VE-Cadherin (E6N7A) Rabbit mAb #93467

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Supporting Data

REACTIVITY	H
SENSITIVITY	Endogenous
MW (kDa)	130, 100
Source/Isotype	Rabbit IgG

Application Key:

WB-Western Blotting
IHC-Immunohistochemistry

Species Cross-Reactivity Key:

H-Human

Product Information

Product Usage Information

Application	Dilution
Western Blotting	1:1000
Immunohistochemistry (Paraffin)	1:200 - 1:800

Storage

Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

For a carrier free (BSA and azide free) version of this product see product #33143.

Protocol

Specificity / Sensitivity

VE-Cadherin (E6N7A) Rabbit mAb recognizes endogenous levels of total VE-Cadherin protein.

Species Reactivity:

Human

Source / Purification

Monoclonal antibody is produced by immunizing animals with recombinant protein specific to the extracellular domain of human VE-Cadherin protein.

Background

Cadherins are a superfamily of transmembrane glycoproteins that contain cadherin repeats of approximately 100 residues in their extracellular domain. Cadherins mediate calcium-dependent cell-cell adhesion and play critical roles in normal tissue development (1). The classic cadherin subfamily includes N-, P-, R-, B-, and E-cadherins, as well as about ten other members that are found in adherens junctions, a cellular structure near the apical surface of polarized epithelial cells. The cytoplasmic domain of classical cadherins interacts with β-catenin, γ-catenin (also called plakoglobin), and p120 catenin. β-catenin and γ-catenin associate with α-catenin, which links the cadherin-catenin complex to the actin cytoskeleton (1,2). While β- and γ-catenin play structural roles in the junctional complex, p120 regulates cadherin adhesive activity and trafficking (1-4). Investigators consider E-cadherin an active suppressor of invasion and growth of many epithelial cancers (1-3). Research studies indicate that cancer cells have upregulated N-cadherin in addition to loss of E-cadherin. This change in cadherin expression is called the "cadherin switch." N-cadherin cooperates with the FGF receptor, leading to overexpression of MMP-9 and cellular invasion (3). Research studies have shown that in endothelial cells, VE-cadherin signaling, expression, and localization correlate with vascular permeability and tumor angiogenesis (5,6). Investigators have also demonstrated that expression of P-cadherin, which is normally present in epithelial cells, is also altered in ovarian and other human cancers (7,8).

Database Links

UniProt ID: P33151

Entrez-Gene Id: 1003

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