Cell Signaling Technology

Product Pathways - Cytoskeletal Signaling

M-Cadherin Antibody #45863

No. Size Price
45863S 100 µl ( 10 western blots ) ¥3,100.00 现货查询 购买询价
45863 carrier free & custom formulation / quantityemail request
Applications Dilution Species-Reactivity Sensitivity MW (kDa) Isotype
W 1:1000 Human,Mouse, Endogenous 130 Rabbit

Species cross-reactivity is determined by western blot.

Applications Key: W=Western Blotting,

Specificity / Sensitivity

M-cadherin recognizes endogenous levels of total M-cadherin protein. This antibody also cross-reacts with a number of unidentified proteins between 40 kDa and 95 kDa.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Arg434 of mouse M-cadherin protein. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from U87, RD, and C2C12 cells using M-Cadherin Antibody.


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 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).

M-cadherin is a cell-cell adhesion molecule expressed in satellite cells, a collection of adult stem cells/myogenic progenitors found in mature muscle tissue (9). Research studies indicate that M-cadherin may be involved in the recognition and fusion of adjacent cells, and may play an important role in activating satellite cell division (10).

  1. Wheelock, M.J. and Johnson, K.R. (2003) Annu Rev Cell Dev Biol 19, 207-35.
  2. Christofori, G. (2003) EMBO J 22, 2318-23.
  3. Hazan, R.B. et al. (2004) Ann N Y Acad Sci 1014, 155-63.
  4. Bryant, D.M. and Stow, J.L. (2004) Trends Cell Biol 14, 427-34.
  5. Rabascio, C. et al. (2004) Cancer Res 64, 4373-7.
  6. Yamaoka-Tojo, M. et al. (2006) Arterioscler Thromb Vasc Biol 26, 1991-7.
  7. Patel, I.S. et al. (2003) Int J Cancer 106, 172-7.
  8. Sanders, D.S. et al. (2000) J Pathol 190, 526-30.
  9. Irintchev, A. et al. (1994) Dev Dyn 199, 326-37.
  10. Marti, M. et al. (2013) J Cell Sci 126, 5116-31.

Application References

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Companion Products

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

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