E-Cadherin (4A2) Mouse mAb (Alexa Fluor® 488 Conjugate) #86770
- IF
- F
Supporting Data
| REACTIVITY | H M R |
| SENSITIVITY | Endogenous |
| MW (kDa) | |
| Source/Isotype | Mouse IgG1 |
Application Key:
- IF-Immunofluorescence
- F-Flow Cytometry
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Description
Product Usage Information
| Application | Dilution |
|---|---|
| Immunofluorescence (Immunocytochemistry) | 1:50 |
| Flow Cytometry (Fixed/Permeabilized) | 1:50 |
Storage
Protocol
Specificity / Sensitivity
E-Cadherin (4A2) Mouse mAb (Alexa Fluor® 488 Conjugate) recognizes endogenous levels of total E-cadherin protein. This antibody does not cross-react with other cadherin proteins. Species cross-reactivity for IF-F and IF-IC is human only.
Species Reactivity:
Human, Mouse, Rat
Source / Purification
Monoclonal antibody is produced by immunizing animals with recombinant protein specific to human E-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).
- Wheelock, M.J. and Johnson, K.R. (2003) Annu Rev Cell Dev Biol 19, 207-35.
- Christofori, G. (2003) EMBO J 22, 2318-23.
- Hazan, R.B. et al. (2004) Ann N Y Acad Sci 1014, 155-63.
- Bryant, D.M. and Stow, J.L. (2004) Trends Cell Biol 14, 427-34.
- Rabascio, C. et al. (2004) Cancer Res 64, 4373-7.
- Yamaoka-Tojo, M. et al. (2006) Arterioscler Thromb Vasc Biol 26, 1991-7.
- Patel, I.S. et al. (2003) Int J Cancer 106, 172-7.
- Sanders, D.S. et al. (2000) J Pathol 190, 526-30.
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