpha M beta 2 activity could be a therapeutic option for patients with advanced RCC.

Altered Wnt and NF-kappa B Signaling in Facet Joint Osteoarthritis: Insights from RNA Deep Sequencing

TOHOKU JOURNAL OF EXPERIMENTAL MEDICINE

Authors: Chen, Chu; Bao, Guo-Feng; Xu, Guanhua; Sun, Yuyu; Cui, Zhi-Ming

Abstract

Facet joint osteoarthritis is common lumbar osteoarthritis characterized by facet joint cartilage degeneration. However, the molecular basis of facet joint osteoarthritis remains largely undetermined. In the current study, we collected facet joint tissue samples from 10 control patients and 48 patients with facet joint osteoarthritis (20 patients with moderate degeneration and 28 with severe degeneration). The control patients underwent internal fixation of the lumbar spine due to vertebral fracture. RNA deep sequencing was performed, and Bioinformatic tools were applied. Among top 30 enriched signaling pathways, we focused on two inflammation-related signaling pathways, Wnt and NF-kappa B signaling pathways. Subsequently, using the quantitative RT-PCR analysis, we confirmed that in Wnt signaling pathway, the mRNA levels of Dickkopf WNT Signaling Pathway Inhibitor 2 (DKK2), Sex-determining Region Y-box 17 (SOX17), MYC, Cyclin D1, Calcium/Calmodulin Dependent Protein Kinase II Alpha (CAMK2A), and Wnt Family Member 11 and 5 were increased in facet joint osteoarthritis, while the mRNA levels of WNT Inhibitory Factor 1, Casein Kinase 1 Alpha 1, Transcription Factor 7/Lymphoid Enhancer Binding Factor 1 (TCF7/LEF1), and VANGL Planar Cell Polarity Protein 2 were decreased. In NF-kappa B signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein Al were decreased. These results suggest that Wnt and NF-kappa B signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.