Cell Signaling Technology

Product Pathways - Adhesion

N-Cadherin Antibody #4061

Applications Reactivity Sensitivity MW (kDa) Source
W H M R Mk (Dg) Endogenous 140 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey  Dg=Dog
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

N-Cadherin Antibody detects endogenous levels of total N-cadherin protein. The antibody does not cross-react with other cadherin family members.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues within the amino-terminus of human N-cadherin. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from A431, MCF-7, C2C12, HUVEC, BAEC, C6 and H-4-II-E cells, using N-cadherin Antibody.

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). Recent studies indicate that cancer cells have up-regulated 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).

  1. Wheelock, M.J. and Johnson, K.R. (2003) Annu. Rev. Cell. Dev. Biol. 19, 207-235.
  2. Christofori, G. (2003) EMBO J. 22, 2318-2323.
  3. Hazan, R.B. et al. (2004) Ann. NY Acad. Sci. 1014, 155-163.
  4. Bryant, D.M. and Stow, J.L. (2004) Trends Cell Biol. 14, 427-434.
  5. Rabascio, C. et al. (2004) Cancer Res. 64, 4373-4377.
  6. Yamaoka-Tojo, M. et al. (2006) Arterioscler. Thromb. Vasc. Biol. 26, 1991-1997.
  7. Patel, I.S. et al. (2003) Int. J. Cancer 106, 172-177.
  8. Sanders, D.S. et al. (2000) J. Pathol. 190, 526-530.

Application References

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Companion Products

For Research Use Only. Not For Use In Diagnostic Procedures.

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