Mouse Angptl4 blocking peptide

Name: Mouse Angptl4 blocking peptide
SKU: CDBP0399
Rating: 5 (1 reviews)

Synthetic Mouse Angptl4 blocking peptide for Apuri, BL, ELISA

COA

SDS

Datasheet

Summary

Product Overview

Blocking/Immunizing peptide for anti-Angptl4 (mouse) antibody

Target

Angptl4 (mouse)

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.

Entrez Gene ID

57875

Antigen Description

This gene encodes a glycosylated, secreted protein containing a C-terminal fibrinogen domain. The encoded protein is induced by peroxisome proliferation activators and functions as a serum hormone that regulates glucose homeostasis, lipid metabolism, and insulin sensitivity. This protein can also act as an apoptosis survival factor for vascular endothelial cells and can prevent metastasis by inhibiting vascular growth and tumor cell invasion. The C-terminal domain may be proteolytically-cleaved from the full-length secreted protein. Decreased expression of this gene has been associated with type 2 diabetes. Alternative splicing results in multiple transcript variants. This gene was previously referred to as ANGPTL2 but has been renamed ANGPTL4.

Function

enzyme inhibitor activity; receptor binding;

Synonyms

ANGPTL4; angiopoietin-like 4; angiopoietin-related protein 4; 425O18-1; secreted protein Bk89; angiopoietin-like protein 4; fasting-induced adipose factor; fibrinogen/angiopoietin-related protein; major histocompatibility complex region NG27; hepatic fibrinogen/angiopoietin-related protein; Arp4; Bk89; Fiaf; Ng27; Pgar; Hfarp; Pgarg; Pp1158;

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

MNK1 signaling induces an ANGPTL4-mediated gene signature to drive melanoma progression

ONCOGENE

Authors: Yang, William; Khoury, Elie; Guo, Qianyu; Prabhu, Sathyen A.; Emond, Audrey; Huang, Fan; Goncalves, Christophe; Zhan, Yao; Plourde, Dany; Nichol, Jessica N.; Dahabieh, Michael S.; Miller Jr., Wilson H.; del Rincon, Sonia Victoria

Abstract

The BRAF(V600E) mutation occurs in more than 50% of cutaneous melanomas, and results in the constitutive activation of the mitogen-activated protein kinases (MAPK) pathway. MAP kinase-interacting serine/threonine-protein kinase 1 and 2 (MNK1/2) are downstream effectors of the activated MAPK pathway, and important molecular targets in invasive and metastatic cancer. Despite the well-known role of MNK1 in regulating mRNA translation, little is known concerning the impact of its aberrant activation on gene transcription. Here, we show that changes in the activity, or abundance, of MNK1 result in changes in the expression of pro-oncogenic and pro-invasive genes. Among the MNK1-upregulated genes, we identify Angiopoietin-like 4 (ANGPTL4), which in turn promotes an invasive phenotype via its ability to induce the expression of matrix metalloproteinases (MMPs). Using a pharmacologic inhibitor of MNK1/2, SEL201, we demonstrate that BRAF(V600E)-mutated cutaneous melanoma cells are reliant on MNK1/2 for invasion and lung metastasis.

Association of a genetic variant in the angiopoietin-like protein 4 gene with cervical cancer

PATHOLOGY RESEARCH AND PRACTICE

Authors: Rahmani, Farzad; Hasanzadeh, Malihe; Hassanian, Seyed Mahdi; Khazaei, Majid; Esmaily, Habibollah; Asef-Agah, Seyed Ami; Naghipour, Alireza; Ferns, Gordon A.; Avan, Amir

Abstract

Background: Cervical cancer is among the most aggressive gynecological tumors and is a consequence of interactions between genetic and epigenetic factors. Several genetic polymorphisms related to cervical cancer have been reported in previous clinical studies. In this study, we aimed to explore the possible relationship between polymorphisms of the ANGPTL4 gene locus and susceptibility to cervical cancer. Methods: We investigated the relationship between a single nucleotide polymorphism (SNP) in the ANPGTL4 gene (rs116843064) and risk of cervical cancer in a total of 378 individuals with (n = 151), or without (n = 227) cancer. DNA was extracted, and genotyped using a Taq-Man based real time PCR. Results: The ANPGTL4 polymorphism was found to be associated with an increased risk of developing cervical neoplasia using dominant model (OR = 12.48, CI = 4.9-31.82, p< 0.0001) and additive model (OR = 30.54, CI = 7.35-126.89, p < 0.0001). Conclusion: Our results indicate that there is a strong association between ANPGTL4 and the susceptibility for cervical cancer suggesting that it is a potential risk factor for cervical neoplasia.