MMP26 peptide

Name: MMP26 peptide
SKU: DAG-P0919
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Nature

Synthetic

Tag/Conjugate

Unconjugated

Purity

> 95 % by SDS-PAGE.

Format

Lyophilized

Preservative

None

Storage

Shipped at 4°C. Upon delivery aliquot and store at -20°C or -80°C. Avoid repeated freeze / thaw cycles. Preservative: None Constituents: 0.001% Tween 20, 30mM HEPES, 2mM EDTA, 150mM Sodium chloride, pH 6.75

Reconstitution

MMP26 peptide is supplied as 1mg of dried peptide. When the peptide is reconstituted in 1 mL strile water, the concentration will be 1 mg/mL.

Introduction

Proteins of the matrix metalloproteinase (MMP) family are involved in the breakdown of extracellular matrix in normal physiological processes, such as embryonic development, reproduction, and tissue remodeling, as well as in disease processes, such as arthritis and metastasis. Most MMPs are secreted as inactive proproteins which are activated when cleaved by extracellular proteinases. The encoded protein degrades type IV collagen, fibronectin, fibrinogen, casein, vitronectin, alpha 1-antitrypsin, alpha 2-macroglobulin, and insulin-like growth factor-binding protein 1, and activates MMP9 by cleavage. The protein differs from most MMP family members in that it lacks a conserved C-terminal protein domain. [provided by RefSeq, Jul 2008]

Entrez Gene ID

56547

Synonyms

MMP26; matrix metallopeptidase 26; matrix metalloproteinase-26; MMP-26; endometase; matrilysin 2; matrilysin-2; matrix metalloproteinase 26;

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

MiR-125b regulates endometrial receptivity by targeting MMP26 in women undergoing IVF-ET with elevated progesterone on HCG priming day

SCIENTIFIC REPORTS

Authors: Chen, Cheng; Zhao, Yue; Yu, Yang; Li, Rong; Qiao, Jie

Abstract

On the women undergoing IVF-ET with elevated progesterone on human chorionic gonadotrophin priming, the assisted reproductive technology outcome is poor. But, due to the unknown mechanism of this process, no effective method has been found to overcome this difficulty. Here, we investigated the roles of miR-125b and its target gene, MMP26, in endometrial receptivity (ER) in these women. The expression of miR-125b was significantly up-regulated in EECs in women with elevated progesterone during the window of implantation, and it showed a progesterone-dependent effect in vitro. Similarly, the expression of miR-125b was significantly up-regulated in the preimplantation period, and was down-regulated in the implantation period and the post-implantation period in mouse EECs. In addition, miR-125b showed a greater decrease at implantation sites than it did at interimplantation sites. The luciferase report assay demonstrated that MMP26 is a target gene of miR-125b. And the expression profile of MMP26 showed an inverse relationship with miR-125b in vivo and in vitro. Overexpression of miR-125b in human EECs inhibited cell migration and invasion. Gain-of-function of miR-125b induced a significant decrease in the number of implantation sites. In conclusion, these data shed new light on how miR-125b triggers ER decline through the regulation of MMP26 function.

A83-01 inhibits TGF-beta-induced upregulation of Wnt3 and epithelial to mesenchymal transition in HER2-overexpressing breast cancer cells

BREAST CANCER RESEARCH AND TREATMENT

Authors: Wu, Yanyuan; Tran, Trinh; Dwabe, Sami; Sarkissyan, Marianna; Kim, Juri; Nava, Miguel; Clayton, Sheilah; Pietras, Richard; Farias-Eisner, Robin; Vadgama, Jaydutt V.

Abstract

The aim of this study is to investigate the mechanisms of interactions between TGF-beta and Wnt/beta-catenin pathways that induce and regulate EMT and promote breast cancer cells to become resistant to treatment. The effect of TGF-beta on Wnt/beta-catenin signaling pathway was examined by using a human Wnt/beta-catenin-regulated cDNA plate array and western blot analysis. The interaction of Twist at promoter of Wnt3 was examined by chromatin immunoprecipitation (ChIP) assay. Secreted Wnt3 level was determined by ELISA assay. HER2-overexpressing breast cancer cells treated with TGF-beta have a reduced response to trastuzumab and exhibited EMT-like phenotype. The TGF-beta-induced EMT in HER2-cells was concordant with upregulation of Wnt3 and beta-catenin pathways. The TGF-beta-induced induction of Wnt3 during EMT was found to be Smad3-dependent. ChIP analysis identified occupancy of Twist at promoter region of Wnt3. Knock-down of Twist by shRNA confirmed the significance of Twist in response to TGF-beta regulating Wnt3 during EMT. Subsequently, TGF-beta-induced matrix metalloproteinases, MMP1, MMP7, MMP9, MMP26, Vascular endothelial growth factors (VEGF), and activation of Wnt/beta-catenin signaling were repressed by the shRNA treatment. TGF-beta R1 ALK5 kinase inhibitor, A83-01 can effectively prevent the TGF-beta-induced Twist and Wnt3. Co-treating A83-01 and trastuzumab inhibited TGF-beta-induced cell invasion significantly in both trastuzumab responsive and resistant cells. Our data demonstrated an important interdependence between TGF-beta and Wnt/beta-catenin pathways inducing EMT in HER2-overexpressing breast cancer cells. Twist served as a linkage between the two pathways during TGF-beta-induced EMT. A83-01 could inhibit the TGF-beta-initiated pathway interactions and enhance HER2-cells response to trastuzumab treatment.