Cell Signaling Technology

Product Pathways - Adhesion

Pan-Cadherin (28E12) Rabbit mAb #4073

Applications Reactivity MW (kDa) Source Isotype
W H M R 130-150 Rabbit IgG

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

Specificity / Sensitivity

Pan-Cadherin (28E12) Rabbit mAb detects endogenous levels of total cadherin proteins.

Source / Purification

Monoclonal antibody is produced by immunizing rabbits with a synthetic peptide (KLH-coupled) corresponding to a conserved region of human N-, R-, E- and P-Cadherin.

Western Blotting

Western Blotting

Western blot analysis of extracts from various cell lines, using Pan-Cadherin (28E12) Rabbit mAb.

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 which are found in adherens junctions (AJ), 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). Unlike β- and γ-catenin, p120 regulates cadherin adhesive activity and trafficking rather than having a structural role in the junctional complex (1-4). E-cadherin is considered an acting 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 over-expression of MMP-9 and cellular invasion (3). In endothelial cells, VE-cadherin signaling, expression and localization are correlated with vascular permeability and tumor angiogenesis (5,6). 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

Rabbit Monoclonals Produced Using Epitomics® Technology, U.S. Patent No. 5,675,063.

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